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The kidney filters ~180 L of plasma per day through 1 million nephrons (glomerular filtration: 125 mL/min), reabsorbs 99% of the filtrate, and excretes 12 L of concentrated urine. The glomerular Starling equation determines GFR: glomerular hydrostatic pressure (P_GC, ~50 mmHg, maintained by the efferent arteriole) drives filtration; oncotic pressure (_GC, ~30 mmHg) retains it.

Renal clearance is the central concept of renal function: Cl_X = (U_X × V)/P_X represents the volume of plasma that is free of substance X per unit of time. If Cl_X = GFR: it is filtered and is not secreted or reabsorbed (inulin, creatinine). If Cl_X < GFR: it is reabsorbed (glucose, Na, HCO). If Cl_X > GFR: it is secreted (uric acid, some drugs).

Tubular glucose reabsorption follows Michaelis-Menten kinetics (T_max 375 mg/min = 2.08 mmol/min). When blood glucose exceeds the threshold (~180 mg/dL = 10 mmol/L), the SGLT2 transporter becomes saturated and glucose appears in the urine (diabetic glycosuria). SGLT2 inhibitors (gliflozins) deliberately lower T_max, increasing glycosuria and reducing blood glucose.

The CKD-EPI equation uses serum creatinine to estimate GFR: creatinine is freely filtered and has minimal tubular secretion, hence its clearance ( GFR). The eGFR allows staging chronic kidney disease (CKD): G1 (>90), G2 (6089), G3 (3059), G4 (1529), G5 (<15 mL/min/1.73m²). eGFR decline typically progresses at 15 mL/min/year in uncontrolled chronic CKD.

The ability to concentrate urine (up to 1200 mOsm/kg) depends on the medullary osmotic gradient (multiplying countercurrent + turnover in the loop of Henle) and ADH (vasopressin), which inserts aquaporins-2 into the collecting duct. In diabetes insipidus (central or nephrogenic), the urine is very dilute (<100 mOsm/kg) and the urine volume may exceed 1015 L/day, causing severe dehydration if not replaced.

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