Mp19-17 Renal Papillary Mapping and Quantification of Randall’s Plaque in Pediatric Calcium Oxalate Stone Formers

Abstract

Chronic Kidney Disease (CKD), it remains unclear which factor has much more worse effects on renal function. We accessed the influence of hyperuricemia on impaired renal function in patients with UA stone components in comparison with community-dwelling population.METHODS: Between 2010 and 2014, we treated 1793 consecutive patients with urolithiasis in our hospital, and identified stone components available 473 patients. Of those, 123 patients with UA stone were included in the present study. Age, sex, and serum UA concentration adjusted control subjects were selected from 3089 community-dwelling population in each group by propensityscore matching (2:1). Subjects were divided into two groups; hyperuricemia or non-hyperuricemia groups according to the serum UA concentrations (UA-low: < 7.0 or UA-high: ¼7.0 mg/mL). We compared renal function between the UA stone and control subjects in each group. The renal function was evaluated as estimated glomerular filtration rate (eGFR). The independent risk factor for impaired renal function were investigated by multivariate logistic regression analysis.RESULTS: We selected pair-matched 166 control subjects and 83 UA stone patients for serum UA-low group. Similarly, 68 control subjects and 34 UA stone patients for serum UA-high group. UA stone patients had significantly lower in eGFR (P<0.01) compared with control subjects regardless of serum UA concentrations. Multivariate logistic regression analysis revealed that age, past-history of cardiovascular disease, serum UA, and stone former were significant factors for stage 3 CKD. UA stone component had 3-fold chance to develop stage 3 CKD than serum UA concentration.CONCLUSIONS: Uric acid stone components may strongly influence on renal function deterioration than hyperuricemia.

Effects of secretome derived from macrophages exposed to calcium oxalate crystals on renal fibroblast activation

“…The main originating site for Randall’s plaque formation is thin ascending limb of Henle’s loop 7 . The plaque at papilla’s tip can then erode into renal pelvis, where CaOx is frequently supersaturated, and serves as the nidus for CaOx stone formation 7 – 9 . An alternative mechanism describes a possibility of paracellular translocation of CaOx crystals to the renal interstitium through the disrupted tight junctions or neocrystallization after the degraded intracellular crystals generate free calcium and oxalate ions that pass through basolateral membranes of renal tubular cells 8 , 10 – 12 .…”