Chronic Kidney Disease

Detailed Overview

CKD is a global health burden predominantly driven by diabetes and hypertension. The progressive loss of nephrons triggers hyperfiltration in remaining nephrons, leading to glomerular sclerosis and further decline. It affects fluid balance, acid-base homeostasis, erythropoiesis, and bone mineral metabolism. Advanced stages lead to uremia requiring renal replacement therapy.

Epidemiology & Demographics

Affects ~15% of the US adult population (37 million people). Higher prevalence in African American and Hispanic populations.

Etiological Mechanism

Diabetic nephropathy (most common, ~40%), hypertensive nephrosclerosis (~27%), glomerulonephritis, polycystic kidney disease.

Primary Causes

Poorly controlled Type 2 Diabetes mellitus, prolonged systemic hypertension, chronic NSAID use.

• Diabetes and Hypertension: The top two risk factors driving microvascular kidney damage.
• Age >60: Natural GFR decline exacerbates comorbid kidney injury.

Initial injury destroys nephrons. Surviving nephrons undergo compensatory hypertrophy and increase single-nephron GFR (hyperfiltration) mediated by efferent arteriolar vasoconstriction (angiotensin II dependent). This increases glomerular capillary hydrostatic pressure, endothelial injury, and podocyte detachment. Protein leaks into the filtrate, causing tubular inflammation and interstitial fibrosis, leading to an irreversible cycle of nephron loss.

Characteristic Clinical Presentation

• Fatigue & Weakness: Secondary to decreased erythropoietin production leading to normocytic anemia.
• Pruritus: Uremic frost and deposition of calcium-phosphate crystals in the skin.
• Peripheral Edema: Sodium and water retention due to decreased filtration.

Physical Examination Signs

• Hypertension
• Asterixis
• Pericardial Friction Rub

• CKD-MBD: Mineral bone disease: high phosphate, low calcium, secondary hyperparathyroidism, renal osteodystrophy.
• Cardiovascular Disease: Leading cause of death in CKD patients due to accelerated atherosclerosis and vascular calcification.

Diagnostic Criteria & Guidelines

eGFR <60 mL/min/1.73m2 OR markers of kidney damage (albuminuria >30 mg/g, abnormal imaging, abnormal biopsy) present for >3 months.

Differential Diagnosis

• Acute Kidney Injury (rapid rise in creatinine, reversible)
• Obstructive Uropathy (BPH, stones)

Laboratory Tests & Biomarkers

• Serum Creatinine: Persistently elevated (>1.2 mg/dL in women, >1.4 mg/dL in men), with reduced eGFR.
• Urine Albumin-to-Creatinine Ratio (UACR): >30 mg/g (microalbuminuria) or >300 mg/g (macroalbuminuria).
• Serum Phosphorus: Elevated (>4.5 mg/dL) due to decreased renal excretion.

Imaging Modalities & Findings

• Renal Ultrasound:

• Stage 3a/b
  eGFR 45-59 / 30-44. Complications like anemia and bone disease begin.
• Stage 4
  eGFR 15-29. Preparation for dialysis.
• Stage 5
  eGFR <15. Requires renal replacement therapy or transplant.

Second-Line & Adjunctive Therapy

Management of complications: Darbepoetin alfa for anemia (target Hb 10-11.5 g/dL). Sevelamer 800 mg PO TID with meals for hyperphosphatemia. Calcitriol 0.25 mcg PO daily for secondary hyperparathyroidism.

Surgical & Procedural Management

Creation of arteriovenous (AV) fistula in Stage 4 for hemodialysis access. Kidney transplantation is the definitive treatment for ESRD.

Recommended Lifestyle Changes

• Low sodium diet (<2g/day).
• Protein restriction (0.6-0.8 g/kg/day) in advanced stages to limit uremia.
• Avoid nephrotoxins (NSAIDs, IV contrast).

Patient Counseling & Advice

Educate that CKD is a silent disease; taking protective medications (ACEi, SGLT2i) is vital even if they feel well. NSAIDs like ibuprofen must be completely avoided.

Follow-Up & Monitoring Schedule

Every 3-6 months: Basic Metabolic Panel, Calcium, Phos, PTH, CBC, UACR.

Preventive Strategies

Strict glycemic control (HbA1c <7%) and BP control in diabetic patients.

Highly dependent on stage and proteinuria. Stage 5 requires lifelong dialysis (5-year survival ~40-50% on dialysis) or transplant.