ACUTE KIDNEY INJURY CLINICAL THERAPEUTICS | PRELIMS (1st Sem)

Dr. Magnolia Reyes

OUTLINE B. WHAT PRECIPITATED THE PATIENT’S RENAL INJURY?

I. I. CASE  Multiple medications (ASA, B-blockers, ACE Inhibitors)
A. Salient Points
II. II. DISCUSSION
 History of Type 2 Diabetes Mellitus
III. III. CLINICAL PEARLS  Worsening angina and hypertension
IV.
V.
IV. DEFINITION OF TERMS
V. CAUSES OF ACUTE KIDNEY INJURY
 Coronary Angiography – due to contrast media
A. Prerenal AKI o This may be the cause of the abrupt increase in the
B. Intrinsic AKI creatinine levels of the patient during the hospital stay
VI. VI. EVALUATION OF ACUTE KIDNEY INJURY
A. Urinalysis o PREVENTION: proper hydration before the procedure
VII. VII. COMPREHENSION QUESTIONS
NOTE: Text in blue are lifted from the book.  C. WHAT ARE THE COMMON CAUSES, EVALUATION,
AND PREVENTION OF AKI IN HOSPITALIZED PATIENT?
I. CASE Causes of AKI
A 54-year-old man with a history of type 2 diabetes and  Prerenal – may be due to S4 gallop (Ventricular Failure)
coronary artery disease is admitted to the coronary care unit  Renal
with worsening angina and hypertension. His pain is controlled o Acute Tubular Necrosis – due to nephrotoxic drugs
with intravenous nitroglycerin, and he is treated with aspirin, (contrast media)
beta-blockers to lower his heart rate, and angiotensin- o Glomerulonephritis
converting enzyme (ACE) inhibitors to lower his blood o Tubulointerstitial nephritis
pressure. Cardiac enzymes are normal. He undergoes  Postrenal – usually due to obstruction, as in:
coronary angiography, which reveals no significant stenosis. o Renal stones
By the next day, his urine output has diminished to 200 mL o Infection
over 24 hours. Examination at that time reveals that he is o Tumors
afebrile, his heart rate is regular at 56 bpm, and his blood o Obstruction of bladder neck secondary to Benign
pressure is 109/65 mm Hg. His fundus reveals dot Prostatic Hyperplasia (BPH)
hemorrhages and hard exudates, his neck veins are flat, his
chest is clear, and his heart rhythm is normal with an S4 gallop  Medications such as aspirin, nonsteroidal anti-
and no murmur or friction rub. His abdomen is soft without inflammatory drugs (NSAIDs), and ACE inhibitors can alter
masses or bruits. He has no peripheral edema or rashes, with intrarenal blood flow and result in prerenal failure.
normal pulses in all extremities.  Intrinsic renal failure is caused by disorders that injure
the renal glomeruli or tubules directly. These include
LABORATORY glomerulonephritis, tubulointerstitial nephritis, and acute
 Na 140 mEq/L (Normal: 135 -145 mEq/L) tubular necrosis (ATN) from either ischemia or nephrotoxic
 K 5.3 mEq/L (Normal: 3.5 – 5.5 mEq/L) drugs.
 Cl 104 mEq/L (Normal: 97 – 107 mEq/L)  Postrenal failure, also referred to as obstructive
 CO2 19 mEq/L (Normal: 22 – 29 mEq /L) nephropathy, implies blockage of urinary flow.
 blood urea nitrogen (BUN) 69 mg/dL (Normal: 7 – 20 o Site of obstruction can be anywhere along the urinary
mg/dL) system, including the intratubular region (crystals),
 Creatinine (Cr) level has risen to 2.9 mg/dL from 1.6 ureters (stones, extrinsic compression by tumor),
mg/dL on admission (Normal: 0.84 – 1.21 mg/dL) bladder, or urethra
o The most common causes of obstructive nephropathy
A. SALIENT POINTS are ureteral obstruction due to malignancy, or
prostatic obstruction due to benign or malignant
 54-year-old man
hypertrophy
 History of Type 2 DM and CAD
o Diagnosed by seeing hydronephrosis on renal UTZ
 Worsening angina and hypertension
 Pain controlled with NTG
C. HOW DO YOU USE URINALYSIS AND CHEMISTRY
 Treated with ASA, B-blockers, ACE Inhibitor VALUES TO CATEGORIZE THE ETIOLOGY AS PRERENAL,
 Undergoes coronary angiography RENAL, AND POSTRENAL?
 Low urine output (Normal: 1-2mL/kg/hr) Prerenal:
 HR regular at 56 bpm; BP 110 / 66 mmHg  Concentrated (High specific gravity)
 Dot hemorrhages and hard exudates  Normal microscopic findings
 Flat neck veins Renal:
 (+) S4 gallop  Protein
 Granular casts
II. DISCUSSION  RBC casts
Note: the answers to these questions are lifted from the recording,
 Urinary eosinophils (d/t allergic reactions to drugs in acute
those in blue are from the book
interstitial nephritis)
Postrenal:
A. WHAT IS THE PATIENT’S NEW CLINICAL PROBLEM?
 Normal specific gravity
 Acute Kidney Injury

