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TABLE OF CONTENTS

Nephrology
1. Anatomy & Embryology
2. Fluid & Filtration Physiology
3. Nephron Transporters
4. Renin-Angiotensin-Aldosterone System
5. Electrolytes
6. Acid-Base Physiology
7. Pathology Diagnostics
8. Nephrotic Syndromes
9. Nephritic Syndromes
10. Nephrolithiasis
11. Urinary Incontinence
12. Kidney Injury
13. Inflammatory
Inflammation Conditions & Malignancy
14. Cystic Kidney Disease
15. Renal Pharmacology
REVIEW OUTLINE

Nephrology:
1. Embryology
A. Pronephros
B. Mesonephros

Anatomy & 2.
C. Metanephros
Developmental Anomalies
A. Potter Sequence

Embryology B. Horseshoe kidney

C. Solitary Functioning Kidney
D. Duplex Collecting System
E. Posterior Urethral Valves
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F. Vesicoureteral reflux
3. Anatomy
A. Renal Cortex
B. Renal Medulla
C. Arterial Supply
D. Additional Structures
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Embryology
● Pronephros:
● Formed at ~3rd-4th week
● Degenerates to become mesonephros
● Mesonephros:
● Formed at ~4 weeks
● Kidney for 1st trimester
● In males, structures persists as the Wolffian duct
■ Forms internal male sex organs (ductus deferens & epidydimis; not the prostate)
● Metanephros:
● Formed at ~5 weeks; permanent kidney
● Nephrogenesis completed at ~36 weeks
● Ureteric bud (metanephric diverticulum): Collecting duct, renal calyces, renal pelvis, ureter
■ Ureteric bud developmental failure → Renal agenesis
● Metanephric mesenchyme (metanephric blastema): Glomerulus, PCT, LoH, DCT (not collecting duct)
■ Abnormal interaction with ureteric bud → Multicystic dysplastic kidney
● Ureteropelvic junction (UPJ)
■ Final structure to canalize; failure → obstruction/hydronephrosis
■ Usually only affects one kidney
■ ↑ Risk of kidney stones & urinary tract infections (UTIs)
 Nephrology: Anatomy & Embryology Bootcamp.com

Developmental Anomalies P - Pulmonary Hypoplasia

O - Oligohydramnios
● Potter Sequence: T - Twisted Face
● Oligohydramnios → ↓ Amniotic fluid ingestion → Intrauterine compression → Fetal deformities T - Twisted Skin
● Internal deformities (e.g., pulmonary hypoplasia); External deformities (e.g., facial and limb abnormalities) E - Extremity Involvement
● Associated with renal agenesis, PUV, placental insufficiency, ARPKD R - Renal Involvement
● Horseshoe kidney:
● Fusion of inferior poles → Inhibited renal ascension by inferior mesenteric a. → Kidney remains inferiorly displaced
■ Typically normal kidney function
■ ↑ Risk in trisomes (13, 18, 21) and Turner syndrome (45,XO)
■ Associated with hydronephrosis, infection, nephrolithiasis, renal cancer
● Solitary Functioning Kidney:
● Multicystic dysplastic kidney (functional) AfraTafreeh.com
■ Failure of ureteric bud differentiation → Non-functioning cystic kidney (Unilateral = asymptomatic)
■ Bilateral = Potter sequence presentation
● Renal agenesis (anatomical)
■ Failure of ureteric bud development → Absent kidney & ureter (Unilateral = asymptomatic)
■ Bilateral = Potter sequence presentation
● Duplex Collecting System:
● Duplication of collecting duct system (Complete vs. incomplete)
● Associated with VUR, ureteral obstruction, ↑ Risk of UTIs
● Posterior Urethral Valves:
● Posterior urethra membrane remnant (males) → Bladder outlet obstruction
● Associated with bilateral hydronephrosis, thickened bladder walls, oligohydramnios (severe obstruction)
● Vesicoureteral Reflux:
● Primary VUR: Abnormal UVJ insertion → Retrograde urine flow
● Secondary VUR: ↑ Bladder pressure → Retrograde urine flow
● Associated with ↑ Risk of UTIs & renal complications (CKD, scarring); < 2 years old
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Anatomy
● Renal Cortex:
● Glomerulus, proximal convoluted tubule (PCT), distal convoluted tubule (DCT), cortical collecting duct
● Renal Medulla:
● Renal pyramids, renal columns, Loop of Henle, medullary collecting duct
● Arterial Supply:
● Renal a. → Segmental a. → Interlobar a. → Arcuate a. → Interlobular a. → Afferent a. → Glomerulus
● Glomerulus → Efferent a. → Peritubular capillaries/vasa recta → Outflow via venous pathway → Renal v.
● Juxtaglomerular Apparatus:
● Macula densa (DCT), juxtaglomerular cells
● Juxtaglomerular cells (afferent arterioles): Secretes renin
● Mesangial cells: Removes debris
● Additional Structures:
● Left renal vein: Longer than right, drains left gonadal v. (vs. right gonadal vein)
■ Nutcracker syndrome: Compression of left renal v. by superior mesenteric artery (SMA)
○ Presentation: Abdominal pain, hematuria, varicocele
● Ureters: Under vas deferens/uterine a. & over common iliac a. (“Water under the bridge”)
○ Complication: Damage to ureter during gynecologic procedures due to close proximity
● Bladder: Ureteral orifice (trigone), internal urethral sphincter (involuntary), external urethral sphincter (voluntary)
■ Detrusor muscle (autonomic)
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Macula densa
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Juxtaglomerular cells
& Mesangial cells Proximal
convoluted
tubule
Renal nerve

Afferent arteriole
(a)
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REVIEW OUTLINE

Nephrology:
1. Overview
2. Fluid Compartments
● A. 60-40-20 Rule

Fluid & 3.
●
Starling Forces
A. Hydrostatic Pressure

Filtration
● B. Oncotic Pressure
● C. Net Fluid Flow
4. Fluid Shifts

Physiology ●
●
5.
A. Osmosis
B. Examples
Glomerular Filtration
● A. Components
● B. Barriers
Nephrology: Fluid & Filtration Physiology Bootcamp.com

Fluid Compartments

60-40-20 Rule:
● Approximately 60% total water, 40% intracellular fluid, 20% extracellular fluid
○ ICF: K+, Mg2+, Phosphate (ATP!)
○ ECF: Na+, Cl-, Bicarbonate, Albumin
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Starling Forces

Hydrostatic Pressure:
● Pushes fluid out across the capillary
○ Pc = Capillary hydrostatic pressure
○ Pi = Interstitial hydrostatic pressure

Oncotic Pressure:
● Pulls fluid in across the capillary Jv = net fluid flow = Kf [(Pc − Pi) − σ(πc − πi)]
○ πc = Plasma oncotic pressure
○ πi = Interstitial oncotic pressure Kf = capillary permeability to fluid
σ = capillary permeability to protein
(reflection coefficient)
Examples:
● Heart Failure = ↑ Pc
● Lymphedema = ↑ πi
● Malnutrition/Liver failure/Nephrotic syndrome = ↓ πc
Nephrology: Fluid & Filtration Physiology Bootcamp.com

Fluid Shifts

Osmosis:
● Osmosis = Water moves from low → high solute concentration
● Osmolarity drives fluid shifts

Examples: AfraTafreeh.com
● Hemorrhage
○ No Δ ICF, ↓ ECF
● Saline infusion
○ No Δ ICF, ↑ ECF
● Mannitol infusion
○ ↓ ICF, ↑ ECF
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Glomerular Filtration

Components:
● Fenestrated capillary endothelium
● Basement membrane (type IV collagen)
● Epithelial Podocytes

Barriers:
● Size
● Charge (negatively charged)
REVIEW OUTLINE

Nephrology:
1. Overview 9. Autoregulation
2. Terminology ● A. Myogenic Mechanism
● A. Secretion ● B. Tubuloglomerular Feedback

Fluid & ●
●
B. Excretion
C. Reabsorption
3. Filtration Fraction
Filtration ●
4.
A. Calculation
Variables Affecting Filtration

Physiology ●
●
●
A. Physiologic Dynamics
B. Effects of Prostaglandins
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C. Effects of Angiotensin
5. Renal Clearance
● A. Definition
● B. Equation
6. Renal Plasma Flow
● A. Definition
● B. Equation
7. Renal Blood Flow
● A. Definition
● B. Equation
8. Glucose Clearance
● A. Normal
● B. Abnormal
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Terminology
● Secretion: substance moved from the blood into the nephron

● Excretion: substance removed from the body

● Reabsorption: substance reabsorbed from the tubules back into the blood
 Nephrology: Fluid & Filtration Physiology Bootcamp.com

Filtration Fraction
● Calculation:
● Filtration Fraction (FF) = GFR / RPF
● GFR is estimated w/ creatinine clearance
○ Normal FF ~ 20%
○ Decreases with age
● RPF estimated w/ PAH clearance

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Variables Affecting Filtration

Physiologic Dynamics:
● Afferent arteriole constriction
○ ↓ GFR; ↓ RPF; No Δ FF
● Efferent arteriole constriction
○ ↑ GFR; ↓ RPF; ↑ FF
● ↑ Plasma oncotic pressure
○ ↓ GFR; No Δ RPF; ↓ FF
● ↓ Plasma oncotic pressure
○ ↑ GFR; No Δ RPF; ↑ FF
● Ureteral constriction
○ ↓ GFR; No Δ RPF; ↓ FF
● Dehydration
○ ↓ GFR; ↓↓ RPF; ↑ FF

Prostaglandins Effects:
● (PDA) Prostaglandins Dilates Afferent arteriole

Angiotensin II Effects:
● (ACE) Angiotensin Constricts Efferent arteriole
 Nephrology: Fluid & Filtration Physiology Bootcamp.com

Renal Clearance
● Definition:
● Volume of plasma cleared of a substance in a defined amount of time

● Equation:
Cx = Clearance of substance ‘X’
Ux = Urine concentration of substance ‘X’
Cx = (UxV)/Px V = Flow rate of urine
Px = Plasma concentration of substance ‘X’

● C = GFR → No net reabsorption or secretion (Inulin)

● C > GFR → Net secretion (PAH, estimates RPF) AfraTafreeh.com
● C < GFR → Net reabsorption (Glucose)
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Renal Plasma Flow

● Definition:
● Volume of plasma flowing through the kidney in a defined amount of time
● Estimated with para-aminohippuric acid (PAH)
○ Nearly 100% excreted (filtered + secreted)

● Equation:

eRPF = (Upah * V)/Ppah

 Nephrology: Fluid & Filtration Physiology Bootcamp.com

Renal Blood Flow

● Definition:
● Volume of blood flowing through the kidney in a defined amount of time
● ~ 20-25% of cardiac output

● Equation:

RPF = RBF * (1 - Hct)

RBF = RPF / (1 - Hct)

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Glucose Clearance
● Normal:
● Ranges from ~ 60-120 mg/dL
● ~100% reabsorbed in PCT
■ SGLT2
● ↑ filtration in pregnancy
■ ↑ GFR

● Abnormal:
● Glucosuria begins at ~ 200 mg/dL
● Splay phenomenon
 Nephrology: Fluid & Filtration Physiology Bootcamp.com

Autoregulation
● Myogenic Mechanism:
● ↑ Stretch from ↑ BP → Afferent arteriole vasoconstriction
● Allows maintenance of GFR & RPF

● Tubuloglomerular Feedback:
● Macula densa senses ↑ NaCl → Afferent arteriole vasoconstriction
● Allows maintenance of GFR & RPF

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REVIEW OUTLINE

Nephrology: 1. Proximal Convoluted Tubule

A. Glucose & Amino Acids

Nephron
B. Bicarbonate
C. Other Transporters
D. Hormone Effects

Transporters
E. Renal Tubular Defect
2. Loop of Henle
A. Thin Descending Loop of Henle
B. Thick Ascending Loop of Henle
C. Renal Tubular Defect
3. Distal Convoluted Tubule
A. Function
B. Hormone Effects
C. Renal Tubular Defect
4. Collecting Duct
A. Function
B. Hormone Effects
C. Types of Cells
D. Renal Tubular Defect
 Nephrology: Nephron Transporters Bootcamp.com

Proximal Convoluted Tubule

● Glucose & Amino Acids:
● Reabsorbs ~ 100%
● Na+/Glucose cotransporter
■ Saturated at ~ 350 mg/dL
■ Blocked by SGLT-2 inhibitors
● Bicarbonate:
● Reabsorbed as CO2 + H2O on apical side
● Reabsorbed ast HCO3- & Na+ on basolateral side
● Key enzyme: Carbonic Anhydrase
● Other Transporters: AfraTafreeh.com
● PCT reabsorbs most Na+, Cl-, PO43-, K+, HCO3-
● Na+/H+ & Na+/K+ counter transport
● Na+/HCO3- & Na+/PO43-cotransport
● Hormone Effects:
● Parathyroid Hormone (PTH) = ↓ Na+/PO43- cotransport
■ ↑ PO43- excretion
● Angiotensin II = ↑ Na+/H+ counter transport
■ ↑ Na+, HCO3- , H2O reabsorption
● Renal Tubular Defect:
● Fanconi syndrome
■ Reabsorption defect of all substances
■ Metabolic acidosis, hypophosphatemia, hypokalemia
■ Various causes
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Loop of Henle
● Thin Descending Loop of Henle:
● Passively reabsorbs H2O
■ Driven by medullary hypertonicity
● Impermeable to Na+
● Concentrates urine (hypertonic)
● Thick Ascending Loop of Henle:
● Actively reabsorbs most Na+, Cl-, K+
■ NKCC transporter
● Paracellular reabsorption of Mg2+, Ca2+
■ + electrochemical potential due to K+
● Impermeable to H2O
● Dilutes urine (hypotonic)
● Renal Tubular Defect:
● Bartter Syndrome
■ Reabsorption defect (NKCC)
● Similar to loop diuretic use
■ Metabolic Alkalosis, hypercalciuria, hypokalemia
■ Autosomal recessive
 Nephrology: Nephron Transporters Bootcamp.com

