Unit 07 — Renal / Urinary · Question Bank

1. Glomerular filtration

Plasma is filtered across the filtration membrane (endothelium + basement membrane + podocytes) driven by the net ultrafiltration pressure, forming a protein-free filtrate (~125 mL/min). It is charge- and size-selective.

2. Tubular reabsorption

The tubule reclaims most of the filtrate: the PCT reabsorbs ~65% (Na⁺, all glucose and amino acids, HCO₃⁻, water); the TAL reabsorbs NaCl (diluting segment); the DCT/collecting duct fine-tune Na⁺ (aldosterone) and water (ADH).

3. Tubular secretion

The tubule secretes substances into the lumen (H⁺, K⁺, NH₄⁺, drugs/organic acids).

Result

Urine = filtered − reabsorbed + secreted.

Glomerular capillary hydrostatic pressure

Set by arterial pressure and afferent/efferent arteriolar tone. ↑Pressure → ↑GFR (afferent dilation or efferent constriction raise it).

Plasma colloid osmotic pressure (πGC)

Opposes filtration — an INVERSE relationship: ↑π → ↓GFR.

Bowman's capsule (tubular) hydrostatic pressure

↑Pressure (e.g. obstruction) → ↓GFR.

Filtration coefficient

Depends on membrane permeability and surface area; ↑Kf → ↑GFR.

Renal blood flow

↑RBF tends to ↑GFR.

Autoregulation

GFR is held nearly constant over a MAP of ~80–180 mmHg by myogenic and tubuloglomerular feedback; below this it falls steeply.

Step 1 — blood glucose exceeds the renal threshold

The hypertonic glucose raises plasma glucose well above the renal threshold (~180 mg/dL), so the filtered glucose load exceeds the tubular transport maximum (Tm) for glucose.

Step 2 — glucose stays in the tubule

The SGLT carriers are saturated, so the excess glucose cannot be reabsorbed and remains in the tubular fluid.

Step 3 — osmotic effect → diuresis

The retained glucose raises the osmotic pressure of the tubular fluid, opposing water reabsorption. Less water is reclaimed, so urine volume increases — this is osmotic diuresis.

Clinical parallel

The same mechanism causes the polyuria of uncontrolled diabetes mellitus.

ADH (antidiuretic hormone, vasopressin)

From the hypothalamus. Released by ↑plasma osmolality or ↓blood volume; it increases WATER reabsorption in the collecting duct/DCT (aquaporin-2), producing concentrated urine. Low ADH → water diuresis (dilute urine).

Aldosterone

From the adrenal cortex. Increases Na⁺ reabsorption and K⁺ secretion in the DCT and collecting duct.

Renin–angiotensin–aldosterone system (RAAS)

↓BP/volume or ↓NaCl at the macula densa or ↑sympathetic activity → renin → angiotensin I → (ACE) angiotensin II → vasoconstriction + aldosterone + ADH/thirst + ↑proximal Na⁺ reabsorption → ↑volume and BP.

Renal sympathetic nerves

↓GFR, ↑renin and ↑NaCl reabsorption.

Bicarbonate reabsorption

Filtered HCO₃⁻ is reclaimed (mostly in the PCT): the tubule secretes H⁺, and for each H⁺ secreted one HCO₃⁻ is reabsorbed (1:1).

H⁺ excretion

The kidney excretes the fixed (non-volatile) acids of metabolism (e.g. sulfuric, phosphoric) as titratable acid (buffered by phosphate) and as ammonium — secreted ammonia (NH₃) binds H⁺ to form NH₄⁺, aiding H⁺ elimination.

Henderson–Hasselbalch

pH = 6.1 + log([HCO₃⁻]/(0.03 × PCO₂)). The kidney sets [HCO₃⁻] (the metabolic component) while the lungs set PCO₂.

Compensation

In metabolic acidosis the lungs hyperventilate (fast) and the kidney increases H⁺ excretion/HCO₃⁻ generation (slow); in respiratory acidosis the kidney raises HCO₃⁻ reabsorption.