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 Prelims (1st Sem) Acute Kidney Injury
Dr. Magnolia Reyes
CLINICAL THERAPEUTICS· September 25, 2020

D. HOW DO YOU MANAGE THIS PATIENT?  Hyperkalemia is treated initially with calcium to stabilize
 Dialysis cardiac membranes; insulin and beta-agonists to
 Note: redistribute potassium intracellularly (sodium bicarbonate if
o No need to change medications. ACE Inhibitors and there is a severe metabolic acidosis); and then loop
ARBs are protective to the kidneys, so it is best to use diuretics, a potassium exchange resin, or hemodialysis to
them in patients with kidney injury. remove excess potassium from the body.
o Do not flush out contrast media through hydration, it  Indications for dialysis: AEIOU
may cause fluid overload in this particular patient. o acidosis
o electrolyte disturbances
E. WHAT IS THE MANAGEMENT OF HYPERKALEMIA? o ingestions
 IV Calcium Gluconate o overload
o Stabilize the cardiac cell membrane against o uremia
undesirable depolarization  preventing arrhythmia
o Calcium will oppose the membrane effects of the high IV. DEFINITION OF TERMS
potassium concentration on the heart, allowing time  ACUTE KIDNEY INJURY
for other methods to lower the potassium level o Abrupt decline in kidney function, measured as
 IV Sodium Bicarbonate glomerular filtration rate (GFR).
o Used in patients with acidosis
o It also promotes intracellular diffusion of potassium
 Insulin + Glucose – via IV drip
o 10 units regular insulin IV + 1 ampule D50 (50 cc)
o Insulin drives potassium into cells, lowering levels o True GFR is difficult to measure, so we rely on
within 30 minutes increases in serum creatinine levels to indicate a
 Oral Kayexalate fall in GFR.
o cationic exchange resin that lowers potassium by o But because creatinine is both filtered and secreted
exchanging sodium for potassium in the colon by the kidneys, changes in serum creatinine

