Renal Circulation in Cirrhosis: Observations Based on Catheterization of the Renal Vein*

Baldus, William P.; Summerskill, W.H.J.; Hunt, Jennifer; Maher, Frank T.

doi:10.1172/jci104993

Cited by 87 publications

(21 citation statements)

References 29 publications

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“…While azotemia usually was present at the time of death, the major terminal event was more often gastrointestinal hemorrhage or hepatic coma. Discussion Previous investigators, using the PAH clearance method (4,5,15,16), have found reduced RBF in patients with hepatic failure. However, clearance techniques may be inaccurate in the oliguric patient.…”

Section: Clinical Observationsmentioning

confidence: 72%

“…While reduced renal perfusion may not be the only factor in the oliguria of severe liver disease, a number of investigators have considered this reduction of prime importance (4,5). That renal vasoconstriction contributes to the low RBF in these patients was confirmed by the finding of high renal vascular resistance and a markedly reduced renal fraction of CO.…”

Section: Clinical Observationsmentioning

confidence: 99%

“…The absence of a history of kidney disease or of a specific histological renal lesion has led to the suggestion that the renal failure may be due to decreased renal perfusion (3), and clearance studies have suggested that renal blood flow is severely reduced (4,5). However, the mechanism of the renal hemodynamic abnormality in this syndrome has not been established.…”

Section: Introductionmentioning

confidence: 99%

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Systemic and Renal Hemodynamics in Oliguric Hepatic Failure: Effect of Volume Expansion*

Tristani¹,

Cohn²

1967

J. Clin. Invest.

171

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Section: Clinical Observationsmentioning

confidence: 72%

Section: Clinical Observationsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Systemic and Renal Hemodynamics in Oliguric Hepatic Failure: Effect of Volume Expansion*

Tristani¹,

Cohn²

1967

J. Clin. Invest.

171

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“…Increases in PVP also were associated with an antidiuresis as urine osmolality increased from 101 to 446 mosmol/kg H20 (P < 0.001). This antidiuresis was significantly blunted INTRODUCTION An impairment in glomerular filtration rate (GFR),' renal blood flow (RBF), and renal water excretion, as well as enhanced renin secretion, have been observed during hepatic cirrhosis (1)(2)(3)(4)(5). The cause of these abnormalities has not been elucidated.…”

mentioning

confidence: 99%

Mechanisms of portal hypertension-induced alterations in renal hemodynamics, renal water excretion, and renin secretion.

Cronin¹,

McDonald²,

Schrier³

1976

J. Clin. Invest.

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A B S T R A C T Clinical states with portal venous hypertension are frequently associated with impairment in renal hemodynamics and water excretion, as well as increased renin secretion. In the present investigation, portal venous pressure (PVP) was increased in anesthetized dogs undergoing a water diuresis. Renal arterial pressure was maintained constant in all studies. As PVP was increased from 6 to 20 mm Hg, decreases in cardiac output (2.5-2.0 liter/min, P < 0.05) and mean arterial pressure (140-131 mm Hg, P < 0.05) were observed. Increases in PVP were also associated with decreases in glomerular filtration rate (GFR, 40-31 ml/min, P <0.001), renal blood flow (RBF, 267-193 ml/min, P < 0.001), and increases in renin secretion (232-939 U/min, P < 0.025) in innervated kidneys. No significant change in either GFR or RBF and a decrease in renin secretion occurred with increases in PVP in denervated kidneys. To dissociate the changes in cardiac output and mean arterial pressure induced by increased PVP from the observed decreases in GFR and RBF, studies were performed on animals undergoing constriction of the thoracic inferior vena cava. In these studies, similar decreases in cardiac output and mean arterial pressure were not associated with significant changes in GFR or RBF. Increases in PVP also were associated with an antidiuresis as urine osmolality increased from 101 to 446 mosmol/kg H20 (P < 0.001). This antidiuresis was significantly blunted but not abolished by acute hypophysectomy. In hypophysectomized animals, changes in free water clearance Dr. Anderson is a Teaching and Research Scholar of the American College of Physicians.Received for publication 24 February 1976 and in revised form 18 June 1976. and urine flow were linearly correlated as PVP was increased. These studies indicate that increases in PVP result in decreases in GFR and RBF and increases in renin secretion mediated by increased renal adrenergic tone. Increased PVP is also associated with antidiuresis; this antidiuresis is mediated both by vasopressin release and by diminished tubular fluid delivery to the distal nephron.

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“…The factors responsible for the limited ability of the kidney to excrete sodium are still not clear. The possibility that the decrease in sodium excretion is due solely to reduced glomerular filtration seems to be eliminated by a number of recent investigations [4,16,27].The necessity of aldosterone to maintain a high rate of tubular sodium reabsorption in edema-forming states of different origin is fairly well estab lished [9,30]. However, several studies make it perfectly clear that an increased mineralocorticoid activity alone does not promote progressive sodium retention [2,21].…”

mentioning

confidence: 99%

Urinary Sodium Excretion and Proximal Tubule Reabsorption in Rats with High-Output Heart Failure

Stumpe¹,

Reinelt²,

Ressel³

et al. 1974

Nephron

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Sodium excretion and proximal tubule function were studied in rats with an aorta-to-vena cava (A-V) fistula using the techniques of micropuncture. 15–28 days after ereation of the fistula, 40% of the rats had developed peripheral edema and ascites. Control rats excreted significantly more sodium in the urine than did the A-V fistula rats. Clearances of inulin and PAH, intrarenal distribution of filtration, and filtration fraction were wholly comparable for the two experimental groups. Also, sodium reabsorption by the proximal tubule was not different for the two groups during either hydropenia or extracellular volume expansion. Transit time through the loop of Henle was prolonged in the A-V rats. The data suggest that an enhanced reabsorption in a distal nephron segment – possibly in the loop of Henle – must play a significant role in sustained salt retention and edema formation of A-V rats. Proximal reabsorption was increased only in ‘acute’ A-V rats (2–6 days after the operation). This alteration of proximal reabsorption does not appear relevant to the chronic state of sodium retention and may be mediated by extracellular fluid volume contraction due to creation of the fistula.

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Renal Circulation in Cirrhosis: Observations Based on Catheterization of the Renal Vein*

Cited by 87 publications

References 29 publications

Systemic and Renal Hemodynamics in Oliguric Hepatic Failure: Effect of Volume Expansion*

Systemic and Renal Hemodynamics in Oliguric Hepatic Failure: Effect of Volume Expansion*

Mechanisms of portal hypertension-induced alterations in renal hemodynamics, renal water excretion, and renin secretion.

Urinary Sodium Excretion and Proximal Tubule Reabsorption in Rats with High-Output Heart Failure

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