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.