+
Loop Diuretics (Furosemide) – to remove excess K concentrations always lag behind and underestimate
o increase urinary flow and excretion of potassium, or, if the decline in the GFR.
the patient does not make sufficient urine o In other words, by the time the serum
 Beta agonist (Albuterol) – drives potassium intracellularly creatinine level rises, the GFR has already
fallen significantly.
F. WHAT ARE THE INDICATIONS FOR ACUTE DIALYSIS?  OLIGURIA
 The indications for dialysis in AKI include o Less than 400 mL of urine output in 24 hours
o fluid overload, such as pulmonary edema o Physiologically, it is the lowest amount of urine a
o metabolic acidosis person on a normal diet can make if he or she
o hyperkalemia is severely dehydrated and does not retain uremic
o uremic pericarditis waste products.
o severe hyperphosphatemia o Oliguria is a poor prognostic sign in acute renal
o uremic symptoms failure (ARF).
o Patients with oliguric renal failure have higher
III. CLINICAL PEARLS mortality rates and less renal recovery than do
 The two main causes of AKI in hospitalized patients are patients who are nonoliguric.
prerenal azotemia and acute tubular necrosis.  ANURIA
 In the anuric patient, one must quickly determine if the o Less than 50 mL of urine output in 24 hours.
kidneys are obstructed or if the vascular supply is o Acute obstruction, cortical necrosis, and vascular
interrupted. catastrophes such as aortic dissection should be
 Treatment of prerenal renal failure is volume replacement; considered in the differential diagnosis.
treatment of postrenal failure is relief of the obstruction.  UREMIA
 The main causes of postrenal failure are obstruction o Nonspecific symptoms of fatigue, weakness,
caused by prostatic hypertrophy in men and bilateral nausea and early morning vomiting, itchiness,
ureteral obstruction caused by abdominal or pelvic confusion, pericarditis, and coma attributed to the
malignancy in either gender. retention of waste products in renal failure but do
 Uremic pericarditis is an indication for urgent not always correlate with the BUN level.
hemodialysis. Other indications include hyperkalemia, o A highly malnourished patient with renal failure may
metabolic acidosis, severe hyperphosphatemia, and have a modestly elevated BUN and be uremic.
volume overload when refractory to medical management. Another patient may have a highly elevated BUN
 Treatment of hyperkalemia: C BIG K (calcium, and be asymptomatic.
bicarbonate/beta-agonist, insulin, glucose, Kayexalate).  AZOTEMIA
- Elevated BUN without symptoms

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 Prelims (1st Sem) Acute Kidney Injury
Dr. Magnolia Reyes
CLINICAL THERAPEUTICS· September 25, 2020

V. CAUSES OF ACUTE KIDNEY INJURY VI. EVALUATION OF PATIENTS WITH AKI

3 BASIC PATHOPHYSIOLOGIC MECHANISMS  Starts with a detailed history and physical examination
 prerenal failure o Does the patient have signs or symptoms of a
 intrinsic renal failure systemic disease, such as heart failure or cirrhosis,
 postrenal failure that could cause prerenal failure?
o Does the patient have symptoms of a disease, such
A. CAUSES OF PRERENAL ACUTE KIDNEY INJURY as lupus, that could cause a glomerulonephritis?
PRERENAL FAILURE o Did the patient receive something in the hospital that
 diminished GFR could cause ATN, such as intravenous contrast or an
o due to marked decreased renal blood perfusion aminoglycoside?
o volume depletion from gastrointestinal fluid loss or o While in the operating room did the patient become
hemorrhage hypotensive from sepsis or from hemorrhage that
 e.g. severe nephrotic syndrome: massive peripheral caused ischemic ATN?
edema present, while the effective arterial blood volume o Is the patient receiving an antibiotic and now has
may be very low as a consequence of the severe allergic interstitial nephritis?
hypoalbuminemia. o In addition to the history and physical examination,
 congestive heart failure may have prerenal failure because urinalysis and measurement of urinary
of a low cardiac ejection fraction, yet be fluid overloaded electrolytes are helpful in making the diagnosis.
with peripheral and pulmonary edema.
 BUN:Cr ratio is more than 20 in prerenal failure. A. URINALYSIS
 Medications such as aspirin, nonsteroidal anti-  The urine findings based on testing
inflammatory drugs (NSAIDs), and ACE inhibitors can alter o reagent paper
intrarenal blood flow and result in prerenal failure. o microscopic examination

