Cellular and Molecular Gateways to Urolithiasis: A New Insight

Abstract

Urolithiasis is a relevant clinical problem in everyday practice with a subsequent burden for the health system. Urolithiasis is classically explained as the derangement in the process of biomineralization involving the equilibrium between promoters and inhibitors of crystallization: a deficit of one or several inhibitors or an excess of one or several promoters plays a pivotal role in the stone formation. The revolutionary introduction of the molecular biology in medicine has given a new insight in urolithiasis too. Genetic factors have also been postulated to play an important role. A review of the current knowledge on urolithiasis based upon a molecular and genetic approach is reported.

Exploring Antiurolithic Effects of Gokshuradi Polyherbal Ayurvedic Formulation in Ethylene-Glycol-Induced Urolithic Rats

“…Studies have shown that calcium oxalate crystal deposition leads to the cellular injury mediated by lipid peroxidation through free oxygen radical generation. Studies revealed that these cellular injuries favor the events of calcium oxalate retention in renal tubules which is significant for further stone development [33–35]. Recent clinical data are also supporting this finding that formation of urinary stones leads to the oxidative stress in patients [36].…”

Kidney Stone Disease: An Update on Current Concepts

“…Many factors contribute to CaOx stone formation such as hypercalciuria (resorptive, renal leak, absorptive, and metabolic diseases), hyperuricosuria, hyperoxaluria, hypocitraturia, hypomagnesuria, and hypercystinuria [ 35 ]. Mostly, urinary pH of 5.0 to 6.5 promotes CaOx stones [ 36 ], whereas calcium phosphate stones occur when pH is greater than 7.5 [ 11 ].…”

“…However, it has to be noted that some cells did not respond to oxalate injury. This may be due to the fact that changes in gene expression could protect from apoptosis and then inhibit from lithiasis [ 35 ]. These findings highlight the need for future studies clarifying novel biochemical targets of kidney stone formation and the utility of p38 MAPK inhibitors in preventing stone formation.…”

Alcea rosea root extract as a preventive and curative agent in ethylene glycol-induced urolithiasis in rats

“…[1] It is largely a recurrent disease with a relapse rate of 50% in 5-10 years, and therefore a condition with substantial economic consequences and a great public health importance. [12] Calcium oxalate (CaOx) and calcium phosphate stones are the highest common calculi which form approximately 80% of stones in the urinary system. [34] Uric acid stones represent about 5-10%, trailed by cystine, struvite, and ammonium acid urate stones.…”