Document Detail


Cardiac remodeling and dysfunction in nephrotic syndrome.
MedLine Citation:
PMID:  17457379     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
There is an increased incidence of heart disease in patients with chronic nephrotic syndrome (NS), which may be attributable to the malnutrition and activated inflammatory state accompanying the sustained proteinuria. In this study, we evaluated renal function, cardiac morphometry, contractile function, and myocardial gene expression in the established puromycin aminonucleoside nephrosis rat model of NS. Two weeks after aminonucleoside injection, there was massive proteinuria, decreased creatinine clearance, and a negative sodium balance. Skeletal and cardiac muscle atrophy was present and was accompanied by impaired left ventricular (LV) hemodynamic function along with decreased contractile properties of isolated LV muscle strips. The expression of selected cytokines and proteins involved in calcium handling in myocardial tissue was evaluated by real time polymerase chain reaction. This revealed that the expression of interleukin-1beta, tumor necrosis factor-alpha, and phospholamban were elevated, whereas that of cardiac sarco(endo)plasmic reticulum calcium pump protein was decreased. We suggest that protein wasting and systemic inflammatory activation during NS contribute to cardiac remodeling and dysfunction.
Authors:
M Moreira-Rodrigues; R Roncon-Albuquerque; T Henriques-Coelho; A P Lourenço; B Sampaio-Maia; J Santos; M Pestana; A F Leite-Moreira
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-04-25
Journal Detail:
Title:  Kidney international     Volume:  71     ISSN:  0085-2538     ISO Abbreviation:  Kidney Int.     Publication Date:  2007 Jun 
Date Detail:
Created Date:  2007-06-07     Completed Date:  2007-07-18     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1240-8     Citation Subset:  IM    
Affiliation:
Unit of Research and Development of Nephrology, University of Porto, Porto, Portugal.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure
Calcium-Binding Proteins / genetics
Down-Regulation
Gene Expression
Heart Ventricles / metabolism,  pathology*,  physiopathology
Interleukin-1beta / genetics
Male
Muscle Contraction
Muscle, Skeletal / pathology
Muscular Atrophy / etiology*,  pathology*
Myocardium / metabolism,  pathology*
Nephrotic Syndrome / chemically induced,  complications*
Puromycin Aminonucleoside / toxicity
Rats
Rats, Sprague-Dawley
Sarcoplasmic Reticulum Calcium-Transporting ATPases / genetics
Sodium / metabolism
Stroke Volume
Tumor Necrosis Factor-alpha / genetics
Up-Regulation
Water-Electrolyte Balance
Chemical
Reg. No./Substance:
0/Calcium-Binding Proteins; 0/Interleukin-1beta; 0/Tumor Necrosis Factor-alpha; 0/phospholamban; 58-60-6/Puromycin Aminonucleoside; 7440-23-5/Sodium; EC 3.6.3.8/Sarcoplasmic Reticulum Calcium-Transporting ATPases

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


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