Kidney Function

Crystal-induced kidney disease refers to kidney injury caused by intratubular crystal deposition of calcium salts, medications, or other chemicals. The major risk factors for crystal deposition include hypercalcemia and/or hypercalciuria, hyperoxalosis and/or hyperoxaluria, and increased serum and/or urinary phosphate levels. The risk of crystal-induced kidney disease is increased further in the presence of hypovolemia and urinary concentration, changes in urinary pH, and decrease in level of urinary inhibitors of crystallization, such as citrate, magnesium, and pyrophosphate. In the case of calcium phosphate crystal deposition, use of angiotensin-converting enzyme inhibitors is considered an additional risk factor. In addition to calcium salts and uric acid, drugs such as sulfonamides, foscarnet, methotrexate, triamterene, phosphate-containing bowel preparations, orlistat, ciprofloxacin, and indinavir can cause crystal-induced kidney disease. Clinical manifestations of crystal-induced kidney disease are wide ranging, from no symptoms to flank pain, hematuria, sterile pyuria, crystalluria, and reduced kidney function. Although crystal-induced kidney disease is well documented in native kidneys, its occurrence in kidney allografts is not. We report 2 cases of crystal-induced kidney disease in transplant recipients that resulted in kidney failure.

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