Abstract
Calcium oxalate nephrolithiasis is a common and highly recurrent disease in urology; however, its precise pathogenesis is still unknown. Recent research has shown that renal inflammatory injury as a result of the cell-crystal reaction plays a crucial role in the development of calcium oxalate kidney stones. An increasing amount of research have confirmed that inflammation mediated by the cell-crystal reaction can lead to inflammatory injury of renal cells, promote the intracellular expression of NADPH oxidase, induce extensive production of reactive oxygen species, activate NLRP3 inflammasome, discharge a great number of inflammatory factors, trigger inflammatory cascading reactions, promote the aggregation, nucleation and growth process of calcium salt crystals, and ultimately lead to the development of intrarenal crystals and even stones. The renal tubular epithelial cells (RTECs)-crystal reaction, macrophage-crystal reaction, calcifying nanoparticles, endoplasmic reticulum stress, autophagy activation, and other regulatory factors and mechanisms are involved in this process.
Highlights
One of the most frequently encountered diseases in urology is kidney stones, which are closely related to multiple factors such as environment, genetics, and metabolic abnormalities; its exact pathogenesis is still unclear [1]
We found that when taurine, N-acetylcysteine (NAC), catalase, or superoxide dismutase (SOD) were added to the rat calcium oxalate (CaOx) kidney stone model, the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and the production of reactive oxygen species (ROS) and LDH decreased, the renal tissue and cell damage and inflammatory reaction triggered by Ox and/ or CaOx crystals were alleviated, the deposition of crystal in the kidney was significantly decreased, and the formation rate of CaOx kidney stones was reduced [21]
We found that oxalic acid or CaOx crystals could prompt oxidative stress in renal tubular epithelial cells (RTECs)
Summary
One of the most frequently encountered diseases in urology is kidney stones, which are closely related to multiple factors such as environment, genetics, and metabolic abnormalities; its exact pathogenesis is still unclear [1]. In vivo as well as in vitro studies have shown that CaOx crystals are capable of inducing the generation of ROS in the kidney, and activating NLRP3 inflammasome to cause inflammatory damage to RTECs and renal tissue, promoting the formation of CaOx stones [10]. We speculate that after macrophages engulf CaOx crystals, up-regulation of ROS may mediate the activation of NLRP3 inflammasomes, induce the secretion of inflammatory factors, and cause aggravation of the inflammatory damage in kidney tissues and RTECs, thereby promoting the formation process of CaOx kidney stones. We speculate that the excessive activation of autophagy mediated by mitochondria-derived ROS could trigger the NLRP3 inflammasome pathway, up-regulate the secretion of inflammatory factors IL-18 and IL-1b, which leads to inflammatory cell invasion and renal interstitial inflammatory injury in the course of CaOx kidney stone formation. The activation of NLRP3 inflammasome may further increase the level of autophagy, resulting in an inflammatory chain reaction in the kidney, and accelerating the formation process of nephrolithiasis
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