Document Detail

The progression of renal disease.
MedLine Citation:
PMID:  3287163     Owner:  NLM     Status:  MEDLINE    
The diversity of its causes, the unpredictability of its clinical course, and our expanding knowledge of the conditions that may exacerbate or retard its progression suggest that glomerular sclerosis cannot be attributed to a single aberration in glomerular physiology. Nonetheless, the welter of clinical and experimental observations is beginning to yield a pattern. Agents or conditions injurious to glomerular epithelium tend to cause glomerular sclerosis. Agents or conditions that induce short-term or long-term activation of mesangial cells may lead to glomerular sclerosis. Indeed, one contribution of the healthy epithelium may be to serve as a tonic inhibitor of the intraglomerular processes arising from mesangial-cell activation. Long-term activation of the mesangium is associated with the proliferation and infiltration of cells and with the expansion of the mesangial matrix--the antecedents of sclerosis. We anticipate that different diseases associated with glomerular sclerosis will be found to depend to varying extents on these two potential mechanisms of sclerosis. Beyond a certain threshold of glomerular injury, glomerular diseases share an additional factor: the capacity of both intrinsic cells and infiltrating cells to alter the microenvironment of the glomerulus so that sclerosis progresses inexorably long after the disappearance of the initiating insult. Several potential risk factors may contribute to the progression of chronic renal disease. These factors include systemic hypertension, proteinuria, hyperlipidemia, high protein intake, and probably conditions that lead to glomerular hypertrophy. Interventions designed to minimize the potential contribution of these factors to the progression of renal insufficiency may halt or slow the loss of function of the kidney. Clinical trials designed to examine the effects of these factors on the progressive course of renal insufficiency will help to establish their role and relative importance in humans.
S Klahr; G Schreiner; I Ichikawa
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  The New England journal of medicine     Volume:  318     ISSN:  0028-4793     ISO Abbreviation:  N. Engl. J. Med.     Publication Date:  1988 Jun 
Date Detail:
Created Date:  1988-07-06     Completed Date:  1988-07-06     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  0255562     Medline TA:  N Engl J Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1657-66     Citation Subset:  AIM; IM    
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.
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MeSH Terms
Kidney Diseases / physiopathology*
Kidney Glomerulus / pathology

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

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