Literature DB >> 2354670

Role of the kidney in congestive heart failure. Relationship of cardiac index to kidney function.

S Ljungman1, J H Laragh, R J Cody.   

Abstract

Because of inappropriate signals from the volume-regulation system and a reduction in renal blood flow, the kidney is not able to prevent sodium and water retention in chronic congestive heart failure (CHF). A brief summary of normal renal function and renal involvement in CHF is given and a study of renal function in patients with moderate or severe chronic CHF is presented. To evaluate the impact of cardiac output reduction on the regulation of the glomerular filtration rate (GFR) in heart failure, GFR (inulin clearance), renal plasma flow [p-aminohippurate (PAH) clearance], invasive haemodynamics, blood volume, plasma renin and plasma catecholamines were measured in 34 patients with chronic CHF. The patients were divided into 3 groups according to their cardiac index (CI): CI greater than 2.0 L/min/m2 (group A), CI 1.5 to 2.0 L/min/m2 (group B), and CI less than 1.5 L/min/m2 (group C). Differences in the relationship between GFR, renal plasma flow and filtration fraction for the 3 groups emerged. Despite an intergroup reduction in the renal fraction of cardiac output and renal blood flow, GFR was similar in groups A and B (62 and 67 ml/min/1.73 m2, respectively), and was accompanied by a compensatory increase in filtration fraction, from 24% in group A to 35% in group B. Group C had a much lower GFR (38 ml/min/1.73 m2), however, the filtration fraction (28%) was intermediate in value between those of groups A and B. The differences in GFR were reflected by blood urea nitrogen levels but not by serum creatinine levels. The occurrence of a non-compensatory filtration fraction response in the patients with the greatest impairment of CI and renal blood flow suggests that GFR becomes dependent on afferent arteriolar flow in the most severe heart failure, despite stimulation of haemodynamic and hormonal pathways, which would normally increase efferent arteriolar tone. It is thus suggested that GFR becomes flow dependent in patients in the most severe stage of chronic CHF.

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Year:  1990        PMID: 2354670     DOI: 10.2165/00003495-199000394-00004

Source DB:  PubMed          Journal:  Drugs        ISSN: 0012-6667            Impact factor:   9.546


  33 in total

1.  Changes in cardiac output with age.

Authors:  M BRANDFONBRENER; M LANDOWNE; N W SHOCK
Journal:  Circulation       Date:  1955-10       Impact factor: 29.690

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Authors:  L WERKO; E VARNAUSKAS; H ELIASCH; J EK; H BUCHT; B THOMASSON; J BERGSTROM
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Authors:  D F DAVIES; N W SHOCK
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Authors:  S Nitter-Hauge; E K Brodwall; K Rootwelt
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5.  Interrelationship of hemodynamic alterations of valvular heart disease and renal function: influences on renal sodium reabsorption.

Authors:  G A Porter; F E Kloster; J D Bristow; H E Griswold
Journal:  Am Heart J       Date:  1972-08       Impact factor: 4.749

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Authors:  N R Levens; M J Peach; R M Carey
Journal:  Circ Res       Date:  1981-02       Impact factor: 17.367

8.  Normal renal function: CIN and CPAH in healthy donors before and after nephrectomy.

Authors:  T K Slack; D M Wilson
Journal:  Mayo Clin Proc       Date:  1976-05       Impact factor: 7.616

9.  Renal response to captopril in severe heart failure: role of furosemide in natriuresis and reversal of hyponatremia.

Authors:  V J Dzau; N K Hollenberg
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10.  Role of angiotensin II in the altered renal function of congestive heart failure.

Authors:  I Ichikawa; J M Pfeffer; M A Pfeffer; T H Hostetter; B M Brenner
Journal:  Circ Res       Date:  1984-11       Impact factor: 17.367

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  64 in total

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Review 9.  Acute kidney injury and 'nephrotoxins': mind your language.

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10.  Importance of venous congestion for worsening of renal function in advanced decompensated heart failure.

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