Literature DB >> 7996806

Calcium oxalate nephrolithiasis, a free or fixed particle disease.

D J Kok1, S R Khan.   

Abstract

The chances of stone formation occurring through a free particle mechanism were calculated using the approach of Finlayson and Reid [1]. For these calculations we used new data on nephron dimensions, supersaturation and crystal growth rates in urine, and also incorporated the size increasing effect of crystal agglomeration. The calculations were performed assuming different levels of oxalate excretion, simulating the diurnal variation and acute hyperoxaluria following a dietary load. In addition urinary flow conditions were varied according to changes in daily urinary volume. It is shown that during the normal transit time of urine through the nephron, particles can obtain a size big enough to be retained in the nephron. This is mainly due to the size-increasing effect of the agglomeration process. The precipitable amount of oxalate present is not limiting for the maximum attainable particle size. However, acute increases in oxalate excretion do pose a risk because supersaturation is reached earlier in the nephron and consequently the crystal particles are allowed more time to increase in size. In conclusion, the present calculations demonstrate that during the normal transit time through the kidney, crystalline particles can be formed which are large enough to be retained because of their size and thus form the nidus of a stone. The highest risk is encountered at the end of those collecting ducts where crystals formed in nephrons with a long loop of Henle meet and agglomerate.

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Year:  1994        PMID: 7996806     DOI: 10.1038/ki.1994.341

Source DB:  PubMed          Journal:  Kidney Int        ISSN: 0085-2538            Impact factor:   10.612


  81 in total

1.  Update on the genetics of nephrolithiasis.

Authors:  Giuseppe Vezzoli; Teresa Arcidiacono; Vera Paloschi; Annalisa Terranegra; Rita Biasion; Laura Soldati
Journal:  Clin Cases Miner Bone Metab       Date:  2008-05

2.  Renal stone disease: a commentary on the nature and significance of Randall's plaque.

Authors:  A P Evan; R J Unwin; J C Williams
Journal:  Nephron Physiol       Date:  2011-09-21

Review 3.  The tubular epithelium in the initiation and course of intratubular nephrocalcinosis.

Authors:  Benjamin A Vervaet; Anja Verhulst; Marc E De Broe; Patrick C D'Haese
Journal:  Urol Res       Date:  2010-08-02

4.  Reactive oxygen species mediated calcium oxalate crystal-induced expression of MCP-1 in HK-2 cells.

Authors:  Pouran Habibzadegah-Tari; Karen G Byer; Saeed R Khan
Journal:  Urol Res       Date:  2006-01-06

Review 5.  The role of calcium phosphate in the development of Randall's plaques.

Authors:  Hans-Göran Tiselius
Journal:  Urolithiasis       Date:  2013-08-21       Impact factor: 3.436

6.  Microstructures of Randall's plaques and their interfaces with calcium oxalate monohydrate kidney stones reflect underlying mineral precipitation mechanisms.

Authors:  Ingo Sethmann; Gunnar Wendt-Nordahl; Thomas Knoll; Frieder Enzmann; Ludwig Simon; Hans-Joachim Kleebe
Journal:  Urolithiasis       Date:  2016-10-01       Impact factor: 3.436

7.  Acidic polyanion poly(acrylic acid) prevents calcium oxalate crystal deposition.

Authors:  Jack G Kleinman; Laura J Alatalo; Ann M Beshensky; Jeffrey A Wesson
Journal:  Kidney Int       Date:  2008-06-18       Impact factor: 10.612

8.  Involvement of VKORC1 in the inhibition of calcium oxalate crystal formation in HK-2 cells.

Authors:  Bo Hu; Hao-Ran Wu; Zhi-Yong Ma; Zhuan-Chang Wu; Ying-Mei Lu; Guo-Wei Shi
Journal:  J Huazhong Univ Sci Technolog Med Sci       Date:  2014-06-18

Review 9.  Genetic basis of renal cellular dysfunction and the formation of kidney stones.

Authors:  Saeed R Khan; Benjamin K Canales
Journal:  Urol Res       Date:  2009-06-11

10.  Studies on the role of calcium phosphate in the process of calcium oxalate crystal formation.

Authors:  Hans-Göran Tiselius; Bengt Lindbäck; Anne-Marie Fornander; Mari-Anne Nilsson
Journal:  Urol Res       Date:  2009-05-15
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