Distal Convoluted Tubule

● Function:
● Impermeable to H2O
● Reabsorbs some Na+, Cl-, Mg2+, Ca2+
● Site of LOWEST osmolarity
● Hormone Effects:
● PTH = ↑ Ca2+ reabsorption (↑ Ca2+/Na+ transporter)
● Renal Tubular Defect:
● Gitelman Syndrome
■ Reabsorption defect of NaCl
● AfraTafreeh.com
Similar to thiazide diuretic use
■ Metabolic alkalosis, hypocalciuria, hypomagnesemia, hypokalemia
■ Autosomal recessive
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Collecting Duct
● Function:
● Reabsorbs Na+, H2O, urea
● Secretes K+ and H+
● Hormone Effects:
● Aldosterone = ↑ Na+/K+ pump, ENaC, H+ & K+ secretion
● ADH = binds to V2 receptor = ↑ free H2O reabsorption
■ Aquaporin channels
● Types of Cells:
● Principal cell = Primary site of Na+ reabsorption
● ⍺-intercalated = Secretes acid, reabsorbs bicarbonate
● β-intercalated = Reabsorbs acid, secretes bicarbonate
● Renal Tubular Defect:
● Liddle Syndrome
■ Gain of function mutation = ↑ Na+ reabsorption
■ Metabolic alkalosis, hypertension, hypokalemia
■ Autosomal dominant
● Syndrome of Apparent Mineralocorticoid Excess
■ Loss of function mutation = ↓ 11ß-HSD = ↑ cortisol = ↓ Aldosterone
■ Metabolic alkalosis, hypertension, hypokalemia
■ Autosomal recessive
REVIEW OUTLINE

Nephrology: 1.
●
Overview
A. Primary Goals

Renin-
● B. Primary Mechanism
● C. Primary Activators
2. Angiotensin II Effects

Angiotensin- ●
●
●
A. Systemic Vasoconstriction
B. Efferent Arteriole Vasoconstriction
C. Aldosterone Secretion

Aldosterone ●
●
D. ADH Release
E. PCT Stimulation
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3. Natriuretic Peptides
System ●
●
A. Systemic Vasoconstriction
B. Molecular Mechanism
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Overview
● Primary Goals:
● Regulate blood pressure
● Balance fluid & electrolytes
● Primary Mechanism:
● Angiotensinogen → Angiotensin I
■ Key enzyme: Renin
● Angiotensin I → Angiotensin II
■ Key enzyme: ACE
● Primary Activators:
● ↓ Blood pressure
● ↓ NaCl filtrate
● ↑ Sympathetic tone (β1-receptors)
 Nephrology: RAAS Bootcamp.com

Angiotensin II Effects
● Systemic Vasoconstriction:
● ATII binds AT1 receptor
● ↑ BP
● Efferent Arteriole Vasoconstriction:
● ↑ Filtration fraction to preserve GFR
● Aldosterone Secretion:
● ↑ Na+ reabsorption & H+/K+ excretion
■ ↑ Na+/K+ pump
■ ↑ ENaC
■ ↑ K+ conductance AfraTafreeh.com
● ADH Release:
● ↑ H2O reabsorption
■ Aquaporins
● PCT Stimulation:
● ↑ Na+/H+ pump
■ ↑ Na+, H2O, HCO3- reabsorption
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Natriuretic Peptides
● Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP):
● Released from cardiac myocytes
● Inhibits RAAS
● Relaxation of vascular smooth muscle
● Molecular Mechanism:
● ↑ cGMP = dilates afferent arteriole
■ ↓ Renin, ↑ GFR
REVIEW OUTLINE

Nephrology: 1. Sodium
A. Basic Physiology

Electrolytes
B. Hypernatremia
C. Hyponatremia
2. Potassium
A. Basic Physiology
B. Hyperkalemia
C. Hypokalemia
3. Calcium
A. Basic Physiology
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B. Hypercalcemia
C. Hypocalcemia
4. Magnesium
A. Basic Physiology
B. Hypermagnesemia
C. Hypomagnesemia
5. Phosphate
A. Basic Physiology
B. Hyperphosphatemia
C. Hypophosphatemia
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Sodium
● Basic Physiology:
● Normal range = 135-145 mEq/L
● Major determinant of volume status & serum osmolality (~285 mOsm/kg)
■ Serum osmolality = (2Na) + (Glucose/18) + (BUN/2.8)
● Hypernatremia:
● 1° causes: Diabetes insipidus, hyperaldosteronism, ↓ H2O intake, ↑ H2O loss (e.g. diuretics, diarrhea, vomiting, burns)
● Presentation: Dehydration symptoms, polyuria, polydipsia, seizures/coma (severe)
● Work-up: Water deprivation test +/- desmopressin (ADH analog)
■ Central DI - Lack of ADH
■ Nephrogenic DI - Resistance to ADH
● Management: Fluid replacement, thiazide diuretics & NSAIDs (Nephrogenic DI), desmopressin (Central DI)
● Caution! “From high to low, your brains will blow” (Cerebral edema/herniation)
● Hyponatremia:
● 1° causes: Based on plasma osmolality and clinical volume status
■ Hypertonic hyponatremia: Hyperglycemia, mannitol
■ Isotonic hyponatremia: “Pseudohyponatremia” → Laboratory artifact, ↑ Lipids/protein
■ Hypotonic hyponatremia: True hyponatremia
● Hypervolemic: CHF, cirrhosis, ↓ urine output, ↓ protein (e.g. nephrotic syndrome)
● Euvolemic: SIADH, ↓ NaCl intake (“tea & toast” diet), psychogenic polydipsia
● Hypovolemic: ↓ volume status, diuretics, Addison’s disease
● Presentation: Headache, N/V, seizures/coma (severe)
● Management: Based on clinical volume assessment
■ Hypervolemic hyponatremia: Fluid restriction +/- loop diuretic
■ Euvolemic hyponatremia: Fluid restriction +/- hypertonic saline, salt tablets, ADH antagonist (SIADH)
■ Hypovolemic hyponatremia: Isotonic saline
● Caution! “From low to high, your pons will die” (Osmotic demyelination syndrome)
 Nephrology: Electrolytes Bootcamp.com

Potassium
● Basic Physiology:
● Normal range = 3.5-5.0mEq/L
● Maintains fluid/electrolyte balance
● Hyperkalemia:
● 1° causes: Intracellular release (TLS, rhabdomyolysis), medications (ACEi, ARBs, potassium-sparing diuretics), ↓
excretion
● 2° causes: ↓ insulin, β-blockers, digoxin toxicity, acidosis
● Presentation: Cardiac abnormalities/arrhythmias, weakness
● ECG findings: Peaked T wave, widened QRS
● AfraTafreeh.com
Management: IV calcium gluconate, insulin + glucose, β-agonist, cation exchange resins, dialysis (severe)
● Hypokalemia:
● 1° causes: GI loss (vomiting/diarrhea), renal loss (RTA type I & II), medications (diuretics)
● 2° causes: Hypomagnesemia, alkalosis
■LossROMK
of ROMK inhibition
inhibition → ↑→↑ urinary
urinary K+ loss
K+ loss
● Presentation: Cardiac abnormalities/arrhythmias, weakness
● ECG findings: U wave, flattened T wave
● Management: Potassium and/or magnesium supplementation as necessary, potassium-sparing diuretics
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Calcium
● Basic Physiology:
● Total serum calcium ~8.5-10.0 mg/dL
● Foundational component of bone & cellular membrane stabilization
● Exists in two primary forms: Albumin bound, ionized free calcium (active)
■ Free Ca2+ exerts physiologic effects
● ↑ H+ → ↑ Free Ca2+
● ↓ H+ → ↓ Free Ca2+
● Homeostasis: PTH, calcitonin, calcitriol
● Hypercalcemia:
● 1° causes: Hyperparathyroidism, sarcoidosis, malignancy
● 2° causes: Milk-alkali syndrome, hypervitaminosis D
● Presentation: Often asymptomatic, recurrent kidney stones, polyuria
■ “Stones, bones, groans & psychiatric overtones”
● Management: Treat underlying cause. If severe: IV NS, calcitonin, bisphosphonates
● Hypocalcemia:
● 1° causes: Hypoparathyroidism
● 2° causes: Hypomagnesemia, CKD, pancreatitis, ↓ Vitamin D
● Presentation: Tetany, seizures, prolonged QT interval
■ Trousseau’s sign - Hand spasm w/ inflation of BP cuff
■ Chvostek’s sign - Face spasm w/ tapping facial nerve
● Management: Mild (>7.5 mg/dL): PO supplementation; Severe (<7.5mg/dL): IV Calcium gluconate
■ Vitamin D & magnesium supplementation
 Nephrology: Electrolytes Bootcamp.com

Magnesium
● Basic Physiology:
● Involved in many physiologic reactions
● Inhibits ROMK channels
■ Hypokalemia persists in setting of hypomagnesemia
● Hypermagnesemia:
● 1° causes: Renal failure, rhabdomyolysis, ↑ oral intake
● Presentation: ↓ DTRs, cardiac abnormalities, hypocalcemia
● Management: Stop Mg2+ containing medications, NS + loop diuretics, calcium gluconate, dialysis (severe)
● Hypomagnesemia:
● AfraTafreeh.com
1° causes: GI loss, renal loss, drugs/medications, malnutrition
● Presentation: Tetany, torsades de pointes, hypocalcemia, hypokalemia
● Management: Magnesium supplementation
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Phosphate
● Basic Physiology:
● Foundational component of bone/teeth, signaling pathways, and ATP reactions
● Urinary buffer for H+
● Hyperphosphatemia:
● 1° causes: Renal failure, hypoparathyroidism, ↑ intake or release (TLS, rhabdomyolysis)
● Presentation: Kidney stones, hypocalcemia, metastatic calcifications (“Calciphylaxis”)
■ PO43- precipitates Ca2+
● Management: Phosphate binders, ↓ intake, dialysis (severe)
■ Calcium carbonate, aluminum hydroxide, sevelamer
● Hypophosphatemia:
● 1° causes: Primary hyperparathyroidism, refeeding syndrome, Fanconi syndrome
● Presentation: Weakness, bone loss, osteomalacia/rickets
● Management: Phosphate supplementation
REVIEW OUTLINE

7. RTA type 1
Nephrology: 1. Overview
A. Fundamental Principles
B. Important Formulas
A. Pathophysiology
B. Common Causes

Acid-Base 2.
C. How To Determine Acid-Base Disorder
Acid-Base Examples 8.
C. Management
RTA type 2
A. Example 1 A. Pathophysiology

Physiology B. Example 2
C. Example 3
B. Common Causes
C. Management
D. Example 4 9. RTA type 4
3. Metabolic Acidosis A. Pathophysiology
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A. Primary Mechanism B. Common Causes
B. Common Causes C. Management
4. Metabolic Alkalosis
A. Primary Mechanism
B. Common Causes
5. Respiratory Acidosis
A. Primary Mechanism
B. Common Causes
6. Respiratory Alkalosis
A. Primary Mechanism
B. Common Causes
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Nephrology: Acid-Base Physiology Bootcamp.com

Overview
● Fundamental Principles:
● Acidosis = ↑ H+; Alkalosis = ↓ H+
● Arterial pH ~7.35-7.45
■ Normal HCO3- ~ 24 mEq/L
■ Normal pCO2 ~ 40 mmHg
● Tightly regulated by two primary mechanisms
■ Kidneys: HCO3- production, H+ excretion
■ Lungs: CO2 excretion
● Important Formulas:
● Henderson-Hasselbalch Equation
■ pH = 6.1 + log (HCO3-/0.03*pCO2)
● Winter’s Formula
■ pCO2 = 1.5(HCO3-) + 8 +/- 2
● Anion Gap
■ AG = Na+ - HCO3- - Cl-
● How To Determine Acid-Base Disorder:
(1) Assess pH (Acidic vs. Alkalotic)
(2) Assess HCO3- (>/< 24 mEq/L) & pCO2 (>/< 40 mmHg)
(3) Determine primary disorder
(4) Calculate anion gap (Metabolic acidosis)
(5) Assess for compensation
 Nephrology: Acid-Base Physiology Bootcamp.com

Acid-Base Examples
● Example 1:
● pH = 7.31
● HCO3- = 28 mEq/L
● pCO2 = 48 mmHg
● Example 2:
● pH = 7.25
● HCO3- = 11 mEq/L How To Determine Acid-Base Disorder:
● pCO2 = 24 mmHg (1) Assess pH (Acidic vs. Alkalotic)
● Example 3: (2) Assess HCO3- (>/< 24 mEq/L) & pCO2 (>/< 40 mmHg)
● pH = 7.15 AfraTafreeh.com (3) Determine primary disorder
● HCO3- = 9 mEq/L (4) Calculate anion gap (Metabolic acidosis)
● pCO2 = 38 mmHg (5) Assess for compensation
● Example 4:
● A 55-year-old patient with a past medical history of poorly controlled
type II DM, CKD, and HTN presents to the ED with worsening nausea,
abdominal pain, and confusion. Serum labs are obtained and the ABG
shows a pH of 7.27 and pCO2 of 25 mmHg. Which of the following is Na+ 138
the most likely underlying cause of this patient’s presentation?
A) Diarrhea K+ 4.9
B) Tachypnea
C) Hyperchloremia Cl- 110
D) Uremia
HCO3- 10
 AfraTafreeh.com
Nephrology: Acid-Base Physiology Bootcamp.com

