Questions: Renal Physiology and Fluid Balance

Question 1

A patient with elevated blood osmolarity will experience which hormonal response to restore fluid balance?

• A. Aldosterone release, causing Na⁺ reabsorption and water retention
• B. ADH release, increasing water permeability of the collecting duct
• C. Aldosterone release, causing K⁺ reabsorption in the distal tubule
• D. ADH release, increasing Na⁺ secretion in the proximal tubule

Answer: (B)

High plasma osmolarity triggers ADH (antidiuretic hormone) release from the posterior pituitary. ADH inserts aquaporin channels into the collecting duct, increasing water reabsorption and producing small volumes of concentrated urine. Aldosterone responds to low blood pressure or low Na⁺ — not directly to osmolarity.

Question 2

Aldosterone directly controls water reabsorption in the collecting duct.

• T. True
• F. False

Answer: False

This is a common misconception. Aldosterone drives Na⁺ reabsorption and K⁺ secretion in the distal convoluted tubule and collecting duct, but water follows Na⁺ passively only when water channels are present. ADH controls water permeability by regulating aquaporin insertion. The two hormones are complementary but distinct in their primary targets.

Question 3

Why does glucose appear in the urine of a patient with uncontrolled diabetes mellitus, even though the kidneys are structurally normal?

Model answer: Blood glucose exceeds the transport maximum (Tmax) of the SGLT2 cotransporter in the proximal convoluted tubule. When the filtered glucose load surpasses ~180 mg/dL, the carriers are saturated and the excess glucose cannot be reabsorbed, so it passes into the urine.

Glycosuria reflects transporter saturation, not kidney damage. The proximal tubule normally reabsorbs 100% of filtered glucose via SGLT2 cotransporters, but these have finite capacity. Above the renal threshold (~180 mg/dL plasma glucose), the filtered load overwhelms transport capacity and glucose spills into the urine.