Renal Physiology — MRCS Urology

🔬 Renal Physiology

Urology Basic Sciences — Topic 3 of 13. Body fluids, GFR, tubular handling, RAAS, aldosterone, ADH, diuretics, and acid–base — with surgical and clinical context throughout.

💧 Body Fluids & Glomerular Filtration

The 60-40-20 Rule — Body Fluid Distribution

Total body water (TBW) is approximately 60% of body weight — about 42 L in a 70 kg adult. This percentage is highest in newborns and adult males, and lowest in adult females and in patients with large amounts of adipose tissue (fat is anhydrous).

TBW — Total Body Water 60% body weight ≈ 42 L

Measured by tritiated water, D₂O, or antipyrene — substances that distribute wherever water goes. The starting denominator for all compartment calculations.

ICF — Intracellular Fluid 40% body weight ≈ 28 L (⅔ TBW)

Major cations: K⁺ and Mg²⁺. Major anions: protein and organic phosphates (ATP, ADP, AMP). Measured indirectly: TBW − ECF. Cannot be directly sampled.

ECF — Extracellular Fluid 20% body weight ≈ 14 L (⅓ TBW)

Major cation: Na⁺. Major anions: Cl⁻ and HCO₃⁻. Measured by sulfate, inulin, or mannitol. Divided into plasma (¼ ECF = 3.5 L) and interstitial fluid (¾ ECF = 10.5 L).

Plasma ¼ ECF = 1/12 TBW ≈ 3.5 L

Measured by Evans blue (binds albumin) or RISA (radioiodinated serum albumin). Major proteins: albumin and globulins. Interstitial fluid is an ultrafiltrate of plasma — same composition but very little protein.

Surgical Relevance — IV Fluid Choices

Understanding fluid compartments explains why different IV fluids distribute differently:
Normal saline / Hartmann’s (isotonic) → stays in ECF only. Does not shift water into or out of cells. Expands both plasma and interstitial compartments. Use: resuscitation, maintenance.
5% Dextrose (hypotonic after glucose metabolised) → distributes as free water across all compartments (⅔ goes intracellular). Risks hyponatraemia and cerebral oedema. Not a resuscitation fluid.
Hypertonic saline → pulls water from ICF into ECF. Used for severe hyponatraemia with neurological symptoms — cautiously (osmotic demyelination if corrected too fast).

Renal Blood Flow & GFR

Renal Blood Flow (RBF)

The kidneys receive approximately 25% of cardiac output — approximately 1.25 L/min in a 70 kg adult — despite accounting for only 0.5% of body weight. This enormous flow relative to metabolic need reflects the filtration function of the kidney, not oxygen demand.

Clearance Equation

C = (U × V) / P

C = clearance (mL/min) | U = urine concentration (mg/mL) | V = urine flow rate (mL/min) | P = plasma concentration (mg/mL)

Renal Plasma Flow — PAH Clearance

RPF = C_PAH = (U_PAH × V) / P_PAH

PAH is filtered AND secreted — so nearly all PAH is removed in one pass. Underestimates true RPF by ~10%. RBF = RPF / (1 − haematocrit)

Glomerular Filtration Rate (GFR)

Normal GFR is approximately 125 mL/min (180 L/day). Measured by inulin clearance — inulin is freely filtered, neither reabsorbed nor secreted. In clinical practice, GFR is estimated from serum creatinine (eGFR), though creatinine slightly overestimates GFR as it is secreted in small amounts by the proximal tubule.

GFR — Inulin Clearance (Gold Standard)

GFR = (U_inulin × V) / P_inulin

Inulin: freely filtered, not reabsorbed or secreted. Filtration fraction = GFR/RPF ≈ 0.20 (20% of RPF is filtered)

Starling Forces at the Glomerulus

Glomerular filtration is driven by the balance of hydrostatic and oncotic pressures across the capillary wall. The diagram below shows the basic unit of the glomerulus with the afferent and efferent arterioles, Bowman’s capsule, and the direction of filtration forces.

Diagram of the glomerulus showing afferent and efferent arterioles, Bowman's capsule, and Starling filtration forces — The glomerulus — afferent arteriole delivers blood at high pressure into the glomerular capillary tuft. P_GC drives filtration into Bowman’s space; π_GC and P_BS oppose it. The efferent arteriole (constricted by angiotensin II) maintains P_GC and GFR.

P_GC — Glomerular Capillary Hydrostatic Pressure Favours filtration (~45 mmHg)

↑ by afferent arteriole dilation or efferent arteriole constriction → ↑ GFR. ↓ by afferent constriction (sympathetic activation, severe hypovolaemia) → ↓ GFR.

π_GC — Glomerular Oncotic Pressure Opposes filtration (~27 mmHg)

Rises along the capillary length as water is filtered out. ↑ with hyperproteinaemia → ↓ GFR. Angiotensin II preferentially constricts efferent arteriole → ↑ P_GC and ↑ π_GC → net ↑ GFR.

P_BS — Bowman’s Space Hydrostatic Pressure Opposes filtration (~10 mmHg)

↑ with ureteral obstruction (stone, stricture, ligation) → ↓ GFR. A ureteral stone → ↑ P_BS → ↓ GFR → rising creatinine. Net filtration pressure = P_GC − P_BS − π_GC = 45 − 10 − 27 = +8 mmHg (favours filtration).

ACE Inhibitors, ARBs & the Efferent Arteriole

Angiotensin II preferentially constricts the efferent arteriole, maintaining GFR when renal perfusion is reduced (e.g. renal artery stenosis, heart failure). ACE inhibitors and ARBs block this — they dilate the efferent arteriole, reduce P_GC, and drop GFR. This is why ACE inhibitors are dangerous in bilateral renal artery stenosis or in a single functioning kidney. In practice: always check creatinine and potassium 1–2 weeks after starting ACE inhibitors. A rise in creatinine of up to 30% is acceptable; greater rises suggest renal artery stenosis. Long-term, ACE inhibitors protect the kidney in diabetic nephropathy by reducing hyperfiltration.

Autoregulation of RBF and GFR

Both RBF and GFR remain constant over a wide range of mean arterial pressure (80–200 mmHg) through two mechanisms:

Myogenic mechanism: Increased pressure stretches afferent arteriole → reflex vasoconstriction → increased resistance → maintained flow.
Tubuloglomerular feedback (TGF): ↑ GFR → ↑ NaCl delivery to macula densa → macula densa signals afferent arteriole to constrict → ↓ GFR back to normal. This couples filtration rate to tubular capacity.

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