Metabolic Acidosis
● Primary Mechanism:
● ↓ pH due to ↑ H+ and/or ↓ HCO3- → ↓ pCO2 (compensation)
● Common Causes:
● ↑ Anion gap (>12 mEq/L)
■ Methanol (Formic acid) – Visual symptoms
■ Uremia – Kidney disease
■ Diabetic ketoacidosis (DKA) – Type 1 diabetic
■ Propylene glycol – No visual symptoms; CNS depression
■ Iron or Isoniazid – Over ingestion
■ Lactic acidosis – Various causes
■ Ethylene glycol (oxalic acid) – Sweet breath smell; Calcium oxalate stones
■ Salicylates (delayed) – Uncoupled oxidative phosphorylation
● Normal anion gap (8-12 mEq/L)
■ Hyperchloremia/Hyperalimentation – HCO3- shifts into cells/↑ HCL
■ Addison disease – ↓ H+ secretion
■ Renal tubular acidosis – Varies
■ Diarrhea – Loss of HCO3-
■ Acetazolamide – ↓ Reabsorption of HCO3-
■ Spironolactone – ↓ H+ secretion
■ Saline – ↓ H+ excretion; HCO3- shifts into cells
 Nephrology: Acid-Base Physiology Bootcamp.com

Metabolic Alkalosis
● Primary Mechanism:
● ↑ pH due to ↓ H+ and/or ↑ HCO3- → ↑ pCO2 (compensation)
● Common Causes:
● Chloride-responsive (Normal urine Cl-)
■ Hypovolemia – Volume contraction alkalosis
■ Loop or thiazide diuretics – Volume contraction alkalosis
■ Vomiting/Gastric suctioning – ↓ HCl/K+
● Chloride-resistant (↑ urine Cl-)
■ Hyperaldosteronism – ↑ H+ secretion
■ AfraTafreeh.com
Renal tubular defects (Except Fanconi syndrome) – Volume contraction
alkalosis
■ Loop or thiazide diuretics – Volume contraction alkalosis
 AfraTafreeh.com
Nephrology: Acid-Base Physiology Bootcamp.com

Respiratory Acidosis
● Primary Mechanism:
● ↓ pH due to ↑ pCO2 → ↑ HCO3- (compensation)
● Common Causes:
● Hypoventilation
■ Lung disease – Pulmonary edema
■ Obstruction – Asthma, COPD
■ CNS depressants – Opioids, trauma
■ Respiratory muscle dysfunction – Myasthenia gravis, ALS, MS, Guillain-Barré syndrome
 Nephrology: Acid-Base Physiology Bootcamp.com

Respiratory Alkalosis
● Primary Goals:
● ↑ pH due to ↓ pCO2 → ↓ HCO3- (compensation)
■ ↑ Respiratory rate (RR) and/or ↑ Tidal volume (TV)
● Common Causes:
● Hyperventilation
■ Anxiety/panic attack
■ Cancer
■ High-Altitude, Hypoxemia
● ↓ pO2 = ↑ RR
● AfraTafreeh.com
Acclimatization: 2,3-Bisphosphoglycerate, acetazolamide
■ Pain
■ Pregnancy
■ Pulmonary Embolism
■ Salicylates (acute)
● Stimulates medulla = ↑ RR
 AfraTafreeh.com

Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis

pH
↓ ↑ ↓ ↑

pCO2
↓ ↑ ↑ ↓

HCO3-
↓ ↑ ↑ ↓

Hyperventilation Hypoventilation ↑ HCO3- reabsorption ↓ HCO3- reabsorption

Compensation
 Nephrology: Acid-Base Physiology Bootcamp.com

RTA Type 1 (Distal)

● Pathophysiology:
● ↓ Secretion H+ in distal tubule → ↓ HCO3- formation → ↓ Serum HCO3- → Normal AG metabolic acidosis
● ↓ Serum K+
● Urine pH: >5.5 (alkaline)
● ↑ Risk for nephrolithiasis, rickets/osteoporosis
● Common Causes:
● Autoimmune diseases (eg, Sjögren’s syndrome, RA, SLE)
● Medications (e.g., amphotericin B, analgesics)
● Management:
● Sodium bicarbonate AfraTafreeh.com
 AfraTafreeh.com
Nephrology: Acid-Base Physiology Bootcamp.com

RTA Type 2 (Proximal)

● Pathophysiology:
● PCT dysfunction → ↓ HCO3- reabsorption → ↑ Urinary HCO3- excretion → Normal AG metabolic acidosis
● ↓ Serum K+
● Urine pH: <5.5 if below reabsorption threshold; ≥5.5 if HCO3- above reabsorption threshold
● ↑ Risk for hypophosphatemic rickets
● Common Causes:
● Fanconi syndrome, multiple myeloma, heavy metal poisoning (e.g., mercury, lead, cadmium)
● Medications (e.g., acetazolamide, topiramate)
● Management:
● Sodium bicarbonate, potassium citrate
 Nephrology: Acid-Base Physiology Bootcamp.com

RTA Type 4 (Hyperkalemic)

● Pathophysiology:
● ↓ Aldosterone or ↑ Aldosterone resistance → Hyperkalemia → ↓ NH3 produced in PCT → ↓ NH4+ excretion → Normal AG metabolic acidosis
● ↑ Serum K+
■ ↑ K+ = ↓ NH3 production
● Urine pH: <5.5
● Common Causes:
● ↓ Aldosterone
■ Hyporeninemic hypoaldosteronism
● Diabetic nephropathy
■ AfraTafreeh.com
Primary adrenal insufficiency (Addison’s)
● Aldosterone Resistance
■ K+ sparing diuretics
● Spironolactone, eplerenone, amiloride, triamterene
■ Trimethoprim-sulfamethoxazole
● Management:
● Fludrocortisone, furosemide
 AfraTafreeh.com
REVIEW OUTLINE

Nephrology: 1. Nomenclature
A. Primary vs Secondary
B. Focal vs Diffuse

Pathology C. Membranous
D. Proliferative
2. Urinalysis Basics
Diagnostics A. Gross Urine
B. Urine Dipstick
C. Urine Sediment
3. Urinary Casts
A. Fatty Casts
B. Granular Casts
C. Hyaline Casts
D. Red Blood Cell (RBC) Casts
E. White Blood Cell (WBC) Casts
F. Waxy Casts
 Nephrology: Pathology Diagnostics Bootcamp.com

Nomenclature
● Primary vs Secondary:
● Primary = Direct disease of glomerulus
■ Ex: Minimal change disease (MCD)
● Secondary = Systemic disease affecting glomerulus
■ Ex: SLE, diabetic glomerulonephropathy
● Focal vs Diffuse:
● < 50% glomerular involvement
■ Ex: FSGS
● > 50% glomerular involvement
■ Ex: DPGN AfraTafreeh.com
● Membranous:
● Thickened glomerular basement membrane (GBM)
■ Ex: Membranous nephropathy
● Proliferative:
● ↑ Number of cells
■ Ex: Membranoproliferative glomerulonephritis
 AfraTafreeh.com
Nephrology: Pathology Diagnostics Bootcamp.com

Urinalysis Basics
● Gross Urine:
● Color:
■ Normal → Yellow/Amber
■ Red → Hematuria, medications, porphyria
■ Black → Alkaptonuria
● Turbidity:
■ Cloudiness = potential sign of infection
● Urine Dipstick:
● pH (Normal ~4.5-8)
● Specific gravity (Normal ~ 1.005-1.030)
● Glucose → Diabetes mellitus
● Protein → Diabetic or hypertensive nephropathy, nephrotic syndrome (>3.5g/day)
● Ketones → DKA
● Leukocyte esterase ⨁ Suggestive of UTI
● Nitrite ⨁ Suggestive UTI
● Heme ⨁ Suggestive of hemoglobinuria, myoglobinuria, or hematuria
■ Confirm with RBC microscopy
● Urine Sediment:
● Microscopic:
■ WBCs, RBCs, acanthocytes
● Urinary casts
 Nephrology: Pathology Diagnostics Bootcamp.com

Urinary Casts
● Fatty Casts:
● Nephrotic syndrome
■ “Maltese cross”
● Granular Casts:
● Acute tubular necrosis
■ “Muddy brown”
● Hyaline Casts:
● Nonspecific
■ Tamm-Horsfall mucoprotein
○ AfraTafreeh.com
UTI prevention via tubular cell secretion
● Red Blood Cell (RBC) Casts:
● Glomerulonephritis, hypertensive emergency
● White Blood Cell (WBC) Casts:
● Acute pyelonephritis, transplant rejection, tubulointerstitial nephritis
● Waxy Casts:
● End-stage renal disease (ESRD)/Chronic kidney disease (CKD)
 AfraTafreeh.com
REVIEW OUTLINE

Nephrology: 1. Glomerular Disease Overview 6.

A. Glomerular Filtration Barrier
B. Nephrotic Syndromes
Diabetic Glomerulonephropathy
A. Pathophysiology
B. Diagnosis

Nephrotic 2.
C. Nephritic Syndromes
Minimal Change Disease
C. Management
D. Associations
A. Pathophysiology

Syndromes B. Diagnosis
C. Management
D. Associations
3. Focal Segmental Glomerulosclerosis
A. Pathophysiology
B. Diagnosis
C. Management
D. Associations
4. Membranous Nephropathy
A. Pathophysiology
B. Diagnosis
C. Management
D. Associations
5. Amyloid Nephropathy
A. Pathophysiology
B. Diagnosis
C. Management
D. Associations
 Nephrology: Nephrotic Syndromes Bootcamp.com

Glomerular Disease Overview

● Glomerular Filtration Barrier:
● Podocytes, basement membrane, endothelium
● Nephrotic Syndromes:
● Pathophysiology: ↑ Cytokines → Podocyte effacement → Loss of (-) charge barrier
■ ↓ Albumin → Edema, proteinuria, dyslipidemia
■ ↓ Antithrombin III → Hypercoagulable state
■ ↓ Immunoglobulins → ↑ Risk for infection
● Classic findings: Frothy urine, edema, proteinuria (>3.5g/24h)
● Workup:
■ Urinalysis (Best initial test) AfraTafreeh.com
● 24h urine (>3.5g/24h)
● UPr/Cr (3.5:1)
■ Renal biopsy
● Nephritic Syndromes:
● Pathophysiology: Inflammation → GBM damage → Dysmorphic RBCs
■ Similar findings to nephrotic syndrome (Less proteinuria)
■ ↓ GFR, ↑ Cr (due to inflammation) → RAAS activation
● Classic findings: Hypertension, RBC casts, hematuria, acanthocytes, edema, proteinuria (<3.5g/24h)
● Workup:
■ Urinalysis
■ Renal biopsy
 AfraTafreeh.com
Nephrology: Nephrotic Syndromes Bootcamp.com

Minimal Change Disease

● Pathophysiology:
● ↑ Cytokines → Podocyte effacement → Loss of (-) charge barrier
● Diagnosis:
● Mostly clinical diagnosis
● Normal glomeruli on LM
● Podocyte effacement on EM
● Management:
● Prednisone (MCD responds well)
● Associations:
● Most common nephrotic syndrome in children
● Hodgkin lymphoma
● Upper respiratory infection (URI)
● Immunization
 Nephrology: Nephrotic Syndromes Bootcamp.com

Focal Segmental Glomerulosclerosis (FSGS)

● Pathophysiology:
● Damage to glomerular filtration barrier, sclerosis of glomeruli
● Diagnosis:
● Segmental sclerosis & hyalinosis on LM
● Podocyte effacement on EM
● Typically (-) IF; Possibly (+) for C1, C3, IgM
● Management:
● Prednisone (FSGS responds poorly), consider immunosuppressants
● Symptomatic management (RAAS inhibition)
● AfraTafreeh.com
Often progresses to chronic renal failure, if untreated
● Associations:
● Often idiopathic
● Congenital malformations
● Higher prevalence in African American & Hispanic populations
● Heroin use
● HIV
● Interferon treatment
● Sickle cell disease
 AfraTafreeh.com
Nephrology: Nephrotic Syndromes Bootcamp.com

Membranous Nephropathy
● Pathophysiology:
● Damage to glomerular filtration barrier → Immune complex deposition → Thickening of glomerular basement membrane
● Diagnosis:
● Antibody test for anti-PLA2R or renal biopsy
● GBM thickening on LM
● “Spike and dome” subepithelial deposits on EM
● (+) IF in “granular” appearance (Immune complex deposits)
● Management:
● Prednisone (MN responds poorly), cyclophosphamide
● Symptomatic management (RAAS inhibition)
● Associations:
● Often idiopathic
● ⊕ Serum anti-PLA2R antibody test
● Systemic lupus erythematosus (SLE)
● Solid tumors (e.g., Lung, prostate, colon cancer)
● Medications (e.g., NSAIDs, penicillamine, gold)
● Infections (e.g., Syphilis, Hep B, Hep C)
 Nephrology: Nephrotic Syndromes Bootcamp.com

Amyloid Nephropathy
● Pathophysiology:
● Buildup of extracellular amyloid proteins
● Diagnosis:
● Apple-green birefringence on congo red stain under polarized LM
● Amyloid fibrils on EM
● Management:
● Treat underlying cause
● Associations:
● Most commonly involves kidney
● Common in elderly patients AfraTafreeh.com
● Multiple myeloma (AL amyloid)
● Chronic inflammatory conditions/rheumatoid arthritis (AA amyloid)
● Dialysis-related (𝛃2 microglobulin)
 AfraTafreeh.com
Nephrology: Nephrotic Syndromes Bootcamp.com

Diabetic Glomerulonephropathy
● Pathophysiology:
● Hyperglycemia → Non-enzymatic glycation → Hyaline arteriosclerosis → Hyperfiltration → Glomerulosclerosis (scarring)
● Diagnosis:
● Eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson nodules), GBM thickening, and mesangial expansion on LM
● Management:
● Glucose control
● Symptomatic management (RAAS inhibition)
● Associations:
● Commonly leads to ESRD
● Additional organ involvement (e.g., retinopathy)
REVIEW OUTLINE

1. Poststreptococcal Glomerulonephritis 6. Alport Syndrome

Nephrology: A. Pathophysiology
B. Diagnosis
A. Pathophysiology
B. Diagnosis

Nephritic
C. Management C. Management
D. Associations D. Associations
2. Rapidly Progressive Glomerulonephritis

