Document Detail


Pathogenesis of idiopathic calcium nephrolithiasis: update 1997.
MedLine Citation:
PMID:  9592625     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Idiopathic calcium nephrolithiasis (ICN) is a frequent disease in Western countries. The physicochemical theory of lithogenesis, which explains stone formation by the precipitation, growth, and crystalline aggregation of lithogenic salts in the urine, has contributed greatly to the understanding of the pathogenesis of calcium urolithiasis. However, several aspects are still unexplained; the co-existence of familial occurrence, primary tubular dysfunctions with ICN, and anomalies in the systemic handling of oxalate and calcium led to the development of a cellular hypothesis of ICN. A number of cellular defects in the handling of ions has been reported that involves both anion and cation transport. These anomalies are probably the expression of a still unknown cellular defect in idiopathic calcium stone formers. We suggested that an anomaly in the cell membrane composition might be responsible for the complex array of cell ion flux abnormalities observed in ICN. Recently, a disorder in the n-6 polyunsaturated fatty acid series has been described; it is characterized by a lower linoleic acid content and a higher arachidonic acid concentration in both plasma and erythrocyte membrane phospholipids of renal calcium stone patients. This anomaly could cause an increased activity of ion carriers; furthermore, it may lead to increased prostaglandin synthesis and to secondary phenomena at the kidney, skeletal, and intestinal level. As a consequence, critical conditions for lithogenesis in the kidney may ensue. The data suggest a common pathogenesis for hypercalciuria and hyperoxaluria. The systemic defect in the phospholipid arachidonic acid level may be both of dietary or genetic origin; experimental data suggest that the increase in delta-6 desaturase activity, the limiting enzyme in the metabolic pathway of polyunsaturated fatty acids, might be relevant to the pathogenesis of lipid abnormalities observed in nephrolithiasis and to the pathogenesis of ICN and its related problems (at the kidney, intestinal, and bone level).
Authors:
B Baggio; M Plebani; G Gambaro
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Critical reviews in clinical laboratory sciences     Volume:  35     ISSN:  1040-8363     ISO Abbreviation:  Crit Rev Clin Lab Sci     Publication Date:  1998 Apr 
Date Detail:
Created Date:  1998-06-23     Completed Date:  1998-06-23     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  8914816     Medline TA:  Crit Rev Clin Lab Sci     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  153-87     Citation Subset:  IM    
Affiliation:
Institute of Internal Medicine, School of Medicine, University of Padua, Italy.
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MeSH Terms
Descriptor/Qualifier:
Calcium / urine*
Calcium Metabolism Disorders / genetics*,  metabolism*,  physiopathology*
Female
Humans
Kidney / metabolism*,  physiopathology*
Male
Pedigree
Urinary Calculi / genetics*,  metabolism*,  physiopathology*
Chemical
Reg. No./Substance:
7440-70-2/Calcium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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