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Renal/Urinary System Pathophysiology

Master kidney function, filtration mechanisms, fluid/electrolyte balance, and pathophysiology of renal disease.

Other Systems

Overview

The renal system maintains fluid and electrolyte balance, regulates blood pressure, and eliminates metabolic wastes. Understanding normal kidney function and renal pathophysiology is essential for nursing assessment and management of fluid/electrolyte disorders and kidney disease. This guide covers nephron function, filtration, and common renal disorders.

Kidney Anatomy & Filtration

Renal Structure

  • Location: retroperitoneal, one per side
  • Cortex: outer layer with glomeruli
  • Medulla: inner region with loops of Henle, collecting ducts
  • Functional unit: ~1 million nephrons per kidney
  • Blood processing: 180 L blood/day → 1.5-2 L urine

Nephron Structure

  • Renal corpuscle: glomerulus + Bowman's capsule (filtration site)
  • Proximal convoluted tubule: reabsorption
  • Loop of Henle: countercurrent multiplier, concentration
  • Distal convoluted tubule: fine-tuning reabsorption
  • Collecting duct: final water reabsorption (ADH-regulated)

Glomerular Filtration

  • GFR: normal 125 mL/min (180 L/day), ↓ with aging/disease
  • Filtration pressure: balance of hydrostatic vs. osmotic forces
  • Barrier: endothelium, basement membrane, podocytes
  • Selectivity: size (molecules <5.5 nm freely filtered) and charge (negative filtered less)
  • Autoregulation: maintains constant GFR over BP 50-150 mmHg

Tubular Reabsorption & Secretion

  • PCT (65% water/ions): glucose, amino acids, sodium active transport
  • Loop of Henle: sodium concentration, osmotic gradient creation
  • DCT & Collecting Duct: aldosterone regulation of sodium, ADH regulation of water
  • Result: 99% of filtered substances reabsorbed, only 1-2% excreted

Fluid & Electrolyte Balance

Water Balance

  • Intake: drinking, food, metabolism (~2-2.5 L/day)
  • Output: urine (1-2 L), insensible losses (lungs, skin ~1 L), feces (0.2 L)
  • Regulation: ADH controls collecting duct water reabsorption
  • ADH triggers: ↑ osmolality (>290), ↓ blood volume, ethanol inhibition

Sodium Balance (Blood Volume Control)

  • Filtered load: 25,000 mEq/day (vs 100-150 mEq/day excretion)
  • Reabsorption sites: PCT (65%), loop (25%), DCT/collecting (10%)
  • Aldosterone: ↑ sodium reabsorption, ↑ potassium secretion (RAAS activation)
  • ANP: ↑ sodium and water excretion (from stretched atrium)

Osmolality & Electrolytes

  • Normal serum osmolality: 285-295 mOsm/kg
  • Hyposmolality (<285): water excess, cell swelling (cerebral edema)
  • Hyperosmolality (>295): water deficit, cell shrinking
  • Potassium: critical for cardiac function (normal 3.5-5.0 mEq/L)
  • Calcium: normal 8.5-10.5 mg/dL (PTH-regulated reabsorption)

Kidney Disease

Acute Kidney Injury (AKI)

  • Onset: hours to days, potentially reversible
  • Prerenal (40-50%): ↓ perfusion (hemorrhage, shock, dehydration) - kidney tubules intact
  • Intrinsic (10-50%): direct kidney damage (ATN, GN, AIN)
  • Postrenal (5-10%): obstruction to urine flow (stones, BPH, tumors)
  • Stages: based on creatinine rise and urine output

Chronic Kidney Disease (CKD)

  • Definition: progressive ↓ GFR over months/years
  • Stages: based on GFR (Stage 1: >90, Stage 5: <15)
  • Common causes: hypertension (30%), diabetes (35%), GN, polycystic kidney disease
  • Consequences: uremia, hypertension, anemia, bone disease, CVD risk
  • Progression: remaining nephrons hyperfiltration → glomerulosclerosis, fibrosis

Glomerulonephritis (GN)

  • Acute GN: rapid onset hematuria, proteinuria, hypertension, edema
  • Nephrotic Syndrome: heavy proteinuria (>3.5 g/day), hypoproteinemia, edema, hyperlipidemia
  • Nephritic Syndrome: hematuria, modest proteinuria, hypertension
  • Causes: post-infectious (strep most common), IgA, lupus, ANCA