Syndromes A. Pathophysiology
B. Diagnosis
C. Management
D. Associations
3. Diffuse Proliferative Glomerulonephritis
AfraTafreeh.com
A. Pathophysiology
B. Diagnosis
C. Management
D. Associations
4. Membranoproliferative Glomerulonephritis
A. Pathophysiology
B. Diagnosis
C. Management
D. Associations
5. IgA Nephropathy (Berger Disease)
A. Pathophysiology
B. Diagnosis
C. Management
D. Associations
 AfraTafreeh.com
Nephrology: Nephritic Syndromes Bootcamp.com

Poststreptococcal Glomerulonephritis (PSGN)

● Pathophysiology:
● Group A β-hemolytic streptococci infection → Immune complex deposition → Complement activation → Glomerular destruction
● Diagnosis:
● Antistreptolysin O antibodies, anti-DNase B antibodies, hypocomplementemia (↓ C3)
● Hypercellular glomeruli on LM
● Subepithelial immune complex humps on EM
● Granular appearance on IF (“starry sky” “lumpy-bumpy”)
■ Immune complexes contain IgM, IgG, C3
● Management:
● Supportive care (Often self-limiting in children)
● Potential renal insufficiency in adults
● Associations:
● Most commonly in children ~2-4 weeks after strep infection (pharynx or skin)
■ Vs. IgA Nephropathy occurring within days of URI
● “Tea” or “cola” colored urine
● Hypertension, edema
 Nephrology: Nephritic Syndromes Bootcamp.com

Rapidly Progressive Glomerulonephritis

● Pathophysiology:
● Dysfunction of GBM → Plasma/cell leakage → ↑ Cytokines → Fibrin clot formation/cellular proliferation → Glomerular destruction
● Diagnosis:
● Crescent moon shape on LM
■ Contains fibrin, macrophages, plasma proteins (e.g., C3b), parietal cells
● Type I, II, III can be distinguished by IF pattern
■ Type I - Linear due to anti-GBM antibodies bind collagen (e.g., Goodpasture syndrome)
■ Type II - Granular due to Immune complex deposition (e.g., PSGN, DPGN, IgA Nephropathy)
■ Type III - Negative/pauci-immune (e.g., Granulomatosis with polyangiitis, eosinophilic granulomatosis, microscopic polyangiitis)
● Management: AfraTafreeh.com
● Immunosuppression (e.g., Glucocorticoids, cyclophosphamide)
● Plasmapheresis for Goodpasture Syndrome
● Associations:
● Poor prognosis, rapid destruction
 AfraTafreeh.com
Nephrology: Nephritic Syndromes Bootcamp.com

Diffuse Proliferative Glomerulonephritis

● Pathophysiology:
● Immune complex deposition in glomeruli → Complement activation → Glomerular destruction
● Diagnosis:
● “Wire looping” of capillaries on LM
● Subendothelial or intramembranous or subepithelial immune complex deposits (IgG, C3) on EM
● Granular appearance on IF
● Management:
● Immunosuppression (e.g., Glucocorticoids, cyclophosphamide, mycophenolate mofetil)
● Symptomatic management
● Associations:
● Presents with hematuria, proteinuria, ↓ GFR, ↓ C3 complement levels
● Systemic Lupus Erythematosus (SLE)
■ Type IV Lupus Nephritis
● Can be seen in IgA Nephropathy, autoimmune, and infectious diseases
 Nephrology: Nephritic Syndromes Bootcamp.com

Membranoproliferative Glomerulonephritis
● Pathophysiology:
● Mesangial cell growth and proliferation → Splitting of GBM
● Type 1: Immunoglobulin mediated
● Type 2: Complement mediated - C3 Nephritic factor
○ IgG autoantibody stabilizes C3 convertase → Complement activation → Hypocomplementemia (↓ C3)
● Diagnosis:
● Type 1 (more common): Granular appearing subendothelial immune complex deposits on IF
● Type 2 (rare): Complement mediated “Dense deposits” on EM
● Both types:
○ AfraTafreeh.com
GBM thickening & splitting in “tram-track” appearance on LM
○ ↓ Serum C3
● Management:
● Immunosuppression
● Symptomatic management
● Associations:
● Can present as nephritic or nephrotic syndrome
● Type 1: Idiopathic or 2° to HBV, HBC, cryoglobulinemia
● Type 2: C3 nephritic factor and can be 2° to HBV, HBC, cryoglobulinemia
 AfraTafreeh.com
Nephrology: Nephritic Syndromes Bootcamp.com

IgA Nephropathy (Berger Syndrome)

● Pathophysiology:
● ↑ IgA antibodies (triggering event) → Immune complex formation → Immune complex deposition (Type III HSR)
● Diagnosis:
● Mesangial proliferation on LM
● Mesangial immune complex deposits on EM
● IgA immune complex deposits on IF
● Management:
● Symptomatic management (RAAS inhibition)
● If severe, glucocorticoids
● Associations:
● Most common 1° glomerulonephritis in adults
● Typically during or following respiratory or GI infection
■ Mucosal membranes ↑ IgA secretion during infection
● Same renal findings in IgA vasculitis
 Nephrology: Nephritic Syndromes Bootcamp.com

Alport Syndrome
● Pathophysiology:
● Type IV collagen defect → Irregularities of glomerular basement membrane
● Diagnosis:
● Urinalysis (Initial test)
● Skin biopsy (Confirmatory test)
■ Absence of collagen type IV alpha-chains
● “Basket-weave” appearance on EM
● Management:
● Symptomatic management (RAAS inhibition)
● May require transplant AfraTafreeh.com
● Associations:
● Typically X-linked inheritance
● Intermittent gross hematuria
● Visual (e.g, retinopathy), hearing (e.g., sensorineural deafness), and renal involvement (e.g., glomerulonephritis)
■ “Can’t see, can’t pee, can’t hear a bee”
 AfraTafreeh.com
REVIEW OUTLINE

1. Nephrolithiasis Overview

Nephrology:
A. Classic Presentation
B. General Risk Factors
C. Diagnostics

Nephrolithiasis 2.
D. General Management
Ammonium Magnesium Phosphate (Struvite) Stones
A. Pathophysiology
B. Precipitation
C. Diagnostics
D. Management
3. Calcium Stones
A. Pathophysiology
B. Precipitation
C. Diagnostics
D. Management
4. Cystine Stones
A. Pathophysiology
B. Precipitation
C. Diagnostics
D. Management
5. Uric Acid Stones
A. Pathophysiology
B. Precipitation
C. Diagnostics
D. Management
 Nephrology: Nephrolithiasis Bootcamp.com

Nephrolithiasis Overview
● Classic Presentation:
● Unilateral flank tenderness
● Colicky radiating pain (e.g., to groin or inner thigh)
● Hematuria
● General Risk Factors:
● ↓ Hydration
○ ↓ Intake, ↑ Excretion (e.g., diuretics)
● ↑ Stone forming substances
○ Hypercalcemia, hyperuricemia, hyperoxaluria
● Diagnostics: AfraTafreeh.com
● Best initial imaging: Non-contrast CT scan
○ In pregnancy: Abdominal ultrasound (limit radiation exposure of fetus)
● Alternative imaging: KUB (Abdominal X-ray), MRI, IV pyelogram
● Urinalysis
● General Management:
● Hydration
● Dietary modifications
○ Limit sodium, oxalate, and excessive vitamin C intake
○ Avoid calcium intake restriction (↑ Risk of hyperoxaluria)
● Pain management (e.g. NSAIDs)
● Antispasmodics (e.g., Tamsulosin, nifedipine)
● Large stones may require ureterorenoscopy or shock wave lithotripsy
 AfraTafreeh.com
Nephrology: Nephrolithiasis Bootcamp.com

Ammonium Magnesium Phosphate (Struvite) Stones

● Pathophysiology:
● Urease (+) infection (e.g., Proteus mirabilis, Staphylococcus saprophyticus, Klebsiella)
● Bacteria converts urea → ↑ Ammonia → Alkaline urine (↑ pH) → Stone formation
○ Characteristic “Staghorn calculi”
● Precipitation:
● ↑ pH (alkaline)
● Diagnostics:
● X-ray: Radiopaque
● CT: Radiopaque
● Urine crystal:
○ Rectangular prisms (Coffin lid)
● Management:
● Treat underlying infection
○ Antibiotics for UTI
● Surgical removal
 Nephrology: Nephrolithiasis Bootcamp.com

Calcium Stones
● Pathophysiology:
● ↑ Urinary calcium, oxalate, or phosphate → Supersaturation → Stone formation
○ Two main types (Oxalate > phosphate)
● Due to ethylene glycol (antifreeze), hypocitraturia, ↑↑ vitamin C use, malabsorption (e.g., Crohn’s disease)
○ Calcium phosphate stones often due to hyperparathyroidism
● Precipitation:
● Calcium oxalate: Hypocitraturia, hypercalciuria, hyperoxaluria
● Calcium phosphate: ↑ pH (alkaline)
● Diagnostics:
● X-ray: Radiopaque AfraTafreeh.com
● CT: Radiopaque
● Urine Crystal:
○ Calcium oxalate: Dumbbell, envelope
○ Calcium phosphate: Wedge shape
● Management:
● Calcium oxalate:
○ Thiazides
○ Alkalinize urine (e.g., citrate)
○ Low-sodium diet
● Calcium phosphate:
○ Thiazides
○ Low-sodium diet
● Avoid calcium restriction!
 AfraTafreeh.com
Nephrology: Nephrolithiasis Bootcamp.com

Cystine Stones
● Pathophysiology:
● Defect in PCT reabsorption → ↓ Absorption of dibasic amino acids → Cystinuria → Stone formation
○ Cystine, Ornithine, Lysine, Arginine
● Sodium cyanide nitroprusside (+)
● Precipitation:
● ↓ pH (acidic)
● Diagnostics:
● X-ray: Weakly radiopaque
● CT: Moderately radiopaque
● Urine crystal:
○ Hexagonal
● Management:
● Alkalinize urine
● Low-sodium diet
● Chelating agents (e.g., penicillamine)
 Nephrology: Nephrolithiasis Bootcamp.com

Uric Acid Stones

● Pathophysiology:
● ↑ Uric acid or acidic urine → Stone formation
○ H+ + Urate- ↔ Uric Acid
● Risk factors
○ Gout
○ ↑ Cell turnover (e.g., TLS, leukemia)
○ Desert climates (↓ Urine volume → ↑ Likelihood stone formation)
● Precipitation:
● ↓ pH (acidic)
● Diagnostics: AfraTafreeh.com
● X-ray: Radiolucent
● CT scan: Visible
● Urine crystal:
○ Rhomboid, rosettes
● Management:
● Alkalinize urine (e.g. potassium bicarbonate, potassium citrate)
● Allopurinol
● ↓ Purine intake
 AfraTafreeh.com
Nephrology: Nephrolithiasis Bootcamp.com

Nephrolithiasis Summary

Struvite Calcium Oxalate Calcium Cystine Uric Acid

(Most common) Phosphate

Key Urease (+) UTI ↑ Calcium/Oxalate Hyperparathyroidism Hereditary Cystinuria Gout, ↑ Uric acid,
Association ↓ Citrate ↑ Cell turnover

Precipitation ↑ pH (alkalotic) ↓ pH (acidic) ↑ pH (alkalotic) ↓ pH (acidic) ↓ pH (acidic)

Diagnostics/ Radiopaque/ Radiopaque/ Radiopaque/ Mildly radiopaque/ Radiolucent/

Shape Rectangular prisms Bipyramidal envelope Wedge shaped Hexagonal Rhomboid, rosettes
(Coffin lid) or dumbbell

Management Treat underlying Alkalinize urine, Thiazides, Alkalinize urine, Alkalinize urine,
condition, Surgery thiazides, ↓ Na+ intake ↓ Na+ intake chelating agents, allopurinol,
↓ Na+ intake ↓ Purine intake
REVIEW OUTLINE

1. Micturition Overview

Nephrology:
A. Bladder Physiology
B. Pharmacology
C. Associations

Urinary 2. Overflow Incontinence

A. Pathophysiology
B. Presentation

Incontinence C. Diagnostics
D. Management
E. Associations
3. Stress Incontinence
AfraTafreeh.com
A. Pathophysiology
B. Presentation
C. Diagnostics
D. Management
E. Associations
4. Urge Incontinence
A. Pathophysiology
B. Presentation
C. Diagnostics
D. Management
E. Associations
 AfraTafreeh.com
Nephrology: Urinary Incontinence Bootcamp.com

Micturition Overview
● Bladder Physiology:
● Anatomic structures: Apex, body, fundus, bladder neck, and trigone
● Detrusor muscle: Pelvic nerve (PNS) → M3 receptor
● Detrusor muscle: Hypogastric nerve (SNS) → NE → β3 receptor
● External urethral sphincter (Voluntary): Pudendal nerve (Somatic) → ACh → Nicotinic receptor
● Internal urethral sphincter (Involuntary): Hypogastric nerve SNS → NE → α1 receptor
● Pharmacology:
● α1-blockers (e.g., tamsulosin) → Relaxation of smooth muscle at bladder neck and prostate (α1 inhibition)
● Muscarinic agonists (e.g., bethanechol) → Contraction of detrusor muscle (M3 stimulation)
● Muscarinic antagonists (e.g., oxybutynin) → Relaxation of detrusor muscle (M3 inhibition)
● Sympathomimetics (e.g., mirabegron) → Relaxation of detrusor muscle (β3 stimulation)
● Associations:
● ↑ Risk of UTIs
● ↑ Frequency with ↑ age; more common in women
 Nephrology: Urinary Incontinence Bootcamp.com

Overflow Incontinence
● Pathophysiology:
● ↓ Detrusor contractility or bladder outlet obstruction → Incomplete emptying → Bladder distention → Involuntary leakage
● Presentation:
● Weak/intermittent urinary stream
● Urinary hesitancy
● Diagnostics:
● ↑ Postvoid residual volume
● Management:
● Intermittent catheterization
● AfraTafreeh.com
Medical management (e.g., ɑ-blockers, bethanechol)
● Surgery (e.g., prostate resection)
● Associations:
● Obstruction (e.g., BPH)
● Neurologic disorders (e.g., Diabetes, MS, SCI)
 AfraTafreeh.com
Nephrology: Urinary Incontinence Bootcamp.com

