Renal tubular acidosis (RTA) is a clinical syndrome characterized by hyperchloremic metabolic acidosis with a normal anion gap (AG), caused by impaired renal acidification due to various etiologies. It may result from a defect in hydrogen ion (H+) secretion in the distal tubules, impaired bicarbonate (HCO3-) reabsorption in the proximal tubules, or a combination of both.
The clinical features include hyperchloremic metabolic acidosis accompanied by disturbances in water and electrolyte balance. These may involve hypokalemia or hyperkalemia, hyponatremia, hypocalcemia, polyuria, polydipsia, renal rickets or osteomalacia, and complications such as nephrolithiasis.
RTA is classified into four types based on the site of dysfunction and underlying mechanism:
- Distal renal tubular acidosis (Type I, dRTA)
- Proximal renal tubular acidosis (Type II, pRTA)
- Mixed renal tubular acidosis (Type III RTA)
- Hyperkalemic renal tubular acidosis (Type IV RTA)
Table 1 Characteristics of different types of RTA
Note: Type III RTA exhibits features of both Type I and Type II RTA.
To be continued