The Nursing Process · 6 min read
Chronic Kidney Disease
Chronic Kidney Disease
Chronic kidney disease (CKD) involves progressive, irreversible nephron loss over months to years. CKD is staged by GFR: Stage 1 (GFR ≥90 with kidney damage), Stage 2 (GFR 60-89), Stage 3a (GFR 45-59), Stage 3b (GFR 30-44), Stage 4 (GFR 15-29), and Stage 5 (GFR <15 or dialysis).
Nephron loss triggers compensatory hyperfiltration in remaining nephrons. This adaptation initially maintains function but eventually causes glomerular hypertension, sclerosis, and further nephron loss, creating a progressive cycle.
Uremic syndrome develops as waste products accumulate. Manifestations affect virtually every organ system including cardiovascular, pulmonary, gastrointestinal, neurological, hematological, musculoskeletal, dermatological, endocrine, and immunological systems.
Glomerular Diseases
Glomerulonephritis involves glomerular inflammation from immune-mediated injury. Primary glomerulonephritis originates in the kidney. Secondary glomerulonephritis results from systemic diseases such as lupus, diabetes, or infections.
Nephrotic syndrome features heavy proteinuria (>3.5 g/day), hypoalbuminemia, edema, and hyperlipidemia. Nephritic syndrome features hematuria, red cell casts, mild proteinuria, hypertension, and reduced GFR.
Tubulointerstitial Diseases
Tubulointerstitial nephritis involves inflammation of tubules and surrounding interstitium. Acute forms result from drugs, infections, or autoimmune disorders. Chronic forms result from prolonged injury, reflux nephropathy, or hereditary conditions.
Vascular Diseases
Renovascular disease involves renal artery stenosis from atherosclerosis or fibromuscular dysplasia. Hypertensive nephrosclerosis results from chronic hypertension causing arteriolar changes. Thrombotic microangiopathies cause microvascular injury and thrombosis.
Etiologies of End-Stage Renal Disease
Diabetes Mellitus
Diabetes is the leading cause of ESRD, accounting for approximately 44% of new cases. Diabetic nephropathy develops through predictable stages over 15-25 years. Early changes include glomerular hyperfiltration, basement membrane thickening, and mesangial expansion. Microalbuminuria (30-300 mg/day) progresses to macroalbuminuria (>300 mg/day) and declining GFR.
Risk factors for progression include poor glycemic control, hypertension, smoking, hyperlipidemia, and genetic susceptibility. Intensive glycemic and blood pressure control slow but do not prevent progression.
Hypertension
Hypertension is the second leading cause of ESRD, accounting for approximately 28% of cases. Hypertensive nephrosclerosis results from chronic elevated pressure causing arteriolar changes, ischemia, and glomerulosclerosis.
African Americans have significantly higher rates of hypertensive ESRD, suggesting genetic susceptibility factors. Malignant hypertension causes accelerated kidney damage with fibrinoid necrosis of arterioles.
Glomerulonephritis
Glomerulonephritis accounts for approximately 8% of ESRD cases. IgA nephropathy is the most common primary glomerulonephritis worldwide. Focal segmental glomerulosclerosis (FSGS) has increasing incidence, particularly in African Americans. Membranous nephropathy, minimal change disease, and membranoproliferative glomerulonephritis are other causes.
Polycystic Kidney Disease
Autosomal dominant polycystic kidney disease (ADPKD) accounts for approximately 2% of ESRD. Mutations in PKD1 or PKD2 genes cause progressive cyst development and kidney enlargement. ESRD typically develops in the fourth to sixth decade. Extrarenal manifestations include liver cysts, intracranial aneurysms, cardiac valve abnormalities, and abdominal hernias.
Other Causes
Congenital anomalies include reflux nephropathy, obstructive uropathy, and renal dysplasia. Interstitial nephritis may result from analgesic abuse, heavy metals, or chronic infections. Lupus nephritis affects up to 50% of systemic lupus erythematosus patients. Multiple myeloma causes cast nephropathy and light chain deposition. HIV-associated nephropathy causes collapsing FSGS.
Laboratory and Diagnostic Testing
Kidney Function Tests
Serum creatinine reflects muscle mass and kidney function. Normal values are approximately 0.7-1.3 mg/dL for men and 0.6-1.1 mg/dL for women. Creatinine rises only after significant GFR decline (>50%), making it an insensitive early marker.
Blood urea nitrogen (BUN) reflects protein intake, catabolism, and kidney function. Normal values are 7-20 mg/dL. The BUN/creatinine ratio helps differentiate prerenal (>20:1) from intrinsic (10-15:1) kidney injury.
GFR estimation uses equations incorporating creatinine, age, sex, and race. The CKD-EPI equation is preferred for adults. Cystatin C-based equations may improve accuracy in certain populations.