Stress Incontinence
● Pathophysiology:
● Urethral hypermobility or intrinsic sphincter deficiency → Urine leakage with ↑ abdominal pressure
● Presentation:
● Urine leakage with coughing, laughing, sneezing, heavy lifting, or pregnancy
● Diagnostics:
● (+) Bladder stress test
● Management:
● Kegel exercises (i.e., pelvic floor strengthening)
● Pessary (pelvic organ support)
● Weight loss
● Midurethral sling
● Associations:
● Hx of prostate surgery
● Pregnancy (↑ Risk w/ vaginal delivery)
● Menopause
● Obesity
 Nephrology: Urinary Incontinence Bootcamp.com

Urge Incontinence
● Pathophysiology:
● Overactive detrusor muscle → Sudden urge to urinate → Involuntary urination
● Presentation:
● Frequent urination (particularly at night)
● Diagnostics:
● Clinical diagnosis
● Management:
● Kegel exercises (i.e., pelvic floor strengthening)
● Anticholinergics (e.g., oxybutynin)
○ AfraTafreeh.com
MOA: Blocks muscarinic Ach receptor → ↓ Detrusor muscle overactivity
● Neurostimulators
● Associations:
● Commonly idiopathic
● Neurologic disorders (e.g., MS, Stroke, SCI)
● ↑ Prevalence with age
● UTI
 AfraTafreeh.com
REVIEW OUTLINE
1. AKI Overview 7. Acute Tubular Necrosis
A. Terminology A. Pathophysiology

Nephrology: B. Presentation
C. Diagnostics
B. Etiology
C. Presentation
D. Diagnostics
2. Prerenal AKI
Kidney Injury A. Pathophysiology
B. Etiology 8.
E. Management
Diffuse Cortical Necrosis
C. Diagnostics A. Pathophysiology
D. Management B. Etiology
3. Intrarenal AKI C. Presentation
A. Pathophysiology D. Diagnostics
B. Etiology E. Management
C. Diagnostics 9. Renal Papillary Necrosis
D. Management A. Pathophysiology
4. Postrenal AKI B. Etiology
A. Pathophysiology C. Presentation
B. Etiology D. Diagnostics
C. Diagnostics E. Management
D. Management 10. Chronic Kidney Disease
5. AKI Summary A. Pathophysiology
6. Acute Interstitial Nephritis B. Etiology
A. Pathophysiology C. Presentation
B. Etiology D. Diagnostics
C. Presentation E. Management
D. Diagnostics F. Complications
E. Management
 Nephrology: Kidney Injury Bootcamp.com

Acute Kidney Injury (AKI) Overview

● Terminology:
● Acute kidney injury (AKI) or acute renal failure (ARF)
■ Prerenal, intrarenal, postrenal
■ Typically reversible
● Chronic kidney disease or chronic renal failure
■ Typically irreversible
● Presentation:
● Can be asymptomatic
● Nausea, vomiting, anorexia
● Oliguric or anuric
AfraTafreeh.com
● Fluid overload (e.g., peripheral or pulmonary edema)
● Volume depletion (e.g., prerenal AKI)
● Signs of ↑ Urea:
■ Asterixis, encephalopathy, pericarditis, platelet dysfunction (↑ Bleeding time)
● Diagnostics:
● ↑ Creatinine and BUN (less filtered)
■ ↑ Cr >= 0.3 over 48 hour period
■ ↑ Cr >= 1.5x baseline within 7 day period
 AfraTafreeh.com
Nephrology: Kidney Injury Bootcamp.com

Prerenal AKI
● Pathophysiology:
● ↓ CO and/or ↓ Effective circulating volume → ↓ RBF/GFR → RAAS activation → ↓ Urinary Na+/H2O (↑ Urine osmolality)
● Etiology:
● Hypotension (e.g., Heart failure, cirrhosis)
● Hypovolemia (e.g., Sweating, diarrhea, hemorrhage, vomiting)
● Renal artery stenosis
● Medications (e.g., Diuretics, NSAIDs, ACE inhibitors)
● Diagnostics:
● Urine osmolality (mOsm/kg): >500
● Urine Na+ (mEq/L): <20
● FeNa+: <1%
● Serum BUN/Cr: >20
● ↑ Serum Cr (e.g., 50% from baseline), ↓ Urine output
● Bland urine sediment (No protein/cells; rarely hyaline casts)
● Management:
● Restore renal perfusion (i.e. IV fluids, blood)
● Discontinue contributing medications (e.g., NSAIDs, ACE inhibitors, ARBs)
● Special scenario: Hepatorenal and cardiorenal syndrome
■ Does NOT respond to fluid administration
 Nephrology: Kidney Injury Bootcamp.com

Intrarenal AKI
● Pathophysiology:
● Renal tubular damage → Decreased reabsorption capacity → ↑ Urinary Na+/H2O (↓ Urine osmolality)
● Etiology:
● Acute Tubular Necrosis
■ Ischemia, nephrotoxic medications (e.g., aminoglycosides, contrast), toxins (e.g., hemoglobin, myoglobin, Bence-Jones proteins)
● Acute Interstitial Nephritis
■ Medications (e.g., diuretics, NSAID, antibiotics, PPIs, rifampin, sulfa drugs)
■ Infections
■ Infiltrative diseases (e.g., amyloidosis, sarcoidosis)
● Glomerulonephritis (e.g., RPGN) AfraTafreeh.com
● Vascular disease (e.g., HUS, TTP, malignant hypertension, vasculitis)
● Diagnostics:
● Urine osmolality (mOsm/kg): <350
● Urine Na+ (mEq/L): >40
● FeNa+: >2%
● Serum BUN/Cr: <15
● Various urine sediment
■ Granular/muddy brown casts, RBC or WBC casts, fatty casts
● Management:
● Treat the underlying cause
● Discontinue contributing medications (nephrotoxic)
 AfraTafreeh.com
Nephrology: Kidney Injury Bootcamp.com

Postrenal AKI
● Pathophysiology:
● Bilateral outflow obstruction → Backload of urine → ↑ Tubular pressure → ↓ GFR
■ Normal GFR can be maintained with one functioning kidney
● Etiology:
● Prostate enlargement (e.g., Prostate cancer, BPH)
● Nephrolithiasis
● Congenital anomalies
■ Posterior urethral valves
● Neurogenic bladder
■ SCI, MS
● Diagnostics:
● Urine osmolality (mOsm/kg): Varies
● Urine Na+ (mEq/L): Varies
● FeNa+: Varies
● Serum BUN/Cr: Varies
● Key feature: Anuria
● Imaging: Ultrasound or non-contrast CT
● Management:
● Bladder obstruction
■ Urethral or suprapubic catheterization
● Renal pelvis or ureteral obstruction
■ Ureteral stent
■ Percutaneous nephrostomy
 Nephrology: Kidney Injury Bootcamp.com

Acute Kidney Injury Summary

Prerenal AKI Intrarenal AKI Postrenal AKI

Etiology Hypovolemia ATN Prostate enlargement

Hypotension AIN Nephrolithiasis
Renal artery stenosis Glomerulonephritis Congenital anomalies
Medications Vascular disease Neurogenic bladder

Urine Osmolality (mOsm/kg) >500 AfraTafreeh.com

<350 Varies

Urine Na+ (mEq/L) <20 >40 Varies

FENa <1% >2% Varies

Serum BUN/Cr >20 <15 Varies

 AfraTafreeh.com
Nephrology: Kidney Injury Bootcamp.com

Acute Interstitial Nephritis (Tubulointerstitial Nephritis)

● Pathophysiology:
● Tubulointerstitial damage due to type IV HSR, tubular obstruction, or inflammatory infiltration
● Etiology:
● Medication reaction (Most common)
■ 5 P’S: Pain killers (NSAIDs), Pee pills (Diuretics), Penicillin (& cephalosporins), PPIs, RifamPin, Sulfa containing medications
● 2° to infection
■ Can be bacterial, viral, fungal, or parasitic
● 2° infiltrative & autoimmune diseases
■ Multiple myeloma, SLE, sarcoidosis, Sjṏgren syndrome
● Presentation:
● Morbilliform rash (i.e., rash that resembles measles)
● Fever, hematuria, pyuria
● Flank pain/CVA tenderness
● Potentially asymptomatic
● Diagnostics:
● Urine osmolarity (mOsm/kg): <350
● Hematologic tests: ↑ BUN, creatinine & eosinophils
● Urine tests: Sterile pyuria, WBC casts, microscopic hematuria, mild proteinuria
● Consider renal biopsy
● Management:
● Supportive care
● Cessation of causative agents
● Manage underlying disease + consider glucocorticoids
 Nephrology: Kidney Injury Bootcamp.com

Acute Tubular Necrosis

● Pathophysiology:
● Ischemic: ↓ RBF → Ischemia/necrosis → Cells slough into tubular lumen → Obstruction → ↓ GFR; ↑ BUN & Cr
● Nephrotoxic: Toxic injury to tubular cells → Cell slough into tubular lumen → Obstruction → ↓ GFR; ↑ BUN & Cr
■ Nephrotoxins include: contrast, aminoglycosides, cisplatin, amphotericin, lead, myoglobin, hemoglobin
● 3 phases:
■ (1) Inciting event - Initial kidney injury (Ischemic or nephrotoxic)
■ (2) Maintenance phase (1-3 weeks) - Oliguric; ↑ Risk of hyperkalemia, uremia, & metabolic acidosis
■ (3) Recovery phase - Polyuric; Tubular epithelialization occurs; ↑ Risk of hypokalemia & loss of electrolytes, ↓ BUN & creatinine
● Etiology:
● Ischemic vs. toxic intrarenal AKI AfraTafreeh.com
● Most common AKI in hospitalized patients
● Presentation:
● Similar to AKI (e.g., oliguria, anuria, volume depletion, edema)
● Can be asymptomatic
● Changes in urine volume production (oliguric vs. polyuric)
● Diagnostics:
● Urine sediment: Muddy brown granular casts
● Electrolyte derangement (depending on phase of ATN)
● Management:
● Stop nephrotoxins
● Supportive care
● Kidney functions typically recovers
● Prevent contrast-induced ATN with hydration before contrast
 AfraTafreeh.com
Nephrology: Kidney Injury Bootcamp.com

Diffuse Cortical Necrosis

● Pathophysiology:
● Vascular vasospasm → Ischemia → Necrosis of renal cortex → Renal obstruction/scarring
■ Exact mechanism is unclear
■ Typically bilateral
● Etiology:
● Septic shock, DIC, HUS, obstetric complications (e.g., Abruptio placentae)
● Presentation:
● Colicky flank pain, CVA tenderness, signs of AKI
● Diagnostics:
● Labs: ↑ BUN & Creatinine
● Imaging: CT urography
● Management:
● Treat underlying cause
● Symptom management
■ Consider dialysis
■ Poor prognosis
 Nephrology: Kidney Injury Bootcamp.com

Renal Papillary Necrosis

● Pathophysiology:
● Ischemia → Necrosis of papilla & renal pyramids → Renal obstruction/scarring
■ Typically bilateral
● Etiology:
● Sickle cell (Disease or trait), acute pyelonephritis, NSAIDs, diabetes mellitus, nephrolithiasis
■ Can be triggered by infection
● Presentation:
● Acute: Colicky flank pain, hematuria, proteinuria
● Chronic: Mild or asymptomatic
● Diagnostics: AfraTafreeh.com
● Labs: ↑ BUN & Creatinine
● Imaging: CT urography (visualize ischemic changes)
● Management:
● Treat underlying cause
● Symptom management
 AfraTafreeh.com
Nephrology: Kidney Injury Bootcamp.com

Chronic Kidney Disease

● Pathophysiology:
● Diabetic nephropathy: Hyperglycemia → Nonenzymatic glycation → Hyalinization of afferent & efferent arterioles → Kidney damage
■ GBM thickening, mesangial cell proliferation, & ↑ ECM proteins → Kimmelstiel-Wilson lesions
● Hypertensive nephropathy: ↑ BP → Nephrosclerosis of arterioles (afferent > efferent) → ↓ Perfusion/Ischemia → Kidney damage
● Glomerulonephritis: Inflammatory or noninflammatory damage to the kidney
● ↓ GFR → ↓ Urine production/↑ Extracellular fluid volume → ↓ Excretion of products (e.g., urea, phosphate, medications)
● ↓ 1-𝛂-hydroxylase → ↓ Active vitamin D → ↓ Ca2+ →↑ PTH (2° hyperparathyroidism)
● ↓ EPO → ↓ Erythropoiesis → ↓ Normocytic anemia
● Etiology:
● Diabetes mellitus, hypertension, glomerulonephritis, medications (e.g., NSAIDs), congenital anomalies (e.g., PKD)
● ↑ Risk for ASCVD
● Presentation:
● Can be asymptomatic, edema due to fluid overload, hypertension, heart failure
● Fatigue, nausea/vomiting, pruritus (↓ GFR/↑ Toxic metabolites)
● Hematologic complications: Anemia (loss of EPO), infection (impaired neutrophils), ↑ Bleeding time (platelet dysfunction)
● Diagnostics:
● Diagnosis requires ↓ GFR and/or signs of kidney damage for > 3 months
● Serum: ↑ Cr & BUN, ↓ GFR, ↑ K+, ↑ PO43-, ↓ Ca2+, ↑ PTH
● Urine: Albuminuria, waxy casts
● Imaging: Ultrasound
● Management:
● ACEis/ARBs, statins, ↓ Protein & Na+ intake, supplementation (vitamin D/Ca2+), phosphate binders, EPO stimulators
● Dialysis; Renal transplant in severe cases
● Complications:
● ↑ Risk for ASCVD, uremic pericarditis, anemia (loss of EPO), infection (impaired neutrophils), platelet dysfunction (↑ Bleeding time)
REVIEW OUTLINE

