Role of Diminished Renal Function in Cardiovascular Mortality
Marker or Pathogenetic Factor?
Robert W. Schrier, MD*
University of Colorado School of Medicine, Division of Renal Diseases and Hypertension, Denver, Colorado.
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Figure 1 Decreased baroreceptor sensitivity in patients with chronic heart failure can worsen cardiac function by increasing renin-angiotensin-aldosterone system (RAAS) and sympathetic activity, enhancing proximal fluid reabsorption, impairing aldosterone escape, and blunting the response to natriuretic peptides. Na = sodium.
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Figure 2 Mechanisms in congestive heart failure whereby negative sodium and water balance by loop diuretics or ultrafiltration therapy may improve myocardial function.
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Figure 3 Pathways whereby vasopressin stimulation of V2 and V1a receptors can contribute to events that worsen cardiac function.
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Figure 4 Myocardial injury can lead to sodium and water retention, which can suppress the renin-angiotensin-aldosterone systems (RAAS) and return cardiac index to a normal range. The dashed lines indicate the pathways of these feedback mechanisms. To exclude myocardial injury when these feedback mechanisms have normalized the RAAS and cardiac index would be a mistake.
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Figure 5 Multiple pathways whereby chronic renal parenchymal disease may increase cardiovascular morbidity and mortality by causing hypertension, atherosclerosis, and/or myocardial dysfunction. GFR = glomerular filtration rate.
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