Renal Allograft With Calcium Oxalate Deposition: Association with Urinary Tract Infection and Development of...

The interaction between calcium oxalate deposition and urinary tract infection is not well established. We aimed to identify the association between these and to determine the role of calcium oxalate deposition on interstitial fibrosis development.

Renal allograft biopsies of 967 patients were reviewed to identify those with calcium oxalate deposition in the renal allograft, with 27 (2.8%) identified. Follow-up biopsies were conducted to reevaluate for calcium oxalate presence and interstitial fibrosis development. At time of biopsy, presence of urinary tract infection and oxaluria was also examined from medical records.

Mean time for development of calcium oxalate deposition in renal allografts was 1.7 ± 0.4 and 32.7 ± 21.6 months in patients with primary and secondary oxalosis, respectively (P < .001). Of 27 patients with calcium oxalate deposition, 7 (25.9%) showed tubulointerstitial nephritis, with 2 also having urinary tract infection. Four patients (14.8%) had only urinary tract infection. Causes of tubulointerstitial nephritis were secondary to bacterial infection in 2 and secondary to viral infection in 5 patients (2 polyomaviruses, 2 cytomegaloviruses, 1 adenovirus). Time until development of interstitial fibrosis after calcium oxalate deposition was 3.5 ± 2.1 and 10.3 ± 4.1 months in patients with primary and secondary oxalosis, respectively (P = .01). Time until graft loss after calcium oxalate deposition was 9.3 ± 7.8 and 21.8 ± 12 months in those with primary and secondary oxalosis (P < .001), with 1-, 3-, and 5-year kidney graft survival of 43%, 28%, and 0% and 100%, 100%, and 67% in those with primary and secondary oxalosis, respectively.

Calcium oxalate deposits increased the risk of urinary tract infection and tubulointerstitial nephritis, with bacteria inducing increased presence of calcium oxalate deposition in a renal allograft. Calcium oxalate deposition had a significant influence on interstitial fibrosis development, therefore negatively affecting graft survival.