1. Acute Cystitis 5. Renal Oncocytoma

A. Pathophysiology

Nephrology:
A. Pathophysiology
B. Etiology B. Etiology
C. Presentation C. Presentation

Inflammatory D. Diagnostics D. Diagnostics

E. Management E. Management
2. Acute Pyelonephritis 6. Nephroblastoma

Conditions & A. Pathophysiology

B. Etiology
A. Etiology
B. Presentation
C. Presentation C. Diagnostics

Malignancy D. Diagnostics
E. Management
AfraTafreeh.com
D. Management
E. Associated Syndromes
3. Chronic Pyelonephritis 7. Urothelial Carcinoma
A. Pathophysiology A. Etiology
B. Etiology B. Presentation
C. Presentation C. Diagnostics
D. Diagnostics D. Management
E. Management E. Associated Syndromes
4. Renal Cell Carcinoma 8. Squamous Cell Carcinoma
A. Pathophysiology A. Pathophysiology
B. Etiology B. Etiology
C. Presentation C. Presentation
D. Diagnostics D. Diagnostics
E. Management E. Management
 AfraTafreeh.com
Nephrology: Inflammatory Conditions & Malignancy Bootcamp.com

Acute Cystitis
● Pathophysiology:
● Bacterial ascension from urethra to bladder → Inflammation of bladder (cystitis)
● Etiology:
● Urinary tract infection (UTI)
■ E. coli (most common), staphylococcus saprophyticus, klebsiella, proteus mirabilis (struvite stones)
● Anatomic risk factors: Female sex (due to shorter urethra), strucutural abnormalities (e.g., BPH, VUR)
● Other risk factors: Pregnancy, DM, sexual activity, catheter-associated UTI (CAUTI)
● Presentation:
● Suprapubic pain, ↑ urinary frequency, urgency, dysuria
● Lacks systemic symptoms
● Diagnostics:
● Primarily a clinical diagnosis
● Best initial test: Urinalysis
■ (+) leukocyte esterase, (+) nitrites, pyuria, bacteriuria
■ Sterile pyuria suggest Neisseria gonorrhoeae or Chlamydia trachomatis
● Typically normal serum WBC
● Management:
● TMP-SMX, nitrofurantoin, fosfomycin
● Fluconazole (Candida-related)
● Phenazopyridine (urinary analgesic)
● Prevention: ↑ Fluid intake, post-coital prophylaxis for recurrent UTIs, clean catheterization
 Nephrology: Inflammatory Conditions & Malignancy Bootcamp.com

Acute Pyelonephritis
● Pathophysiology:
● Bacterial ascension from urethra to kidney → Inflammation of kidney/Interstitial neutrophil infiltration
● Etiology:
● Urinary tract infection (UTI)
■ E. coli (most common), Staphylococcus saprophyticus, klebsiella, proteus mirabilis (struvite stones)
● Anatomic risk factors: Female sex (due to shorter urethra), strucutural abnormalities (e.g., BPH, VUR)
● Other risk factors: Pregnancy, DM, sexual activity, catheter-associated UTI (CAUTI)
● Presentation:
● Fever, flank pain, CVA tenderness, dysuria
● Presents with systemic symptoms AfraTafreeh.com
● Can lead to renal papillary necrosis
● Diagnostics:
● Best initial test: Urinalysis
■ (+) Leukocyte esterase, (+) Nitrites, pyuria, bacteriuria +/- WBC casts, hematuria
● Typically ↑ serum WBC
● Consider CT imaging to assess for abscess or obstruction (not routine)
● Management:
● Fluoroquinolones (e.g., ciprofloxacin)
● Fluconazole (Candida-related)
● Pyelonephritis in pregnancy: Broad spectrum antibiotics + cephalosporin
■ Avoid TMP-SMX and fluoroquinolones!
 AfraTafreeh.com
Nephrology: Inflammatory Conditions & Malignancy Bootcamp.com

Chronic Pyelonephritis
● Pathophysiology:
● Recurrent/inadequately treated pyelonephritis
● Xanthogranulomatous pyelonephritis: Subtype of chronic pyelonephritis
■ Typically unilateral
● Etiology:
● Associated with Proteus mirabilis infection
● Risk factors: VUR, chronic obstruction (kidney stones)
● Presentation:
● Flank pain, fever, malaise
● Diagnostics:
● Urinalysis: Pyuria, proteinuria +/- WBC casts
● CT scan shows corticomedullary scarring and blunted calyces
■ Xanthogranulomatous pyelonephritis: Bear’s paw sign
● Histology: “thyroidization” of the kidney
● Management:
● Antibiotics
● Treat underlying causes (remove obstruction)
● Nephrectomy for xanthogranulomatous pyelonephritis
 Nephrology: Inflammatory Conditions & Malignancy Bootcamp.com

Renal Cell Carcinoma

● Pathophysiology:
● Clear cell RCC (most common) originates in epithelial cells of PCT
■ Sporadic mutations (single tumor, older smoker)
■ Inherited mutations (multiple/bilateral tumors, younger patient)
● Etiology:
● ↑ Risk with smoking, obesity, hypertension, occupational exposures (e.g., asbestos), genetic mutations
■ Clear cell associated with Von-Hippel-Lindau (VHL) gene deletion on chromosome 3
● Autosomal Dominant
■ Less commonly associated with Tuberous sclerosis
● Presentation: AfraTafreeh.com
● Classic triad: flank pain, palpable mass, hematuria
● ~50-70 y/o male, fever, weight loss, potentially asymptomatic
● Paraneoplastic syndromes: PTHrP, EPO, ACTH, Renin (Memory Aide: “PEAR”)
● Can present with thrombosis and/or varicocele due to invasion of renal vein
■ Commonly metastasizes to the lungs and bones
● Diagnostics:
● Urinalysis: Hematuria
● Imaging: Abdominal CT
● Histopathology: Polygonal clear cells with high content of carbohydrates and lipids (golden-yellow color)
● Management:
● Nephrectomy
● Immunotherapy (e.g., Aldesleukin)
● Checkpoint inhibitors (e.g., Nivolumab, Ipilimumab)
● Poor response to radiation and chemotherapy
 AfraTafreeh.com
Nephrology: Inflammatory Conditions & Malignancy Bootcamp.com

Renal Oncocytoma
● Pathophysiology:
● Benign epithelial tumor originating from intercalated cells in collecting duct
● Etiology:
● Unclear, potentially genetic
● Presentation:
● Often asymptomatic
● Painless hematuria, flank pain, abdominal mass
● Diagnostics:
● Imaging: Abdominal CT, ultrasound
● Macroscopic pathology: Well circumscribed brown tumor with central scarring
● Microscopic pathology: Eosinophilic cells without perinuclear clearing & abundant mitochondria
● Management:
● Surgical resection to exclude malignancy (e.g., RCC)
 Nephrology: Inflammatory Conditions & Malignancy Bootcamp.com

Nephroblastoma (Wilms Tumor)

● Etiology:
● Often unknown
● Genetics
■ Can be due to a loss-of-function mutation of tumor suppressor gene (WT1 or WT2)
● Presentation:
● Classically early childhood (~2-4 y/o)
● Large, palpable unilateral flank mass +/- abdominal pain
■ Typically does not cross the midline
● Hematuria
● Hypertension
AfraTafreeh.com
● Diagnostics:
● Urinalysis: Hematuria
● Imaging: Ultrasound
■ Consider CT/MRI for staging and/or surgical planning
● Management:
● Nephrectomy +/- chemotherapy/radiation
● Good prognosis: >90% survival rate
● Associated Syndromes:
● Beckwith-Wiedemann: Macrosomia, macroglossia, hemihyperplasia, organomegaly (WT2 mutation)
● Denys-Drash syndrome: Pseudohermaphroditism, early onset nephrotic syndrome (WT1 mutation)
● WAGR complex: Wilms tumor, Aniridia, Genitourinary malformation, Range of developmental delays (WT1 deletion)
■ GU anomalies: Pseudohermaphroditism, early onset nephrotic syndrome
 AfraTafreeh.com
Nephrology: Inflammatory Conditions & Malignancy Bootcamp.com

Urothelial Carcinoma of the Bladder (Transitional Cell Carcinoma)

● Etiology:
● Most common malignancy of the urinary tract system (typically bladder)
● Phenacetin, Smoking tobacco (#1 Risk factor), Aromatic amines, Cyclophosphamide
● Presentation:
● Painless hematuria
● Urinary frequency, urgency, dysuria
● Diagnostics:
● Urinalysis: Hematuria; (-) RBC casts
● Imaging: Cystoscopy + biopsy, CT urography
● Histopathology: Dysplastic urothelium, papillary tumor with fibrovascular core
● Management:
● Bladder carcinoma: Transurethral resection of bladder tumor (TURBT); Radical cystectomy
■ TURBT if no smooth muscle invasion
● Ureters or renal pelvis carcinoma: Nephroureterectomy +/- chemotherapy
 Nephrology: Inflammatory Conditions & Malignancy Bootcamp.com

Squamous Cell Carcinoma of the Bladder

● Etiology:
● Chronic bladder irritation
● Risk factors: Smoking, chronic cystitis, chronic nephrolithiasis, Schistosoma haematobium (Typically found in Africa or the Middle East)
● Presentation:
● Painless hematuria
● Urinary frequency, urgency, dysuria
● Diagnostics:
● Urinalysis: Hematuria; (-) RBC casts
● Management:
●
AfraTafreeh.com
Bladder carcinoma: Transurethral resection of bladder tumor (TURBT) without smooth muscle invasion
● Radical cystectomy
 AfraTafreeh.com
REVIEW OUTLINE

1. Autosomal Dominant Polycystic Kidney Disease (ADPKD)

Nephrology:
A. Pathophysiology
B. Presentation
C. Diagnostics

Cystic Kidney 2.
D. Management
Autosomal Recessive Polycystic Kidney Disease (ARPKD)
A. Pathophysiology

Disease B. Presentation
C. Diagnostics
D. Management
3. Autosomal Dominant Tubulointerstitial Kidney Disease (ADTKD)
A. Pathophysiology
B. Presentation
C. Diagnostics
D. Management
 Nephrology: Cystic Kidney Disease Bootcamp.com

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

● Pathophysiology:
● Autosomal dominant mutation in PKD1 (chromosome 16) or PKD2 (chromosome 4)
● Development of numerous cysts in renal cortex and medulla → Bilaterally enlarged kidneys
● Presentation:
● Typically presents in adult, kidneys appear normal at birth
● Flank pain, hematuria, hypertension, urinary tract infection, can progress to renal failure (↑ Cr, uremia, volume overload)
● Associated findings: liver cysts (most common), pancreas cysts, intracranial aneurysms, mitral valve prolapse, diverticulosis
● Diagnostics:
● Ultrasound: bilaterally enlarged kidneys with multiple cysts of varying sizes
● CT, if US unclear AfraTafreeh.com
● Genetic testing (not routine)
● Management:
● ACE inhibitors, ARBs for HTN and to slow proteinuria/progression to ESRD
● Tolvaptan: Slows growth of renal cysts
■ Selective vasopressin 2 receptor antagonists → ADH inhibition → ↓ Water reabsorption
● Dialysis, if severe
● Only curative option: Transplant
 AfraTafreeh.com
Nephrology: Cystic Kidney Disease Bootcamp.com

Autosomal Recessive Polycystic Kidney Disease (ARPKD)

● Pathophysiology:
● Autosomal recessive mutation in PKHD1 (chromosome 6)
● Presentation:
● Typically presents in childhood
● Hypertension (can be unresponsive to monotherapy), oliguria, Potter sequence in utero, chronic renal failure
● Associated findings: Hepatic fibrosis → Portal hypertension, possible liver failure
● Diagnostics:
● Ultrasound: Bilaterally enlarged kidneys with multiple cysts of equal sizes
● Consider CT if US unclear
● Genetic testing (not routine)
● Management:
● Similar to ADPKD
● ACE inhibitors, ARBs for HTN and to slow proteinuria/progression to ESRD
● Tolvaptan: Slows growth of renal cysts
■ Selective vasopressin 2 receptor antagonists → ADH inhibition → ↓ Water reabsorption
● Dialysis, if severe
● Only curative option: Transplant
 Nephrology: Cystic Kidney Disease Bootcamp.com

Autosomal Dominant Tubulointerstitial Kidney Disease (ADTKD)

● Pathophysiology:
● Also called medullary cystic kidney disease
● Most commonly AD mutation in UMOD
● Tubulointerstitial fibrosis → Renal atrophy/insufficiency → Renal failure
● Presentation:
● Progressive renal insufficiency → Renal failure (↑ Cr, uremia, volume overload)
● Diagnostics:
● Renal US: Small kidney in advanced disease, medullary cysts may or may not be visualized
● Management:
● Symptom management (e.g., ACEi, ARBs) AfraTafreeh.com
● Only curative option: Transplant
● Poor prognosis
 AfraTafreeh.com
REVIEW OUTLINE

1. Carbonic Anhydrase Inhibitors

Nephrology:
A. Mechanism of Action
B. Clinical Use
C. Adverse Effects

Renal 2. Osmotic Diuretics

A. Mechanism of Action
B. Clinical Use

Pharmacology 3.
C. Adverse Effects
Loop Diuretics
A. Mechanism of Action
B. Clinical Use
C. Adverse Effects
4. Thiazide Diuretics
A. Mechanism of Action
B. Clinical Use
C. Adverse Effects
5. Potassium-sparing Diuretics
A. Mechanism of Action
B. Clinical Use
C. Adverse Effects
6. ACEi, ARBs, Direct renin inhibitors
A. Mechanism of Action
B. Clinical Use
C. Adverse Effects
 Nephrology: Renal Pharmacology Bootcamp.com

