Urolithiasis and the major urinary protein

The pathogenetic approach to metaphylaxis of urolithiasis is a widespread, socially significant healthcare issue due to the increasing incidence and, particularly, its recurrent nature, despite advances in pharmacotherapy and the application of lithotripsy. Pathological crystal genesis is viewed as a consequence of exceeding the solubility threshold of various urinary mineral components on one hand, and as a result of post-translational defects in the main proteome of urine formation – uromodulin (UMOD), which demonstrates a sanogenetic system in healthy individuals for maintaining biophysical homeostasis stability: the colloidal properties of urine. However, in addition to this, UMOD, by binding mannose-dependent pili of infectious agents, blocks bacterial contact with urothelial cells, given that urinary tract infection is a known factor in urolithiasis. By modeling the urine of healthy individuals through co-incubation with E. coli bacteria, a decrease in the concentration of polymerized uromodulin in urine has been demonstrated as a factor increasing the risk of calcium oxalate crystal formation.