Nephrocalcinosis in a Transplanted Kidney: A New Sign of Chronic Tacrolimus Nephrotoxicity.

Calcineurin inhibitors are potent immunosuppressive drugs in solid-organ transplantation and multiple autoimmune diseases. Their use is associated with the acute impairment of glomerular filtration and chronic interstitial fibrosis. The latter is mediated by the accumulation of matrix proteins. In this case report, we present a kidney transplant patient with chronic and progressive allograft failure that was associated with nephrocalcinosis. He did not have hypercalcemic-hypercalciuric states such as hyperparathyroidism, sarcoidosis, and hyper-vitaminosis D; normocalcemic-hypercalciuric states such as distal renal tubular acidosis, medullary sponge kidney, excessive use of high-dose loop diuretics, and beta-thalassemia; hyperphosphaturic conditions; and hyperoxaluria. Moreover, his calcifications were limited to the transplanted kidney and spared the native kidneys and extrarenal tissues, and his renal function had improved and stabilized for 6 months after discontinuation of prolonged-release tacrolimus (Advagraf), indicating a cause and an effect phenomenon. Nephrocalcinosis was suspected after ultrasonography and confirmed by computed tomography scanning. Hence, allograft nephrocalcinosis may indicate chronic tacrolimus nephrotoxicity.

"Recurrent Papillary Necrosis and Nephrocalcinosis Induced by Nonsteroidal Anti-Inflammatory Drugs for Gouty Arthritis Associated with Congenital Chloride-Losing Diarrhea: A Major Risk for Kidney Loss".

Congenital chloride-losing diarrhea (CCLD) is a rare genetic disorder due to autosomal recessive mutation in the SLC26A3 gene on chromosome 7. It is characterized with chronic watery diarrhea with high fecal chloride (Cl: >90 mmol/L), low potassium (K), and metabolic alkalosis with low urinary Cl and K. The overall long-term prognosis is favorable with optimal life-long salt and K supplementation. In this case report, we describe a man with progressive renal failure and small kidneys that showed nephrocalcinosis and papillary necrosis. His disease was diagnosed since birth and was confirmed by our tests. He was incompliant with therapy and had developed gout. The latter complication of his disease has led to excessive NSAID use over the past years. Reinstitution of diet, drug therapy, and allopurinol had stabilized his renal disease for 1 year of follow-up. In conclusion, excessive analgesic use is a risk factor for renal failure in CCLD.