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Non-Modifiable Risk Factors: Modifiable Risk Factors

Non-modifiable risk factors for chronic kidney disease include age, gender, and family history, while modifiable risk factors are diet, lifestyle, and use of NSAIDs. Specific conditions that can lead to chronic kidney disease are chronic glomerulonephritis, recurrent pyelonephritis, diabetes mellitus, polycystic kidney disease, systemic lupus erythematosus, and tubulointerstitial inflammation. Chronic kidney disease is staged based on glomerular filtration rate, with later stages being associated with increased kidney damage, decreased kidney function, and eventually end stage renal disease where dialysis is required.

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Kimberly Bomediano
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1K views

Non-Modifiable Risk Factors: Modifiable Risk Factors

Non-modifiable risk factors for chronic kidney disease include age, gender, and family history, while modifiable risk factors are diet, lifestyle, and use of NSAIDs. Specific conditions that can lead to chronic kidney disease are chronic glomerulonephritis, recurrent pyelonephritis, diabetes mellitus, polycystic kidney disease, systemic lupus erythematosus, and tubulointerstitial inflammation. Chronic kidney disease is staged based on glomerular filtration rate, with later stages being associated with increased kidney damage, decreased kidney function, and eventually end stage renal disease where dialysis is required.

Uploaded by

Kimberly Bomediano
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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Non-modifiable Risk factors: Age Gender Familial history

Modifiable Risk factors: Diet Lifestyle Use of NSAIDs (nephrotoxic)

Chronic Glomerulonephritis

Recurrent Pyelonephritis

Diabetes Mellitus

Polycystic kidney disease

Systemic lupus erythematus

Tubulointerstitial inflammation

Elevated glucose levels Large fluid filled cyst in the tubules and collecting ducts enlarge and multiply

Tissue fibrosis

Increased formation of advanced glysosylated end products

Production of large variety of antibodies against selfantigens. (RBC, Nucleic acid, RNA, coagulation proteins etc.)

Kidney enlarge

antibodies react with their corresponding antigen

Glomerular basement membrane thickening and proliferation of masangial cells

Renal blood vessels and nephrons are compressed and obstructed

Formation of immune complex

Diffuse intercapillary glomerulosclerosis

Deposition of immune complexes in the kidneys and blood vessels Destruction of renal tissue/cells

Trigger an inflammatory response and damages the kidneys

Dec. renal blood flow

Loss of nephrons Glomerular capillary hypertension

Angiotensin II

Decrease renal reserve

Increase Glomerular permeability

Promotes Mesangial cell proliferation and cytokine production

Proteinuria

CHON ultrafiltrates are toxic to the proximal tubules

Tubulointerstitial inflammation and fibrosis Stage 1: GFR <90mL/min/1.73 m2

Metoprolol 100 mg bid Systemic hypertension

Renal scarring

BP above 140/90

Stage 2: GFR 60-89 mL/min/1.73 m2

50% damage to kidney Progression of Kidney damage

Stage 3: GFR 30-59 mL/min/1.73 m2 2 ) Renal insufficiency

75% damage to the kidney

Changes in the cell morphology of the remaining nephrons

Decrease in number of functional nephrons Increase workload for the remaining nephrons

Hypertrophy Hyperfiltration of the remaining nephrons as compensatory mechanism

Further damage to Kidney Hypertrophy of remaining nephrons

90% damage

Stage 4: GFR 15-29 ml/min

H Retention
Metabolic acidosis

Decreased Creatinine clearance

Decreased excretion of Blood urea nitrogen

K excretion Water retention

Na+ retention

Hypokalemia

K+ = 2.95 mmol/L Azotemia Pitting edema E Urine output

Urine output <30 cc/hr

Decreased production of Vitamin D in the kidneys

Inability of the kidney to excrete water

Lower Extremety

Decreased Calcium absorption in the GI tract

Fluid overload

Fluid shifting

lungs

DOB/SOB Crackles Nocturnal paroxysmal dyspnea Ineffective breathing pattern

Hypocalcemia

Hyperphosphatemia

Phosphate > 4.1 mg/dl

Increase bone resorption CaCO3 500mg tid

HEMODIALYSIS

Less than 10 % remaining renal function

Stage 5: GFR <15 ml/min/1.73 m2

END STAGE RENAL DISEASE


Hypertrophy of the remaining nephrons

No more compensation mechanism done by the kidney

Dilute Polyuria

Inability of the kidney to concentrate urine

Na+ loss

hyponatremia

Further loss of nephron function

Loss of kidneys excretory functions

G Toxins impair WBCs, humoral & cell mediated immunity

Decrease production of erythropoietin in the juxtaglomerular apparatus

Suppression of immune system Decrease RBC production -Low hamatocrit count -RBC Count < 4.2 million Delayed wound healing infection

Anemia

Fatigue Increase RR Increase PR Dizziness Pail mucous membranes

Eprex FeSO4

Activity intolerance

References: S. Smeltzer, B. Bare, J. Hinkle, K. Cheever, Brunner and Suddarths Textbook of Medical-Surgical Nursing 10th edition, Lippincot Williams & Wilkins, 2009, pages 1325-1333 S. Huether, K. McCance Understanding Pathophysiology 4th edition, Mosby Elsevier, pages 802-806

L. Schumacher, C. Chernecky Real World Nursing Surival Guide: Criticalcare and Emergency Nursing, Elsevier saunders, pages 243-250

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