Carbonic Anhydrase Inhibitors

● Mechanism of Action:
● Medication: Acetazolamide
● Inhibition of carbonic anhydrase → ↓ Reabsorption of HCO3- → ↑ HCO3- excretion
■ Brain: ↓ Production of CSF
■ Eyes: ↓ Production of aqueous humor
● Weak diuretic effect
● Site of action: Proximal tubule
● Clinical Use:
● Acute glaucoma
● Alkalinize urine AfraTafreeh.com
● Altitude sickness
■ ↓ pO2 at high altitude → Hyperventilation → ↓ CO2 → Respiratory alkalosis
■ Acetazolamide ↑ HCO3- excretion which balance out the respiratory alkalosis
● Idiopathic intracranial hypertension (IIH) (Pseudotumor cerebri)
● Metabolic alkalosis
■ Due to ↑ HCO3- excretion
● Adverse Effects:
● Hypokalemia
● Kidney stone formation (↑ Urine pH)
● Paresthesias
● Proximal renal tubular acidosis (RTA type 2)
● Sulfa allergy
 AfraTafreeh.com
Nephrology: Renal Pharmacology Bootcamp.com

Osmotic Diuretics
● Mechanism of Action:
● Medications: Mannitol, urea
● ↑ Osmolality → ↑ Osmotic pressure/pull → ↓ Water reabsorption → ↑ Urine output
■ ↓ Intracranial and/or intraocular pressure
● Clinical Use:
● Acute angle glaucoma
● ↑ Intracranial pressure (ICP)
■ Draws fluid out of the brain
● ↑ Intraocular pressure (IOP)
■ Draws fluid out of the eye
● Adverse Effects:
● Dehydration due to excessive fluid loss
● Pulmonary edema
● Hyper- or hyponatremia
● Contraindications: Heart failure, anuria
■ Draws fluid out of the tissue into intravascular space → Worsening HF
 Nephrology: Renal Pharmacology Bootcamp.com

Loop Diuretics
● Mechanism of Action:
● Medications: Furosemide, torsemide, bumetanide, ethacrynic acid
● Inhibition of NKCC (Na+, K+, 2 Cl-) cotransporter → ↓ Interstitial tonicity → ↑ Urine output
■ ↓ K+ backleak into lumen → ↓ Ca2+ and Mg2+ reabsorption
■ ↑ Na+ exchange for K+ & H+ in collecting duct → ↑ K+ & H+ excretion
● Site of action: Thick ascending Loop of Henle
● Clinical Use:
● Edematous states
■ Decompensated CHF
■ Pulmonary edema
AfraTafreeh.com
■ Cirrhosis
● Hypercalcemia
● Hypertension (not first line)
● Adverse Effects:
● Ototoxicity
● Metabolic contraction alkalosis
● Acute interstitial nephritis
● Allergic reaction (Sulfa allergy)
■ Ethacrynic acid for sulfa allergy (↑ Ototoxicity)
● Electrolyte abnormalities
■ Hypokalemia, hypomagnesemia
■ Hyperuricemia (gout), hyperglycemia
 AfraTafreeh.com
Nephrology: Renal Pharmacology Bootcamp.com

Thiazide Diuretics
● Mechanism of Action:
● Medications: Hydrochlorothiazide (HCTZ), chlorothiazide, chlorthalidone, metolazone
● Inhibition of Na-Cl cotransporter → ↑ Na-Cl excretion/delivery to collecting duct
● ↑ K+ and H+ excretion, ↑ Ca2+ reabsorption (↑ Activity of Ca2+/Na+ exchanger)
● Site of action: Early DCT
● Clinical Use:
● Hypertension
● Edematous states
■ Decompensated CHF
■ Pulmonary edema
■ Cirrhosis
● Nephrogenic diabetes insipidus
● Recurrent calcium kidney stones (↓ Urinary calcium)
● Osteoporosis (↑ Serum calcium)
● Adverse Effects:
● Metabolic contraction alkalosis
● Allergic reaction (Sulfa allergy)
● Electrolyte abnormalities
■ Hypokalemia
■ Hyponatremia
■ HyperGlycemia
■ HyperLipidemia
■ HyperUricemia (Gout)
■ HyperCalcemia
 Nephrology: Renal Pharmacology Bootcamp.com

Potassium-Sparing Diuretics
● Mechanism of Action:
● Medications: Aldosterone antagonists - Spironolactone, eplerenone; ENaC blockers - Triamterene, amiloride
● Aldosterone antagonists: Inhibits aldosterones effects → ↓ Na+ reabsorption, ↓ K+ excretion → ↑ Urine output
■ ↓ H+ excretion → Metabolic acidosis
● ENaC blockers: Inhibition of ENaC channels → ↓ Na+ reabsorption, ↓ K+ excretion → ↑ Urine output
● Site of action: Late DCT and cortical collecting duct
● Clinical Use:
● Congestive heart failure (↓ Mortality)
● Cirrhosis
● Hypertension AfraTafreeh.com
● Hyperaldosteronism
● Potassium wasting (loop or thiazide diuretics)
● LIthium-induced nephrogenic diabetes insipidus (amiloride)
● Adverse Effects:
● Hyperkalemia
■ Can be used with loop or thiazide diuretics to offset K+ loss
● Antiandrogenic effects (typically spironolactone)
■ Gynecomastia
■ Amenorrhea
■ Erectile dysfunction
 AfraTafreeh.com
Nephrology: Renal Pharmacology Bootcamp.com

ACEi, ARBs, Direct renin inhibitors

● Mechanism of Action:
● Medication(s): ACEi - Lisinopril, enalapril, captopril; ARB - Losartan, valsartan; Direct renin inhibitor: Aliskiren
● ACEi: Inhibition of ACE → ↓ Conversion of angiotensin I to angiotensin II → ↓ Angiotensin II
■ ↑ Renin (loss of negative feedback) → ↑ AT I → ↓ AT II → ↓ Aldosterone → ↓ Na+ reabsorption
■ ↓ Vasoconstriction → ↓ Blood pressure
■ Efferent arteriole dilation → ↓ GFR
■ ↓ Breakdown of bradykinin
● ARBs: Inhibition of angiotensin II (AT1 receptor)
■ ↑ Renin (loss of negative feedback) → ↑ AT I → ↑ AT II → ↓ Aldosterone → ↓ Na+ reabsorption
■ Similar to ACEi
● Direct renin inhibitors: Inhibition of renin → ↓ Angiotensinogen to angiotensin I → ↓ Angiotensin II
■ ↑ Renin → ↓ AT I → ↓ AT II → ↓ Aldosterone → ↓ Na+ reabsorption
■ ↓ Vasoconstriction → ↓ Blood pressure
● Clinical Use:
● ACEi, ARB:
■ Hypertension, CKD, proteinuria, heart failure, hx of MI
● Aliskiren (not first line):
■ Hypertension
● Adverse Effects:
● ACEi: Cough, angioedema (↑ Bradykinin; contraindicated in C1 esterase inhibitor deficiency)
■ Switch to ARB
● All: Teratogenic, ↑ Cr (↓ GFR), hypotension, hyperkalemia, rash, angioedema
 Nephrology: Embryology & Anatomy Bootcamp.com

References
-Slide 2: <a href="https://commons.wikimedia.org/wiki/File:Intermediate_mesoderm.png">Jessica Xu</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>,
via Wikimedia Commons
-Slide 4 & 5: <a href="https://commons.wikimedia.org/wiki/File:Blausen_0592_KidneyAnatomy_01.png">BruceBlaus. When using this image in external sources it can be cited
as:Blausen.com staff (2014). &quot;Medical gallery of Blausen Medical 2014&quot;. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.</a>, <a
href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons
-Slide 3: <a href="https://commons.wikimedia.org/wiki/File:Hufeisenniere_05_mit_Appendizitis_-_CT_-_axial_-_031.jpg">Hellerhoff</a>, <a
href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via Wikimedia Commons
-Slide 6: <a href="https://commons.wikimedia.org/wiki/File:Posterior_Urethral_Valve.svg">ColnKurtz</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>,
via Wikimedia Commons
-Slide 2: CT image <https://radiopaedia.org/cases/normal-kidneys-on-4-phase-ct-study>
AfraTafreeh.com
-Slide 2 & 3: <a href="https://commons.wikimedia.org/wiki/File:Blausen_0592_KidneyAnatomy_01.png">BruceBlaus. When using this image in external sources it can be cited
as:Blausen.com staff (2014). &quot;Medical gallery of Blausen Medical 2014&quot;. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.</a>, <a
href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons
-Slide 4: Kidney Blood Flow <a href="https://commons.wikimedia.org/wiki/File:2612_Blood_Flow_in_the_Kidneys.jpg">OpenStax College</a>, <a
href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons
-Slide 4: Nephron Blood Flow <a href="https://commons.wikimedia.org/wiki/File:Physiology_of_Nephron.png">Madhero88</a>, <a
href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons
-Slide 5: Juxtaglomerular Apparatus <a href="https://commons.wikimedia.org/wiki/File:2615_Juxtaglomerular_Apparatus.jpg">OpenStax Anatomy and PhysiologyOpenStax</a>, <a
href="https://creativecommons.org/licenses/by/4.0">CC BY 4.0</a>, via Wikimedia Commons
-Slide 5: Renal Corpuscle <a href="https://commons.wikimedia.org/wiki/File:Renal_corpuscle.jpg">Ed Uthman (Pathologist), website: [2]</a>, <a
href="https://creativecommons.org/licenses/by-sa/2.0">CC BY-SA 2.0</a>, via Wikimedia Commons
-Slide 6: <a href="https://commons.wikimedia.org/wiki/File:201405_kidney.png">DBCLS 統合TV</a>, <a href="https://creativecommons.org/licenses/by/4.0">CC BY 4.0</a>, via
Wikimedia Commons
-Slide 8: <a href="https://commons.wikimedia.org/wiki/File:2605_The_Bladder.jpg">OpenStax College</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via
Wikimedia Commons
 AfraTafreeh.com
Nephrology: Fluid & Filtration Physiology Bootcamp.com

References
-Slide 2: Image created with BioRender.com (2021)

-Slide 3: Image created with BioRender.com (2021)

-Slide 5: Image created with BioRender.com (2021)

-Slide 3:
● https://commons.wikimedia.org/wiki/File:Juxtaglomerular_Apparatus_and_Glomerulus.jpg
● <a href="https://commons.wikimedia.org/wiki/File:Juxtaglomerular_Apparatus_and_Glomerulus.jpg">OpenStax College</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY
3.0</a>, via Wikimedia Commons>

-Slide 4, 5, 6:
● https://commons.wikimedia.org/wiki/File:Physiology_of_Nephron.png
● <a href="https://commons.wikimedia.org/wiki/File:Physiology_of_Nephron.png">Madhero88</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia
Commons

-Slide 7:
● https://commons.wikimedia.org/wiki/File:1901_Composition_of_Blood.jpg
● <a href="https://commons.wikimedia.org/wiki/File:1901_Composition_of_Blood.jpg">OpenStax College</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via
Wikimedia Commons
 Nephrology: Nephron Transporters Bootcamp.com

References
-Slide 2:
● https://app.biorender.com/illustrations/61c13edffb628800a9b39d6d
● Created with Biorender.com (2021)

-Slide 3:
● https://app.biorender.com/illustrations/61c13edffb628800a9b39d6d
● Created with Biorender.com (2021)

-Slide 4:
● https://app.biorender.com/illustrations/61c13edffb628800a9b39d6d
● Created with Biorender.com (2021)

-Slide 5:
● https://app.biorender.com/illustrations/61c13edffb628800a9b39d6d AfraTafreeh.com
● Created with Biorender.com (2021)
 AfraTafreeh.com
Nephrology: RAAS Bootcamp.com

References
-Slide 2: https://commons.wikimedia.org/wiki/File:Juxtaglomerular_Apparatus_and_Glomerulus.jpg<ahref="https://commons.wikimedia.org/wiki/File:Juxtaglomerular_Apparatus_and_Glomeru
us.jpg">OpenStax College</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons>

-Slide 2, 3, 4: Adapted from “Renin-Angiotensin System”, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-templates
 Nephrology: Electrolytes Bootcamp.com

References
-Slide 2: https://app.biorender.com/illustrations/61f5e8f9c62308009da9e301 Created with BioRender.com (2022).

-Slide 4: https://app.biorender.com/illustrations/61f5e8f9c62308009da9e301 Created with BioRender.com (2022).

-Slide 6: https://app.biorender.com/illustrations/61f5e8f9c62308009da9e301 Adapted from BioRender.com (2022).

● https://commons.wikimedia.org/wiki/File:Calciphylaxis.png
<a href="https://commons.wikimedia.org/wiki/File:Calciphylaxis.png">Niels Olson</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via Wikimedia
Commons

AfraTafreeh.com
 AfraTafreeh.com
Nephrology: Acid-Base Physiology Bootcamp.com

References
-Slide 2: https://app.biorender.com/illustrations/621930463a0700004c3fc63a
● Created with BioRender.com (2022).

-Slide 6: https://app.biorender.com/illustrations/62153f8f65e704004c2bc518
● Created with BioRender.com (2022).

-Slide 7: https://app.biorender.com/illustrations/62153f8f65e704004c2bc518
● Created with BioRender.com (2022).

-Slide 8: https://app.biorender.com/illustrations/62153f8f65e704004c2bc518
● Created with BioRender.com (2022).
 Nephrology: Pathology Diagnostics Bootcamp.com

References
-Slide 3:
● https://commons.wikimedia.org/wiki/File:Clinical_urine_tests.jpg
● <a href="https://commons.wikimedia.org/wiki/File:Clinical_urine_tests.jpg">www.scientificanimations.com</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>,
via Wikimedia Commons
● https://commons.wikimedia.org/wiki/File:HematuriaGross.jpg
● <a href="https://commons.wikimedia.org/wiki/File:HematuriaGross.jpg">James Heilman, MD</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>, via
Wikimedia Commons
● https://commons.wikimedia.org/wiki/File:Chemstrip1.jpg
● <a href="https://commons.wikimedia.org/wiki/File:Chemstrip1.jpg">J3D3</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via Wikimedia Commons

-Slide 4:
● Granular Cast, https://www.nature.com/articles/srep40521, CC by 4.0 https://creativecommons.org/licenses/by/4.0/
● Hyaline Cast, https://www.nature.com/articles/srep40521, CC by 4.0 https://creativecommons.org/licenses/by/4.0/
AfraTafreeh.com
 AfraTafreeh.com
Nephrology: Nephrotic Syndromes Bootcamp.com

References
-Slide 2:
● Created with BioRender.com (2022).

