New insights into the presence of sodium hydrogen urate monohydrate in Randall's plaque

Abstract

International audienceCalcium oxalate nephrolithiasis is a common ailment. Frequent risk factors associated with are low diuresis, dietary imbalance, inherited or acquired metabolic disorders. Another important factor, namely the presence of a mineral deposit made of apatite at the surface of the papilla, named Randall's plaque (RP), has been recently underlined. In most cases, RP which serves as a nidus for kidney stone formation is made of calcium phosphate apatite (CA). However, RP does not seem to be composed exclusively of CA. We would like to assess the case of RP where sodium hydrogen urate monohydrate (NaUr) is also present in its chemical composition. To attain this goal, a set of experiments including Environmental Scanning Electron Microscopy (ESEM) and Synchrotron Radiation Fourier Transform InfraRed (SR-FTIR) has been performed to analyze papillae of six kidneys randomly selected after they were surgically removed for cancer. NaUr crystals were found in two samples. We show through ESEM an usual morphology of RP present at the surface of kidney stones in the presence of NaUr. Moreover, we discuss the presence of NaUr in the renal parenchyma and its spatial repartition with CA. The complete set of data indicates that different biochemical mechanisms are probably involved in the pathogenesis of RP. The next step will be to establish a significant relationship between these physicochemical data and the clinical and biochemical data of the patients

Randall’s plaque as the origin of idiopathic calcium oxalate stone formation: an update

“…Additionally, the high zinc content of Randall's plaque described by Carpentier et al [72] points towards an inflammatory mechanism involved in Randall's plaque formation, as zinc has been demonstrated to be implicated in inflammation [116,117]. Further, the presence of sodium hydrogen urate, although rare, in Randall's plaque, was accompanied by various cells, suggesting an inflammatory process [62]. It is known that not only sodium hydrogen urate, but also many other crystals, are involved in inflammation by triggering the nod-like receptor protein 3 (NLRP3) inflammasome pathway and other pathways leading to IL-1 production and innate immune cell recruitment [118].…”

“…Amorphous carbonated calcium phosphate is more predominantly found at the core of the Randall's plaque, suggesting that it is the first crystalline phase formed, with subsequent formation of the more stable apatite at the surface [61]. Sodium hydrogen urate can be detected in 3.4% of Randall's plaque identified during morphoconstitutional kidney stone analysis [4,62]. Additionally, whitlockite is detected in 1.0% of Randall's plaques, identified at kidney stone surface [4] and has also been observed in incipient Randall's plaque in the papilla [32].…”

“…Although Randall initially hypothesized Randall's plaque to act as a nidus for the formation of different types of stones including calcium oxalate, calcium phosphate and uric acid [6], it is now known that the bulk of stones formed on Randall's plaque are COM stones [17,46]. Analysed by FTIR, 89.5% of 10462 Randall's plaque-associated kidney stones were made of COM pure or mixed with COD [62]. Alternatively, 88% of calcium oxalate stone formers have endoscopic evidence of Randall's plaque [21] and 66.1% of spontaneously passed COM stones display papillary umbilication [4].…”

Scanning electron microscopy—a powerful imaging technique for the clinician

“…Randall's plaque represents a major issue in urology [80,81]. Several papers report evidence that Randall's plaque (RP) present at the tip of the renal papilla may initiate whewellite (Figure 5a) and more rarely weddellite stones [82][83][84][85][86][87][88][89][90][91]. Some of these investigations have been dedicated to the pathogenesis of this pathological calcification; recent data show clearly that vitamin D and calcium supplementation accelerates the formation of RP in a murine model [91].…”

Crystal size in μcrystalline pathologies and its clinical implication

“…Taking into account a large data bank including 50,000 stones acquired over the past three decades, CA has been identified by selective infrared analysis in 80% of all stones in both sexes, in most cases as a minor component [75]. It is worth underlining that despite its low proportion, CA is often clinically relevant as an initiating phase of the lithogenic process, as observed in stones developed from a Randall's plaque [76][77][78][79][80][81]. XRD as well as PND experiments have been performed on CA typical of physiological (bones) as well as pathological (Randall's plaque) calcifications [85][86][87].…”