Nephrocalcinosis in Kidney Allografts

Background: Nephrocalcinosis is characterized by tubular and interstitial calcium deposition in the kidney. Nephrocalcinosis may contribute to poor allograft function, particularly in kidney transplant recipients with long dialysis vintage, but its prevalence is poorly understood. This study aims to characterize the clinical, histologic, and laboratory features of calcium deposition in the kidney allograft. Methods: We performed a retrospective review of kidney allograft biopsies performed between 2010 and 2022 at Stanford University with histologic evidence of nephrocalcinosis. We quantified the amount of calcium deposition present in biopsy specimens. Demographic, clinical, and laboratory data were extracted from the electronic health record and analyzed descriptively. Results: We identified 19 kidney transplant recipients with histologic evidence of nephrocalcinosis in the kidney allograft. The mean (SD) age was 44.3 + 15.2 years. Time from kidney transplant to nephrocalcinosis diagnosis occurred within the first year of transplantation in approximately 70% of patients. Median dialysis vintage was 6.5 years. Average pre-transplant parathyroid hormone level was 1,238 pg/mL and average peak calcium was 11.4 mg/dL. Of the patients who completed a 24-hour urine collection (n=5), all had hypocitraturia. Finally, 5 out of 19 patients progressed to graft failure with a mean graft survival time of 5 years. On histologic examination of a subset of patients (n=5), the number of calcium deposits per mm2 ranged from 0.52 to 1.5. Calcification was seen in the absence of calcineurin inhibitor toxicity, tubular atrophy and fibrosis. Von Kossa staining of allograft biopsies for further delineation of calcification is pending. Conclusion: Long dialysis vintage, elevated parathyroid hormone levels, and hypocitraturia were common clinical characteristics in kidney transplant recipients with histologic evidence of nephrocalcinosis. The presence of calcification without evidence of calcineurin inhibitor toxicity and fibrosis raises the possibility that calcium deposition in the allograft may be an independent contributor to chronic injury and graft dysfunction. Further studies are warranted to identify modifiable risk factors for nephrocalcinosis in the transplant population. Funding: NIDDK Support