CAUSES OF PRERENAL ACUTE KIDNEY INJURY PRERENAL FAILURE

TRUE VOLUME DEPLETION  High specific gravity
 Gastrointestinal losses  Normal microscopic findings
 Renal losses (diuretics)
REDUCED EFFECTIVE ARTERIAL BLOOD VOLUME POSTRENAL FAILURE
 Nephrotic syndrome  Unable to concentrate the urine, so the urine osmolality is
 Cirrhosis with portal hypertension equal to the serum osmolality (isosthenuria) and the
 Severe burns specific gravity is 1.010.
 Sepsis  Microscopic findings vary depending on the cause of the
 Systemic Inflammatory Response Syndrome (SIRS) obstruction: hematuria (crystals or stones), leukocytes
MEDICATIONS (prostatic hypertrophy), or normal (extrinsic ureteral
 ACE Inhibitors compression from a tumor)
 NSAIDs
DECREASED CARDIAC OUTPUT INTRINSIC RENAL FAILURE
 Congestive heart failure  Ischemic and nephrotoxic
 Pericardial tamponade o Isosthenuric, often with proteinuria, and containing
B. CAUSES OF INTRINSIC ACUTE KIDNEY INJURY “muddy brown” granular casts on microscopy
 Glomerulonephritis
CAUSES OF INTRINSIC ACUTE KIDNEY INJURY o Moderate to severe proteinuria, sometimes
ACUTE TUBULAR NECROSIS microscopic hematuria and red blood cell (RBC) casts
Nephrotoxic Agents  Tubulointerstitial nephritis
 Aminoglycosides o Isosthenuric (the tubules are unable to concentrate
 Radiocontrast the urine), with mild proteinuria, and on white cell
 Chemotherapy casts, and urinary eosinophils
Ischemic
 Hypotension
 Vascular catastrophe
GLOMERULONEPHRITIS
 Post-infectious
 Vasculitis
 Immune complex diseases (lupus, Mesangioproliferative
Glomerulonephritis, cryoglobulinemia)
 Cholesterol emboli syndrome
 Hemolytic uremic syndrome / thrombotic thrombocytopenic
purpura
TUBULOINTERSTITIAL NEPHRITIS
 Medications (cephalosporins, methicillin, rifampin)
 Infection (pyelonephritis, HIV)

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 Prelims (1st Sem) Acute Kidney Injury
Dr. Magnolia Reyes
CLINICAL THERAPEUTICS· September 25, 2020

EVALUATION OF ACUTE RENAL FAILURE

ETIOLOGY URINALYSIS FENA (%) UNA 2. A 49-year-old man with a long-standing history of chronic
(mEq/L) renal failure as a consequence of diabetic nephropathy is
Prerenal Concentrated (high < 1% <20 brought to the emergency room for nausea, lethargy, and
failure specific gravity) with confusion. His physical examination is significant for an
normal sediment elevated jugular venous pressure, clear lung fields, and
ATN Isosthenuric with >1% >20 harsh systolic and diastolic sounds heard over the
muddy brown precordium. Serum chemistries reveal K 5.1 mEq/ L, CO2
granular casts 17 mEq/ L, BUN 145 mg/ dL, and creatinine 9.8 mg/ dL.
Glomerulo- Moderate to severe <1% varies Which of the following is the most appropriate therapy?
nephritis proteinuria with
A. Administer IV insulin and glucose.
RBC and RBC casts
B. Administer IV sodium bicarbonate.
Interstitial Mild to moderate >1% >20
nephritis C. Administer IV furosemide.
proteinuria with
RBC, WBC, and D. Urgent hemodialysis.
WBC casts
Postrenal Variable depending <1% <20 3. A 62-year-old diabetic man underwent an abdominal aortic
failure on cause (early) (early) aneurysm repair 2 days ago. He is being treated with
>1% >20 gentamicin for a urinary tract infection. His urine output has
(late) (late) fallen to 300 mL over 24 hours, and his serum creatinine
has risen from 1.1 mg/ dL on admission to 1.9 mg/ dL.
VII. COMPREHENSION QUESTIONS Which of the following laboratory values would be most
1. A 63-year-old woman with a history of cervical cancer consistent with a prerenal etiology of his renal
treated with hysterectomy and pelvic irradiation now insufficiency?
presents with acute oliguric renal failure. On physical A. FENa of 3%
examination, she has normal jugular venous pressure, is B. Urinary sodium level of 10 mEq/ L
normotensive without orthostasis, and has a benign C. Central venous pressure reading of 10 mm Hg
abdominal examination. Her urinalysis shows a specific D. Gentamicin trough level of 4 μg/mL
gravity of 1.010, with no cells or casts on microscopy.
Urinary FENa is 2% and the Na level is 35 mEq/ L. Which References
of the following is the best next step? Toy, E., Patlan Jr., J. and Warner, M., 2017. Case Files
A. Bolus of intravenous fluids Internal Medicine. 5th ed. United States: McGraw-Hill
B. Renal ultrasound Education, pp.276 - 285.
C. Computed tomographic (CT) scan of the abdomen with
intravenous contrast Dr. Reyes’ ppt
D. Administration of furosemide to increase her urine output

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