-Slide 3:
● Created with BioRender.com (2022).
● MCD Light Microscopy, https://www.nature.com/articles/s41598-017-11553-x, CC by 4.0 https://creativecommons.org/licenses/by/4.0/
● MCD Electron Microscopy, https://bmcnephrol.biomedcentral.com/articles/10.1186/s12882-020-02066-3, CC by 4.0 https://creativecommons.org/licenses/by/4.0/

-Slide 4:
● https://commons.wikimedia.org/wiki/File:Focal_segmental_glomerulosclerosis_-_high_mag.jpg, <a
href="https://commons.wikimedia.org/wiki/File:Focal_segmental_glomerulosclerosis_-_high_mag.jpg">Nephron</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA
3.0</a>, via Wikimedia Commons
● FSGS, https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0241745, CC by 4.0 https://creativecommons.org/licenses/by/4.0/

-Slide 5:
● https://commons.wikimedia.org/wiki/File:Membranous_nephropathy_-_pas_-_very_high_mag.jpg <a
href="https://commons.wikimedia.org/wiki/File:Membranous_nephropathy_-_pas_-_very_high_mag.jpg">Nephron</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA
3.0</a>, via Wikimedia Commons
● MN Electron Microscopy,
https://www.cureus.com/articles/61533-rapidly-progressing-primary-membranous-nephropathy-in-a-hispanic-male-with-elevated-levels-of-anti-phospholipase-a2-receptor-antibodies#article-di
sclosures-acknowledgementsm, CC by 4.0 https://creativecommons.org/licenses/by/4.0/
● MN Immunofluorescence,
https://www.cureus.com/articles/61533-rapidly-progressing-primary-membranous-nephropathy-in-a-hispanic-male-with-elevated-levels-of-anti-phospholipase-a2-receptor-antibodies#article-di
sclosures-acknowledgementsm, CC by 4.0 https://creativecommons.org/licenses/by/4.0/

-Slide 6:
● Congo-red stain, https://www.cureus.com/articles/80767-renal-amyloidosis-a-clinicopathological-study-from-a-tertiary-care-hospital-in-pakistan#article-disclosures-acknowledgements, CC by
4.0 https://creativecommons.org/licenses/by/4.0/

-Slide 7:
● https://commons.wikimedia.org/wiki/File:Diabetic_glomerulosclerosis_(4)_PAS.jpg, <a href="https://commons.wikimedia.org/wiki/File:Diabetic_glomerulosclerosis_(4)_PAS.jpg">No
machine-readable author provided. KGH assumed (based on copyright claims).</a>, <a href="http://creativecommons.org/licenses/by-sa/3.0/">CC BY-SA 3.0</a>, via Wikimedia Commons
 Nephrology: Nephritic Syndromes Bootcamp.com

References
-Slide 2:
● https://commons.wikimedia.org/wiki/File:Post-infectious_glomerulonephritis_-_very_high_mag.jpg <a
href="https://commons.wikimedia.org/wiki/File:Post-infectious_glomerulonephritis_-_very_high_mag.jpg">Nephron</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA
3.0</a>, via Wikimedia Commons
● PSGN EM, https://www.cureus.com/articles/14052-role-of-steroids-in-post-streptococcal-glomerulonephritis-without-crescents-on-renal-biopsy#article-disclosures-acknowledgements, CC by
4.0 https://creativecommons.org/licenses/by/4.0/
● PSGN IF, https://www.cureus.com/articles/14052-role-of-steroids-in-post-streptococcal-glomerulonephritis-without-crescents-on-renal-biopsy#article-disclosures-acknowledgements, CC by
4.0 https://creativecommons.org/licenses/by/4.0/

-Slide 3:
● https://commons.wikimedia.org/wiki/File:Crescentic_glomerulonephritis_-_very_high_mag.jpg, <a
href="https://commons.wikimedia.org/wiki/File:Crescentic_glomerulonephritis_-_very_high_mag.jpg">Nephron</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA
3.0</a>, via Wikimedia Commons
AfraTafreeh.com
-Slide 4:
● https://commons.wikimedia.org/wiki/File:Diffuse_proliferative_lupus_nephritis_-b-_very_high_mag.jpg, <a
href="https://commons.wikimedia.org/wiki/File:Diffuse_proliferative_lupus_nephritis_-b-_very_high_mag.jpg">Nephron</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC
BY-SA 3.0</a>, via Wikimedia Commons

-Slide 5:
● https://commons.wikimedia.org/wiki/File:Membranoproliferative_glomerulonephritis_-_very_high_mag.jpg, <a
href="https://commons.wikimedia.org/wiki/File:Membranoproliferative_glomerulonephritis_-_very_high_mag.jpg">Nephron</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC
BY-SA 3.0</a>, via Wikimedia Commons

-Slide 6:
● https://commons.wikimedia.org/wiki/File:Purpura2.JPG, <a href="https://commons.wikimedia.org/wiki/File:Purpura2.JPG">The original uploader was Okwikikim at English Wikipedia.</a>,
Public domain, via Wikimedia Commons
 AfraTafreeh.com
Nephrology: Nephrolithiasis Bootcamp.com

References
-Slide 2:
● https://commons.wikimedia.org/wiki/File:KidneyStone.JPG, <a href="https://commons.wikimedia.org/wiki/File:KidneyStone.JPG">James Heilman, MD</a>, <a
href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via Wikimedia Commons

-Slide 3:
● https://commons.wikimedia.org/wiki/File:Staghorn_Kidney_Stone_08779.jpg, <a href="https://commons.wikimedia.org/wiki/File:Staghorn_Kidney_Stone_08779.jpg">© Nevit Dilmen</a>, <a
href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via Wikimedia Commons
● Struvite Stone Formation, Created with Biorender.com (2022)

-Slide 4:
● Effect of dietary sodium intake on stone formation, Created with Biorender.com (2022)

-Slide 5:
● https://commons.wikimedia.org/wiki/File:Cystine_Crystals_in_Canine_Urine_Sediment.jpg, <a
href="https://commons.wikimedia.org/wiki/File:Cystine_Crystals_in_Canine_Urine_Sediment.jpg">Lance Wheeler</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA
4.0</a>, via Wikimedia Commons
● Cystinuria, Created with Biorender.com (2022)

-Slide 6:
● https://commons.wikimedia.org/wiki/File:Uric_acid_crystals_(urine)_-_%C3%9Crik_asit_kristalleri_(idrar)_-_03.png, <a
href="https://commons.wikimedia.org/wiki/File:Uric_acid_crystals_(urine)_-_%C3%9Crik_asit_kristalleri_(idrar)_-_03.png">Doruk Salancı</a>, <a
href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via Wikimedia Commons
 Nephrology: Urinary Incontinence Bootcamp.com

References
-Slide 2:
● https://commons.wikimedia.org/wiki/File:2605_The_Bladder.jpg, <a href="https://commons.wikimedia.org/wiki/File:2605_The_Bladder.jpg">OpenStax College</a>, <a
href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons

-Slide 3:
● Overflow incontinence, Created with Biorender.com (2022)

-Slide 4:
● Stress incontinence, Created with Biorender.com (2022)

-Slide 5:
● Urge incontinence, Created with Biorender.com (2022)

AfraTafreeh.com
 AfraTafreeh.com
Nephrology: Kidney Injury Bootcamp.com

References
-Slide 3:
● Bowman’s Capsule, Created with Biorender.com (2022)

-Slide 5:
● https://commons.wikimedia.org/wiki/File:Normal-vs-enlarged-prostate.jpg, <a href="https://commons.wikimedia.org/wiki/File:Normal-vs-enlarged-prostate.jpg">Akcmdu9</a>, <a
href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via Wikimedia Commons

-Slide 7:
● Morbilliform rash: Kulkarni R B, Lederman Y, Afiari A, et al. (July 21, 2020) Morbilliform Rash: An Uncommon Herald of SARS-CoV-2. Cureus 12(7): e9321. doi:10.7759/cureus.9321
● https://commons.wikimedia.org/wiki/File:Acute_Interstitial_Nephritis.jpg, <a href="https://commons.wikimedia.org/wiki/File:Acute_Interstitial_Nephritis.jpg">Libertas Academica (citing Figure 2
of An Unusual Presentation of Classic Idiopathic Polyarteritis Nodosa as Acute Interstitial Nephritis, in Clinical Medicine Insights: Case Reports, first author Ravi Sunderkrishnan)</a>, <a
href="https://creativecommons.org/licenses/by/2.0">CC BY 2.0</a>, via Wikimedia Commons

-Slide 8:
● Muddy Brown Cast, https://www.researchgate.net/publication/319861970_Practical_approach_to_detection_and_management_of_acute_kidney_injury_in_critically_ill_patient/figures, CC by
4.0 https://creativecommons.org/licenses/by/4.0/
● Nephron, Created with Biorender.com (2022)

-Slide 9:
● https://commons.wikimedia.org/wiki/File:Renal_cortical_infarction_showing_coagulative_necrosis_4X.jpg, <a
href="https://commons.wikimedia.org/wiki/File:Renal_cortical_infarction_showing_coagulative_necrosis_4X.jpg">Calicut Medical College</a>, <a
href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>, via Wikimedia Commons
● Kidney Cross-section, Created with Biorender.com (2022)

-Slide 10:
● Kidney Cross-section, Created with Biorender.com (2022)

-Slide 11:
● https://commons.wikimedia.org/wiki/File:CKD_-_Chronic_kidney_disease.jpg, <a
href="https://commons.wikimedia.org/wiki/File:CKD_-_Chronic_kidney_disease.jpg">https://www.scientificanimations.com/</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC
BY-SA 4.0</a>, via Wikimedia Commons
● https://upload.wikimedia.org/wikipedia/commons/1/18/Bowman%27s_capsule_and_glomerulus.svg, <a
href="https://commons.wikimedia.org/wiki/File:Bowman%27s_capsule_and_glomerulus.svg">Mikael Häggström</a>, CC0, via Wikimedia Commons
 Nephrology: Inflammatory Conditions & Malignancy Bootcamp.com

References
-Slide 2:
● https://commons.wikimedia.org/wiki/File:Urinary_System_(Female).png, <a href="https://commons.wikimedia.org/wiki/File:Urinary_System_(Female).png">BruceBlaus</a>, <a
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-Slide 3:
● https://commons.wikimedia.org/wiki/File:Urinary_System_(Female).png, <a href="https://commons.wikimedia.org/wiki/File:Urinary_System_(Female).png">BruceBlaus</a>, <a
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-Slide 4:
● https://commons.wikimedia.org/wiki/File:Thyroidization_of_the_kidney_--_high_mag.jpg, <a
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via Wikimedia Commons
● https://radiopaedia.org/cases/xanthogranulomatous-pyelonephritis-3?lang=us
AfraTafreeh.com
-Slide 5:
● https://commons.wikimedia.org/wiki/File:Clear_cell_renal_cell_carcinoma_high_mag.jpg, <a
href="https://commons.wikimedia.org/wiki/File:Clear_cell_renal_cell_carcinoma_high_mag.jpg">Nephron</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>,
via Wikimedia Commons

-Slide 6:
● https://commons.wikimedia.org/wiki/File:Renal_oncocytoma3.jpg, <a href="https://commons.wikimedia.org/wiki/File:Renal_oncocytoma3.jpg">Nephron</a>, <a
href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via Wikimedia Commons
● https://commons.wikimedia.org/wiki/File:Renal_oncocytoma.jpg, <a href="https://commons.wikimedia.org/wiki/File:Renal_oncocytoma.jpg">Emmanuelm at English Wikipedia</a>, <a
href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons

-Slide 8:
● https://commons.wikimedia.org/wiki/File:Papillary_urothelial_carcinoma_(low-grade),_very_high_mag.2.jpg, <a
href="https://commons.wikimedia.org/wiki/File:Papillary_urothelial_carcinoma_(low-grade),_very_high_mag.2.jpg">CoRus13</a>, CC0, via Wikimedia Commons
 AfraTafreeh.com
Nephrology: Cystic Kidney Disease Bootcamp.com

References
-Slide 2:
● Kidney tumor adult pkd, https://www.pathologyoutlines.com/topic/kidneytumoradultpkd.html
● https://commons.wikimedia.org/wiki/File:Polycystic_Kidney.png, <a href="https://commons.wikimedia.org/wiki/File:Polycystic_Kidney.png">BruceBlaus</a>, <a
href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>, via Wikimedia Commons

-Slide 3:
● https://commons.wikimedia.org/wiki/File:Polycystic_Kidney.png, <a href="https://commons.wikimedia.org/wiki/File:Polycystic_Kidney.png">BruceBlaus</a>, <a
href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>, via Wikimedia Commons
 Nephrology: Renal Pharmacology Bootcamp.com

References
-Slide 2:
● PCT, Created with Biorender.com (2022)

-Slide 3:
● https://commons.wikimedia.org/wiki/File:Physiology_of_Nephron.png, <a href="https://commons.wikimedia.org/wiki/File:Physiology_of_Nephron.png">Madhero88</a>, <a
href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons

-Slide 4:
● Loop of Henle, Created with Biorender.com (2022)

-Slide 5:
● DCT, Created with Biorender.com (2022)

-Slide 6: AfraTafreeh.com
● Collecting duct, Created with Biorender.com (2022)

-Slide 7:
● https://upload.wikimedia.org/wikipedia/commons/1/18/Bowman%27s_capsule_and_glomerulus.svg, <a
href="https://commons.wikimedia.org/wiki/File:Bowman%27s_capsule_and_glomerulus.svg">Mikael Häggström</a>, CC0, via Wikimedia Commons