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PY7.1-9 | Renal Physiology — Part 4

Principles of Dialysis (PY7.7)

Haemodialysis vs Peritoneal Dialysis

Feature	Haemodialysis	Peritoneal Dialysis
Membrane	Synthetic hollow-fibre dialyser	Peritoneal membrane (biological)
Access	AV fistula, graft, or central catheter	Tenckhoff peritoneal catheter
Frequency	3-4 times/week, 4 hours each	Daily/continuous exchanges (CAPD or APD)
Setting	Hospital or dialysis centre	Home-based
Solute removal	Rapid, efficient (diffusion + ultrafiltration)	Gentler, continuous
Key complication	Hypotension, vascular access infection	Peritonitis
Fluid removal	Transmembrane pressure (ultrafiltration)	Osmotic gradient (hypertonic glucose dialysate)

Haemodialysis vs Peritoneal Dialysis

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.

Feature	Haemodialysis	Peritoneal Dialysis
Membrane	Synthetic hollow-fibre dialyser	Peritoneal membrane (biological)
Access	AV fistula, graft, or central catheter	Tenckhoff peritoneal catheter
Frequency	3-4 times/week, 4 hours each	Daily/continuous exchanges (CAPD or APD)
Setting	Hospital or dialysis centre	Home-based
Solute removal	Rapid, efficient (diffusion + ultrafiltration)	Gentler, continuous
Key complication	Hypotension, vascular access infection	Peritonitis
Fluid removal	Transmembrane pressure (ultrafiltration)	Osmotic gradient (hypertonic glucose dialysate)

Haemodialysis vs Peritoneal Dialysis

Feature	Haemodialysis	Peritoneal Dialysis
Membrane	Synthetic hollow-fibre dialyser	Peritoneal membrane (biological)
Access	AV fistula, graft, or central catheter	Tenckhoff peritoneal catheter
Frequency	3-4 times/week, 4 hours each	Daily/continuous exchanges (CAPD or APD)
Setting	Hospital or dialysis centre	Home-based
Solute removal	Rapid, efficient (diffusion + ultrafiltration)	Gentler, continuous
Key complication	Hypotension, vascular access infection	Peritonitis
Fluid removal	Transmembrane pressure (ultrafiltration)	Osmotic gradient (hypertonic glucose dialysate)

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.

Diuretics: Mechanisms and Clinical Uses (PY7.8)

Diuretics — Classification by Nephron Site

Class	Site	Mechanism	Example	Key Clinical Use	Main Side Effect
Loop diuretics	Thick ascending limb	Block NKCC2	Furosemide	Pulmonary oedema, heart failure	Hypokalaemia, hypomagnesaemia, ototoxicity
Thiazides	DCT	Block NCC	Hydrochlorothiazide	Hypertension (first-line)	Hypokalaemia, hyperuricaemia, hypercalcaemia
K+-sparing (aldosterone antagonist)	Collecting duct	Block aldosterone receptor	Spironolactone	Heart failure, ascites, Conn's syndrome	Hyperkalaemia, gynaecomastia
K+-sparing (ENaC blocker)	Collecting duct	Block ENaC directly	Amiloride	Combined with loop/thiazide	Hyperkalaemia
Carbonic anhydrase inhibitors	PCT	Inhibit CA → less HCO3- reabsorption	Acetazolamide	Glaucoma, altitude sickness	Metabolic acidosis
Osmotic diuretics	PCT, loop of Henle	Increase tubular osmolarity → hold water	Mannitol	Raised intracranial pressure, acute glaucoma	Volume expansion, pulmonary oedema

Diuretics — Classification by Nephron Site

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.

Class	Site	Mechanism	Example	Key Clinical Use	Main Side Effect
Loop diuretics	Thick ascending limb	Block NKCC2	Furosemide	Pulmonary oedema, heart failure	Hypokalaemia, hypomagnesaemia, ototoxicity
Thiazides	DCT	Block NCC	Hydrochlorothiazide	Hypertension (first-line)	Hypokalaemia, hyperuricaemia, hypercalcaemia
K+-sparing (aldosterone antagonist)	Collecting duct	Block aldosterone receptor	Spironolactone	Heart failure, ascites, Conn's syndrome	Hyperkalaemia, gynaecomastia
K+-sparing (ENaC blocker)	Collecting duct	Block ENaC directly	Amiloride	Combined with loop/thiazide	Hyperkalaemia
Carbonic anhydrase inhibitors	PCT	Inhibit CA → less HCO3- reabsorption	Acetazolamide	Glaucoma, altitude sickness	Metabolic acidosis
Osmotic diuretics	PCT, loop of Henle	Increase tubular osmolarity → hold water	Mannitol	Raised intracranial pressure, acute glaucoma	Volume expansion, pulmonary oedema

Diuretics — Classification by Nephron Site

Class	Site	Mechanism	Example	Key Clinical Use	Main Side Effect
Loop diuretics	Thick ascending limb	Block NKCC2	Furosemide	Pulmonary oedema, heart failure	Hypokalaemia, hypomagnesaemia, ototoxicity
Thiazides	DCT	Block NCC	Hydrochlorothiazide	Hypertension (first-line)	Hypokalaemia, hyperuricaemia, hypercalcaemia
K+-sparing (aldosterone antagonist)	Collecting duct	Block aldosterone receptor	Spironolactone	Heart failure, ascites, Conn's syndrome	Hyperkalaemia, gynaecomastia
K+-sparing (ENaC blocker)	Collecting duct	Block ENaC directly	Amiloride	Combined with loop/thiazide	Hyperkalaemia
Carbonic anhydrase inhibitors	PCT	Inhibit CA → less HCO3- reabsorption	Acetazolamide	Glaucoma, altitude sickness	Metabolic acidosis
Osmotic diuretics	PCT, loop of Henle	Increase tubular osmolarity → hold water	Mannitol	Raised intracranial pressure, acute glaucoma	Volume expansion, pulmonary oedema

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⁻)