What pathophysiologic factors influence the formation of renal stones?
- Renal stones result from hereditary or acquired disorders causing supersaturation of stone precursors, deficiency of stone inhibitors, and possibly excess promoters.
- Supersaturation causes crystallization with mineral precursors, such as calcium and oxalate.
- Calcium oxalate crystals bind to anionic sialic acid–containing glycoproteins on the apical surfaces of renal tubular epithelial cells, allowing further growth.
- Other factors that increase stone formation include urinary stasis (medullary sponge kidney), decreased flow (obstruction), increased urine ammonium (infection), dehydration (concentrated urine), and increased urinary alkalinity (renal tubular acidosis [RTA]).
- Type I RTA promotes stone formation through the increased release of calcium and phosphorus from bone to buffer the chronic acidemia, with resulting hypercalciuria and hyperphosphaturia.
- The acidemia enhances proximal tubule reabsorption of citrate, with resulting hypocitraturia. The alkaline urine of RTA promotes precipitation of calcium phosphate stones.
- Acidemia with a positive urine anion gap (UNa + UK − UCl) is a clue to the presence of RTA.
