When assessing renal tubular acidosis, which type shows a defect in HCO3 reabsorption?

Type II renal tubular acidosis (RTA), also known as proximal renal tubular acidosis, is characterized by a defect in the reabsorption of bicarbonate (HCO3-) in the proximal tubule of the nephron. In this condition, the proximal tubule is unable to efficiently reabsorb bicarbonate from the urine, leading to its excessive loss in the urine and resulting in systemic acidosis.

The inability to reabsorb bicarbonate effectively causes a normal initial plasma bicarbonate concentration to decrease as bicarbonate is lost in the urine. This usually happens until the bicarbonate levels fall to a certain threshold (~15 mEq/L), at which point the distal nephron can compensate by increasing H+ secretion, helping to maintain acid-base balance to some extent.

Understanding this defect is crucial for diagnosing and managing patients with RTA. In contrast, other types of RTA involve different mechanisms; for example, Type I (distal RTA) is associated with an inability to secrete hydrogen ions, whereas Type IV RTA is typically due to aldosterone deficiency or resistance, leading to a hyperkalemic state and a different pathophysiological process. Each type has distinct clinical features, causes, and implications for treatment.