Document Detail

Cushing's syndrome, glucocorticoids and the kidney.
MedLine Citation:
PMID:  20655918     Owner:  NLM     Status:  MEDLINE    
Glucocorticoids (GCs) affect renal development and function in fetal and mature kidneys both indirectly, by influencing the cardiovascular system, and directly, by their effects on glomerular and tubular function. Excess GCs due to endogenous GC overproduction in Cushing's syndrome or exogenous GC administration plays a pivotal role in hypertension and causes increased cardiac output, total peripheral resistance and renal blood flow. Glucocorticoids increase renal vascular resistance (RVR) in some species and experimental settings and decrease RVR in others. Short term administration of adrenocorticotrophic hormone or GCs causes an increased glomerular filtration rate (GFR) in humans, rats, sheep and dogs. Interestingly, chronic exposure may cause a decreased GFR in combination with a higher cardiovascular risk in human patients with Cushing's syndrome. Glomerular dysfunction leads to proteinuria and albuminuria in canine and human Cushing's patients, and some cases also show histological evidence of glomerulosclerosis. Tubular dysfunction is reflected by an impaired urinary concentrating ability and disturbed electrolyte handling, which can potentially result in increased sodium reabsorption, hypercalciuria and urolithiasis. Conversely, chronic kidney disease can also alter GC metabolism. More research needs to be performed to further evaluate the renal consequences of Cushing's syndrome because of its implications for therapeutic aspects as well as the general well-being of the patient. Because there is a high incidence of Cushing's syndrome in canines, which is similar to the syndrome in humans, dogs are an interesting animal model to investigate the link between hypercortisolism and renal function.
Pascale Smets; Evelyne Meyer; Bert Maddens; Sylvie Daminet
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2010-07-23
Journal Detail:
Title:  General and comparative endocrinology     Volume:  169     ISSN:  1095-6840     ISO Abbreviation:  Gen. Comp. Endocrinol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-14     Completed Date:  2011-01-11     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370735     Medline TA:  Gen Comp Endocrinol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1-10     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Small Animal Medicine and Clinical Biology, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium.
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MeSH Terms
Cushing Syndrome / metabolism*,  pathology
Glucocorticoids / metabolism*
Kidney / metabolism*,  pathology
Reg. No./Substance:

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