Kidney stones are mainly lodged in the kidney(s). Therefore, this review has intended to provide a compiled up-to-date information on kidney stone etiology, pathogenesis, and prevention approaches. Thus, further understanding of the pathophysiology of kidney stone formation is a research area to manage urolithiasis using new drugs. Currently, there is no satisfactory drug to cure and/or prevent kidney stone recurrences.
The exposure of renal epithelial cells to oxalate causes a signaling cascade which leads to apoptosis by p38 mitogen-activated protein kinase pathways. It is also noted that cellular injury promotes retention of particles on renal papillary surfaces. These steps are modulated by an imbalance between factors that promote or inhibit urinary crystallization. The mechanism of stone formation is a complex process which results from several physicochemical events including supersaturation, nucleation, growth, aggregation, and retention of urinary stone constituents within tubular cells.
The most common type of kidney stone is calcium oxalate formed at Randall's plaque on the renal papillary surfaces. The etiology of kidney stone is multifactorial. It has been associated with an increased risk of end-stage renal failure. It is an increasing urological disorder of human health, affecting about 12% of the world population. Kidney stone disease is a crystal concretion formed usually within the kidneys.
0 kommentar(er)
