Origin of monosodium urate Randall's plaques.

Abstract

In 3.4% of Randall's plaques, monosodium urate can be detected. The formation mechanism of these Randall's plaques is unrevealed and the clinical and biochemical characteristics of affected patients are unknown. In this single centre study, we retrospectively analysed the clinical and biochemical characteristics of patients with kidney stone formation related to monosodium urate-containing Randall's plaques (NaUr ^pos RP) and those with stone formation related to "classical" Randall's plaques (NaUr ^neg RP). There was a significantly higher urinary calcium and magnesium excretion in the NaUr ^neg RP group (6.09 vs. 4.61 mmol/24 h, p = 0.03 and 4.78 vs. 3.55 mmol/24 h, p = 0.02). There was no significant difference in urinary uric acid excretion or urinary pH between both groups. The NaUr ^pos RP group tended to have more frequent hyperuricemia (71.4 vs. 44.8%, p = 0.08) and to be more frequently male (92.9 vs. 70.1%, p = 0.10) and had higher median age (53.5 vs. 27.5, p < 0.001) and serum creatinine (96.4 vs. 77.0 µmol/L, p < 0.001). Additionally, there was a signal of higher prevalences of hypertension, dyslipidemia, cardiovascular disease and gout in the NaUr ^pos RP group. Different formation mechanisms seem implicated in the formation of NaUr ^pos RP and NaUr ^neg RP - associated kidney stones. We hypothesize a mechanism of interstitial monosodium urate precipitation at the renal papilla driven by high systemic uric acid serum concentration to be involved in NaUr ^pos RP formation. Treatment with xanthine oxidase inhibitors may reduce the risk of recurrent stone formation on this specific Randall's plaque.