Pathophysiology of Nephrolithiasis

Abstract

The incidence of nephrolithiasis has risen over the last twenty years and continues to rise. Although it is often referred to as a disease, recent advances in the understanding of the pathophysiology suggest that it is a systemic disorder. We conducted a PubMed based literature review on the recent advances in the pathophysiology of kidney stone formation. There is a link between diabetes, metabolic syndrome, obesity, insulin resistance and nephrolithiasis. Along with the aging population and a Western diet, these are the main reasons for the rising incidence and prevalence of nephrolithiasis. Different theories as to the pathophysiological mechanisms of lithogenesis have been proposed, including the free and fixed particle theories, and Randal’s plaque hypothesis. Among the different types of kidney stones, those containing calcium are the most common, followed by those containing uric acid, struvite and cystine. Supersaturated urine, acidic urine pH and reductions in kidney stone inhibitors in the urine are the main recognized causes that contribute to the formation of all these stonetypes. Nephrolithiasis is considered a systemic pathology that may lead to end-stage renal disease. Although much progress has been made, the underlying pathophysiological mechanisms of kidney stone formation are still not fully understood

Kidney Stone Disease With Special Regard to Drug-Induced Kidney Stones – A Contemporary Synopsis

“…The promoters form a surface on which precipitation may take place, which reduces the energy necessary for crystallisation [5,11]. The homogeneous nucleation mechanism is consistent with the general hypothesis of the "free particles", while the heterogeneous one meets the criteria of the "fixed particles" concept, which is also often mentioned in the literature [13].…”

Sleep and circadian rhythm disturbance in kidney stone disease: a narrative review

“…Crystal formation from supersaturated urine retained in the kidney is the driving force ( 16 , 34 ). Then, the crystals gather together to grow to a size as further aggregation, which can interact with intrarenal structures (also called crystal-cell interaction) to cause renal tubular epithelial cell (RTEC) injury ( 34 , 35 ). Crystal-cell interaction leads to the movement of crystals from the basolateral side of cells to the basement membrane and results in the retention of crystals in the kidney or collecting duct to eventually form the clinical stone ( 34 , 36 ).…”

Experimental Urolithiasis Model to assess Phyto-fractions as Anti-lithiatic Contributors: A Herbaceutical Approach

“…Stones containing calcium are a common type of calculi with a prevalence of 70-80%, of which calcium phosphate and calcium oxalate dominate (Han et al, 2015). Supersaturation of urine in presence of calcium and oxalate facilitates calcium oxalate stone development (Paliouras et al, 2012). Following are the factors which affect the formation of calcium oxalate stones; acidic urine, low volume of urine, hypercalciuria (increased concentration of calcium in urine leads to precipitation of calcium salts), hyperoxaluria (high concentration of oxalate excreted in urine), hypocitraturia (excretion of a lower amount of citrate in urine which leads to high pH) and hyperuricosuria (acidic urine dissolves uric acid, leading to stone formation).…”