Uremia: Kidney failure → urea accumulates in blood → nausea, vomiting, fatigue, coma. Treatment: haemodialysis or kidney transplant. Blood urea nitrogen (BUN) and serum creatinine are clinical markers of renal function.

Renal Calculi (Kidney Stones): Most common = calcium oxalate (~70–80%). Uric acid stones form in acidic urine (gout patients). Obstruction → severe flank pain (renal colic) + blood in urine (haematuria). Prevention: high fluid intake, reduced dietary oxalate and animal protein.

Glomerulonephritis (Nephritic Syndrome): Post-streptococcal or autoimmune inflammation of glomeruli → filtration barrier damaged → red blood cells and proteins leak into filtrate → haematuria + proteinuria. Reduced GFR → oliguria + oedema (Na+/water retention). Compared to nephrotic syndrome (massive proteinuria, no haematuria, severe oedema, normal BP).

Nephrotic Syndrome: Glomerular barrier damage → massive protein loss (>3.5 g/day) → hypoalbuminaemia → reduced plasma oncotic pressure (Starling forces disrupted) → fluid shifts from capillaries to interstitium → generalised oedema (anasarca).

Diabetes Insipidus: Central DI = ADH deficiency. Nephrogenic DI = kidney unresponsive to ADH. Both cause polyuria $\frac{up to 20 L}{day}$, very dilute urine, dehydration, polydipsia. NOT diabetes mellitus (no glucose involved).

Hyperaldosteronism (Conn's Syndrome): Excess aldosterone → excess Na+ retention → hypertension + hypokalaemia + suppressed renin. Can cause metabolic alkalosis.

SIADH: Excess ADH → excess water retention → dilutional hyponatraemia → confusion, seizures. Serum Na+ falls despite body fluid excess.

Heart Failure and Oedema: Low cardiac output → perceived as low BP → RAAS activated + ADH released → Na+ and water retained → fluid overload. ANF is elevated but overwhelmed by RAAS/aldosterone.

Clinical Drug Connections: ACE inhibitors reduce angiotensin II → less aldosterone → hyperkalaemia risk. Loop diuretics (furosemide) block NKCC2 in thick ascending limb → abolish medullary gradient → potent diuresis. Spironolactone blocks aldosterone receptors → natriuresis + hyperkalaemia.

Dialysis principle: Semipermeable membrane separates blood from dialysing fluid. Waste products diffuse down concentration gradient out of blood. Dialysing fluid contains glucose and amino acids at normal plasma levels to prevent their loss.