On the origin of calcium oxalate monohydrate papillary renal stones.

Abstract

Calcium oxalate monohydrate (COM) papillary calculi can be initiated by subepithelial calcification of the renal papillae. Hydroxyapatite disruption of the papillary epithelial layer can become the nidus of a COM papillary calculus. This study evaluated the causes of papillary tissue calcifications in 60 patients with calcium oxalate lithiasis, 30 with COM papillary and 30 with calcium oxalate dihydrate (COD) calculi. Urinary redox potential was higher in the COM than the COD group, suggesting that the former is more deficient in antioxidants due to increased oxidative stress. Urinary calcium was significantly higher in the COD group, whereas urinary oxalate was significantly higher in the COM group, suggesting a greater degree of oxidative injury of renal cells. Evaluations of their diets showed that both groups consumed low amounts of phytate-rich products. Of chronic diseases possibly associated with urolithiasis, only the prevalence of gastroduodenal ulcer differed significantly, being higher in the COM group and suggesting that epithelial lesions are common to gastroduodenal ulcers and COM papillary renal stones. Occupational exposure to cytotoxic products occurred in 47 % of the COM and 27 % of the COD group, but this difference was not statistically significant. These findings indicate that oxidative stress is associated with injury to papillary tissue and that this is the origin of intrapapillary calcifications. The continuation of this process is due to modulators and/or deficiencies in inhibitors of crystallization. Identifying and eliminating the causes of injury may prevent recurrent episodes in patients with papillary COM calculi.