![]() ![]() Small stones (≤5 mm) often pass without medical intervention, but larger stones (≥10 mm) usually must be removed. An acute renal colic that is caused by a tiny stone’s passing down the ureter can be extremely painful. The difference between stone formers and non–stone formers is that crystals stay behind in kidneys of stone formers. The formation of crystals in the kidney is normal and harmless provided that they are excreted with the urine. Kidney stones are built from numerous tiny crystals that commonly are pasted together with organic material. #RENAL CALCULUS HOW TO#Despite enormous developments in nephrology and urology, we still do not know exactly how kidney stones are formed and how to prevent them. Renal stone disease has tormented people throughout the ages. It remains to be determined whether one or both forms of renal crystal retention are involved in the development of kidney stones (nephrolithiasis). Crystal binding to HA leads to crystal retention in the renal tubules (nephrocalcinosis) and to the formation of calcified plaques in the renal interstitium (Randall’s plaques). ![]() HA is an excellent crystal-binding molecule because of its size, negative ionic charge, and ability to form hydrated gel-like matrices. HA is a major constituent of the extracellular matrix in the renal medullary interstitium and the pericellular matrix of mitogen/stress-activated renal tubular cells. ![]() The precipitation of poorly soluble calcium salts (crystal formation) in the kidney is the inevitable consequence of producing concentrated urine. Much attention is dedicated to hyaluronan (HA), an extremely large glycosaminoglycan that may play a central role in renal stone disease. In this article, the various concepts that have been proposed during the past century are reviewed briefly and integrated into current insights. The mechanisms that are involved in renal stone disease are not entirely clear. ![]()
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