#1846 Oxalate nephropathy in diabetic kidney disease: another factor to take into account?

Abstract

Abstract Background and Aims Patients with diabetes mellitus (DM) have an increased urinary excretion of oxalate. Around 40% of patients with oxalate nephropathy have DM. The aim of this study was to describe the prevalence of tubular deposits of calcium oxalate (CaOx) crystals in patients with diabetic kidney disease (DKD) and investigate its association with renal survival. Method We performed an observational retrospective study that included patients with DKD in renal biopsies performed at our centre between January 1999 and December 2021. We revised the biopsy specimens for the presence of intratubular CaOx crystals. We excluded patients with a histological findings of non-diabetic kidney disease and those lost to follow-up. Renal survival was defined as a state free from developing end-stage kidney disease (ESKD) requiring renal replacement therapy. Results The study included 87 patients with a mean age of 63.1 ± 13 years, 73.5% were male, and 88.5% had type 2 DM (11.5% type 1 DM). Baseline GFR at the moment of kidney biopsy was 38.5 ± 23 ml/min, and baseline median proteinuria was 3.46 (1.35-5.70) g/day. We found intratubular CaOx deposits in 11 biopsies (12.6%). These findings were only found in patients with type 2 DM (14.3% vs 0%), and was more frequently present in patients with a history of renal stones (33.3% vs 11.1%). There were no differences in baseline GFR, proteinuria or vintage of DM between patients with intratubular CaOx deposits and those with no signs of oxalte nephropathy. CaOx deposition was not associated with other histological lesions such as percentage of glomerular sclerosis, grade of interstitial fibrosis and/or tubular atrophy, interstitial inflammation, arterial hyalinosis or arteriosclerosis. After a median follow-up of 41 months, 49.4% of patients developed ESKD while 26.4% died without progressing to ESKD. The patients who progressed to ESKD had a higher baseline serum creatinine (2.56 ± 1.45 vs 1.98 ± 1.07 ml/min, p = 0.037) and lower serum albumin (3.08 ± 0.70 vs 3.57 ± 0.74 g/dl, p = 0.003). In the regression analysis there was no association between intratubular CaOx deposits and progression to ESKD (OR = 2.96, 95% CI 0.73-12.03). In the adjusted model, no histological lesions were associated with renal survival. In the survival analysis, the presence of intratubular CaOx deposits was not associated with neither renal nor patient survival. Conclusion Oxalate nephropathy, defined as the presence of intratubular CaOx deposits in kidney biopsies, may be found in patients with DKD. In our cohort, 14.3% of type 2 DM patients with DKD had concomitant oxalate nephropathy. Its presence was not associated with a worse renal or patient survival.