Creatinine clearance measured from 24-hour urine collection provides direct GFR assessment. Accuracy depends on complete urine collection.
Urinalysis
Dipstick testing evaluates pH, specific gravity, protein, glucose, blood, leukocyte esterase, nitrites, ketones, and bilirubin. Microscopic examination identifies cells, casts, crystals, and organisms.
Proteinuria quantification uses spot urine protein/creatinine ratio or 24-hour urine collection. Albuminuria is specifically measured to detect early diabetic nephropathy.
Electrolytes and Minerals
Sodium abnormalities reflect water balance disorders. Hyponatremia in ESRD usually results from water excess. Hypernatremia is uncommon.
Potassium elevation occurs with declining GFR. Hyperkalemia (>5.5 mEq/L) causes cardiac arrhythmias. Dietary restriction and dialysis manage potassium levels.
Phosphorus levels rise with declining GFR. Hyperphosphatemia contributes to secondary hyperparathyroidism and vascular calcification. Target levels are 3.5-5.5 mg/dL for dialysis patients.
Magnesium may accumulate with severe kidney impairment. Magnesium-containing medications should be avoided.
Acid-Base Status
Metabolic acidosis develops as kidneys lose capacity to excrete acid and regenerate bicarbonate. Serum bicarbonate levels below 22 mEq/L indicate metabolic acidosis. Anion gap calculation helps identify causes.
Hematology
Complete blood count reveals anemia of CKD from erythropoietin deficiency. Normocytic, normochromic anemia typically develops when GFR falls below 30 mL/min. Target hemoglobin is 10-11 g/dL for dialysis patients.
Iron studies include serum iron, total iron-binding capacity, transferrin saturation, and ferritin. Iron deficiency is common and limits erythropoietin response. Target transferrin saturation is >20% and ferritin >100 ng/mL.
Lipid Panel
Dyslipidemia is common in ESRD with elevated triglycerides, low HDL, and variable LDL. Cardiovascular disease is the leading cause of death in dialysis patients.
Parathyroid Hormone
Intact PTH levels guide management of secondary hyperparathyroidism. Target ranges vary by CKD stage. For dialysis patients, PTH 2-9 times the upper normal limit is generally acceptable.
Peritoneal Equilibration Test
The PET assesses peritoneal membrane transport characteristics. A 4-hour dwell with 2.5% dextrose solution measures dialysate-to-plasma (D/P) creatinine ratio and glucose absorption. Results classify patients as high, high-average, low-average, or low transporters. Transport type guides modality selection and prescription optimization.
Adequacy Testing
Kt/V urea measures dialysis dose. Weekly Kt/V target is ≥1.7 for peritoneal dialysis. Creatinine clearance targets are ≥50 L/week/1.73m². Residual kidney function contributes significantly to overall clearance and must be measured separately.
Pharmacology
Phosphate Binders
Phosphate binders reduce intestinal phosphorus absorption. Calcium-based binders (calcium carbonate, calcium acetate) are effective and inexpensive but contribute to calcium load and potential vascular calcification. Non-calcium binders include sevelamer (hydrochloride or carbonate), lanthanum carbonate, and sucroferric oxyhydroxide. Aluminum-based binders are avoided due to toxicity risk.
Binders must be taken with meals to bind dietary phosphorus. Timing is critical; taking binders between meals provides no benefit.
Vitamin D Analogues
Calcitriol is active vitamin D (1,25-dihydroxyvitamin D). Native vitamin D supplements (cholecalciferol, ergocalciferol) treat deficiency but require kidney activation. Active vitamin D analogues include paricalcitol, doxercalciferol, and alfacalcidol. These suppress PTH secretion and improve calcium absorption. Calcium and phosphorus levels must be monitored to avoid hypercalcemia and hyperphosphatemia.
Calcimimetics
Cinacalcet increases calcium-sensing receptor sensitivity on parathyroid glands, suppressing PTH secretion. It is used for secondary hyperparathyroidism when vitamin D therapy alone is insufficient. Hypocalcemia is a potential adverse effect.
Erythropoiesis-Stimulating Agents
Epoetin alfa and darbepoetin alfa stimulate red blood cell production. Administration is subcutaneous or intravenous. Dosing is individualized to maintain hemoglobin 10-11 g/dL. Higher targets increase cardiovascular risk. Adequate iron stores are essential for response. Hypertension and pure red cell aplasia are potential complications.
Iron Supplements
Oral iron (ferrous sulfate, ferrous gluconate) is often poorly tolerated and absorbed. Intravenous iron (iron sucrose, ferric gluconate, iron dextran, ferumoxytol, ferric carboxymaltose) provides reliable repletion. Anaphylaxis risk exists, particularly with iron dextran.
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