Posttransplant nephrocalcinosis is associated with poor renal allograft function: a single-center experience

Nephrocalcinosis, characterized by intratubular and/or parenchymal deposition of calcium phosphate and calcium oxalate crystals, is frequently seen in renal allograft biopsies; however, the clinical consequence of this histologic finding remains unknown. Kidney transplant recipients with good allograft function usually demonstrate improvement in biochemical parameters; however, persistent hyperparathyroidism remains prevalent in this population of patients. We identified renal allografts with nephrocalcinosis and evaluated the effects on renal allograft function and survival.

We conducted a single-center, retrospective review of kidney allograft biopsies performed at our center from December 1, 2006 to November 30, 2012. Biopsies with nephrocalcinosis as the primary diagnosis were included in the final analysis. Biochemical parameters at the time of biopsy included serum creatinine, phosphate, calcium, intact parathyroid hormone (iPTH), 25-hydroxy vitamin D, and albumin. Serum creatinine was measured at 1, 3, 6, and 12 months after nephrocalcinosis was diagnosed. The use of calcimimetics, vitamin D analogs, active vitamin D, and bisphosphonates was also reviewed.

We identified 12 patients with nephrocalcinosis as the primary diagnosis on renal biopsy. The average age of these patients was 52.2 ± 11.9 years, and the average time since transplantation was 2.3 ± 2.7 years. The baseline serum creatinine was 1.37 ± 0.4 mg/dL before the onset of acute kidney injury (AKI). Mean iPTH and 25-hydroxy vitamin D at the time of AKI were 495.66 ± 358.9 pg/mL and 19.9 ± 13.3 ng/mL, respectively. Renal function deteriorated in all patients, and mean serum creatinine at 12-month follow up was 2.37 ± 1.3 mg/dL (P=0.028). One patient progressed to end-stage renal disease at the end of the study period.

The histologic finding of nephrocalcinosis is associated with poor renal allograft function. Metabolic abnormalities including hyperparathyroidism persist in renal allograft recipients despite normal allograft function and may be associated with the development of nephrocalcinosis in renal transplant recipients.