Renal Tubular Acidosis

Renal tubular acidosis refers to a group of tubular disorders that result in acidosis and its subsequent complications, including metabolic bone disease, kidney stones, and growth failure in children. There are two main types of renal tubular acidosis: proximal tubular disorders that affect bicarbonate reabsorption and distal tubular defects that affect the secretion of fixed metabolic acids. 

The proximal tubule is the site where 90% to 95% of the filtered bicarbonate is reabsorbed. With the onset of impaired tubular bicarbonate absorption, there is a loss of bicarbonate in the urine that reduces plasma bicarbonate levels. The concomitant loss of sodium in the urine that accompanies the bicarbonate loss leads to contraction of the extracellular fluid volume with increased aldosterone secretion and a resultant decrease in serum potassium levels (see Chapter 26). With proximal tubular defects in acid-base regulation, the distal tubular sites for secretion of the fixed acids into the urine continue to function, and the reabsorption of bicarbonate by the proximal cells eventually resumes, albeit at a lower level of serum bicarbonate. Whenever serum levels rise above this decreased level, bicarbonate is lost in the urine. The proximal tubular defect in bicarbonate reabsorption can extend to other substances, such as glucose, amino acids, and phosphate. Defects in calcium and phosphate reabsorption may accentuate bicarbonate losses. 

The most common type of distal tubular acidosis usually is a defect in the secretion of hydrogen ions with failure to acidify the urine. Because the secretion of hydrogen ions in the distal tubules is linked to sodium reabsorption, failure to secrete hydrogen ions results in a net loss of sodium bicarbonate in the urine. There is a resultant contraction of fluids in the extracellular fluid compartment, a compensatory increase in aldosterone levels, and development of hypokalemia. The persistent acidosis, which requires buffering by the skeletal system, causes calcium to be released from bone. Increased losses of calcium in the urine lead to increased levels of parathyroid hormone, osteomalacia, bone pain, impaired growth in children, and development of kidney stones.