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PY7.1-9 | Renal Physiology — SDL Guide (Part 4)

Principles of Dialysis (PY7.7)

When GFR falls below 10–15 mL/min (end-stage renal disease, ESRD), the kidneys can no longer maintain homeostasis — renal replacement therapy is needed.

Haemodialysis (HD):
Blood is pumped through an extracorporeal circuit across a semipermeable membrane (dialyser) against a dialysate solution (an electrolyte solution of desired composition).

Mechanisms:
- Diffusion: Solutes (urea, creatinine, K⁺) move down concentration gradient from blood to dialysate. Dialysate K⁺ is kept low (1–2 mEq/L) to drive K⁺ out of blood.
- Ultrafiltration: Hydrostatic pressure difference across membrane removes excess water.
- No active transport; cannot remove protein-bound toxins efficiently.

Typically 3 sessions/week × 4 h each. Vascular access: AV fistula (preferred) or tunnelled dialysis catheter.

Peritoneal dialysis (PD):
The patient's own peritoneal membrane (highly vascular, ~2 m² surface area) acts as the dialysis membrane.
Dialysate is instilled into the peritoneal cavity, dwells for hours, then drained.

CAPD (Continuous Ambulatory PD): 4 exchanges/day, patient performs at home. Dialysate uses glucose as osmotic agent to drive ultrafiltration.

Advantages of PD over HD: continuous (less haemodynamic stress), home-based (better quality of life for Indian rural patients), cheaper in long-term.
Disadvantage: peritonitis risk, protein loss in dialysate, less efficient for large patients.

Principles of Dialysis (PY7.7) — Four-panel illustration showing the haemodialysis extracorporeal circuit, diffusion and ultrafiltration mechanisms across the dialyser membrane, peritoneal dialysis using the peritoneal membrane, and a comparison of haemodialysis versus peritoneal dialysis.

Summary

Diuretics: Mechanisms and Clinical Uses (PY7.8)

Diuretics increase urine output by reducing tubular reabsorption of Na⁺ and water. Classified by site of action:

Class	Site	Mechanism	Example	Use
Osmotic	PCT, loop	Non-reabsorbable solute draws water	Mannitol	Cerebral oedema, IOP
Carbonic anhydrase inhibitors	PCT	Block CA → ↓ H⁺ secretion → ↓ HCO₃⁻ reabsorption	Acetazolamide	Glaucoma, altitude sickness
Loop diuretics	TAL	Block NKCC2	Furosemide	Pulmonary oedema, acute heart failure, hypercalcaemia
Thiazides	DCT	Block NCC (Na-Cl co-transporter)	Hydrochlorothiazide	Hypertension, heart failure
K⁺-sparing	Collecting duct	Block ENaC (amiloride) or aldosterone receptor (spironolactone)	Spironolactone	Hyperaldosteronism, heart failure (cardioprotective)
ADH antagonists (vaptans)	Collecting duct	Block V2 receptor → no aquaporin insertion	Tolvaptan	SIADH, hyponatraemia

Key side effects to know:
- Loop diuretics: hypokalaemia, hyponatraemia, ototoxicity (high dose IV)
- Thiazides: hypokalaemia, hyperuricaemia, hyperglycaemia, hypercalcaemia
- Spironolactone: hyperkalaemia (dangerous with ACE inhibitors), gynaecomastia
- Acetazolamide: metabolic acidosis (loses HCO₃⁻)

Diuretics: Mechanisms and Clinical Uses (PY7.8) — Four-panel illustration showing the four major diuretic classes mapped to their nephron sites of action: loop diuretics blocking NKCC2, thiazides blocking NCC, K+-sparing diuretics blocking aldosterone/ENaC, and carbonic anhydrase inhibitors in the PCT.