Diabetic Nephropathy

  • Pathophysiology: glomerular basement membrane thickening, nodular glomerulosclerosis
  • Progression: hyperfiltration → proteinuria → nephrotic syndrome → CKD
  • Prevention: tight glucose control, blood pressure control (especially ACE-I/ARB)
  • Prevalence: leading cause of ESRD in developed countries

Common Urinary Disorders

  • UTI: cystitis (lower), pyelonephritis (upper), E. coli most common
  • Kidney Stones: calcium oxalate (75%), calcium phosphate, uric acid
  • Polycystic Kidney Disease: multiple cysts, ADPKD (85%), progressive renal failure
  • Renal Artery Stenosis: narrowed renal artery, hypertension, ischemic nephropathy

Electrolyte Abnormalities

Hyperkalemia & Hypokalemia

  • Hyperkalemia (>5.0): peaked T waves → arrhythmias, muscle weakness
  • Causes: decreased excretion (CKD, ACE-I), increased release (tumor lysis, hemolysis)
  • Hypokalemia (<3.5): muscle weakness, arrhythmias, constipation
  • Causes: GI losses (diarrhea), diuretics, inadequate intake

Hypernatremia & Hyponatremia

  • Hypernatremia (>145): hypertonic plasma, cell dehydration (brain cells → seizures)
  • Causes: water loss (DI, insensible), inadequate intake, excess salt
  • Hyponatremia (<135): hypotonic plasma, cell swelling (cerebral edema)
  • Causes: SIADH, diuretics, dilute fluid intake, heart failure

Hypercalcemia & Hypocalcemia

  • Hypercalcemia (>10.5): nephrogenic DI (polyuria), stones, constipation, altered mental status
  • Causes: malignancy (PTHrP), hyperparathyroidism, vitamin D excess
  • Hypocalcemia (<8.5): Chvostek's/Trousseau's signs, tetany, seizures
  • Causes: vitamin D deficiency, hypoparathyroidism, CKD

Clinical Assessment

Urinary Symptoms & Signs

  • Dysuria: painful urination (UTI, urethritis)
  • Hematuria: gross (visible) or microscopic, painless = cancer risk
  • Proteinuria: nephrotic (>3.5 g/day) vs. nephritic (0.5-3.5 g/day)
  • Pyuria: WBCs in urine (>5/hpf abnormal)
  • Casts: RBC (glomerular bleeding), WBC (infection/inflammation), hyaline (normal)

Diagnostic Tests

  • Serum: creatinine, BUN, eGFR, electrolytes, albumin, lipids
  • Urinalysis: appearance, pH, protein, glucose, cells, casts, crystals
  • Urine Electrolytes: sodium, osmolality, FENa (assess prerenal vs. intrinsic AKI)
  • Imaging: ultrasound (kidney size, cysts), CT (stones), Doppler (stenosis)
  • Biopsy: kidney biopsy (immunofluorescence, electron microscopy for GN)

Management Principles

AKI Management

  • Prerenal: fluid resuscitation, improve cardiac output
  • Intrinsic: remove offending agent, supportive care, dialysis if severe
  • Postrenal: remove obstruction
  • Monitor: urine output, creatinine, potassium, fluid balance

CKD Management

  • BP control: ACE-I/ARB (slows progression), target <130/80
  • Diabetes control: tight glycemic control, SGLT2 inhibitors
  • Bone/mineral: phosphate binders, active vitamin D, calcimimetics
  • Anemia: ESA (erythropoietin-stimulating agents)
  • Renal replacement: dialysis (hemodialysis, peritoneal) or transplantation

Electrolyte Management

  • Hyperkalemia: urgent treatment if >6.5 (calcium, insulin/glucose, K+ removal)
  • Hyponatremia: fluid restriction (SIADH), hypertonic saline (acute symptomatic)
  • Hypercalcemia: hydration, diuretics, bisphosphonates, calcitonin
  • Hyperphosphatemia: phosphate binders, dietary restriction

Study Questions

1. Compare and contrast acute kidney injury (AKI) and chronic kidney disease (CKD) in terms of pathophysiology, reversibility, and clinical presentation.

2. Explain the pathophysiology of nephrotic syndrome, including why proteinuria leads to edema and hypercoagulability.

3. A patient with CKD stage 4 develops hyperkalemia and metabolic acidosis. Explain the mechanisms for both complications.

4. Compare prerenal, intrinsic, and postrenal causes of AKI in terms of pathophysiology, urinary findings, and reversibility.

5. Explain why ACE inhibitors are effective in slowing the progression of diabetic nephropathy.

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