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.