Calcium Crystal Deposits in Kidney Allografts: The Interplay of PTH Levels and Phosphaturia

Rationale & Objective: Hyperparathyroidism is common in kidney transplant recipients and may contribute to graft injury through calcium crystal deposition. We investigated the association between pretransplant parathyroid hormone (PTH) levels and calcium crystal deposits (CCDs) and whether fractional excretion of phosphate (FePi) mediates this relationship. Study Design: Retrospective single-center observational study. Setting & Participants: Forty-one kidney transplant recipients undergoing protocol biopsies at 3 and 12 months posttransplantation. Exposure: Pretransplant PTH levels. Outcome(s): Presence of calcium crystal deposits in graft biopsies. Analytical Approach: Logistic regression models and mediation analysis were used to evaluate associations between PTH levels, FePi, and CCDs. Results: CCDs were detected in 33% of biopsies at 3 months and 45% at 12 months. Higher pretransplant PTH levels were associated with increased odds of CCDs. Mediation analysis showed that approximately 72% of this effect was explained using FePi levels. At 24 months posttransplantation, no meaningful difference in estimated glomerular filtration rate was observed between patients with and without CCDs. Limitations: Retrospective design, small sample size, absence of fibroblast growth factor 23 level measurements, and limited adjustment for potential confounders. Conclusions: Elevated pretransplant PTH levels are associated with calcium crystal deposition in kidney allografts, largely mediated by phosphate wasting. However, no clear impact on graft function was observed within the first 2 years posttransplantation. Plain-Language Summary: After kidney transplantation, disturbances in mineral metabolism are common and may contribute to subtle damage to the transplanted kidneys. In this study, we explored whether high levels of parathyroid hormone before transplantation are linked to the formation of calcium crystal deposits in the kidney graft. We analyzed biopsy samples collected after transplantation and examined how the kidney handles phosphate. We found that higher parathyroid hormone levels were associated with the presence of these deposits, largely through increased loss of phosphate in the urine. However, these deposits did not appear to affect kidney function within the first 2 years after transplantation. These findings suggest that better control of mineral metabolism before transplantation may help reduce early changes in the kidney graft.