PY7.1-9 | Renal Physiology — Summary & Reflection

REFLECT

Return to our opening case — the 52-year-old farmer with diabetic nephropathy (eGFR 18, 3+ proteinuria, BP 160/100, peripheral oedema).

1. Using your knowledge of Starling forces and the filtration barrier, explain mechanistically why he has proteinuria and oedema.
2. His serum K⁺ is 5.8 mEq/L (hyperkalaemia). Why do CKD patients develop hyperkalaemia? (Hint: which tubular mechanism is impaired?)
3. His doctor prescribes furosemide AND spironolactone. What is the physiological rationale for combining a loop diuretic with a K⁺-sparing diuretic?
4. If his eGFR falls to 8 mL/min, what does dialysis do that his kidneys can no longer do? Compare haemodialysis vs. CAPD for a patient in rural Tamil Nadu who lives 80 km from the nearest hospital.

KEY TAKEAWAYS

• GFR (125 mL/min) is driven by net filtration pressure (NFP = Pgc − Pbs − πgc = 10 mmHg). Autoregulation (myogenic + TGF) keeps GFR stable from MAP 80–180 mmHg.
• Renal clearance: C = (U × V)/P. Inulin clearance = GFR; PAH clearance = RPF; creatinine clearance ≈ GFR.
• PCT reabsorbs 65% of everything. Glucose follows Na⁺ via SGLT2 (Tm = 375 mg/min; threshold 180 mg/dL). Osmotic diuresis occurs above Tm.
• Counter-current multiplier (loop of Henle) builds medullary hyperosmolality to 1200 mOsm. ADH (aquaporin-2 in collecting duct) determines final urine concentration: 50–1200 mOsm.
• Acid excretion: HCO₃⁻ reabsorption (recycles H⁺), titratable acidity (phosphate buffer), ammonium excretion (most adaptable).
• Micturition: Storage = sympathetic (β3 relaxes detrusor, α1 closes internal sphincter) + voluntary closure of external sphincter. Voiding = parasympathetic (M3) + pontine coordination.
• Diuretics act at specific nephron segments; know the site, mechanism, and key side effect for each class.
• eGFR < 15 = ESRD → dialysis (haemodialysis via diffusion/ultrafiltration; CAPD uses peritoneum as membrane).