Changes in plasma renin activity in cirrhosis: a reappraisal based on studies in 67 patients and "low-renin" cirrhosis.

Wilkinson, Stephen; Smith, I. K.; Williams, Roger

doi:10.1161/01.hyp.1.2.125

Cited by 59 publications

(23 citation statements)

References 19 publications

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“…No significant differences were noted at three months between these groups in terms of urine volume, uri nary sodi um excretion , creatinine clearance, plasma rcnin activity and serum a ldosterone (fable 4) DISCUSSION This study confirms previous observations that p lasma renin activity levels a re usually eleva ted in subjects with ascites (13)(14)(15)(16)(17) but that in some individuals levels may be found within the nonnal range ( 10, 13,18).…”

Section: Individual Natriuretic Response To Pvssupporting

confidence: 86%

Renin-Aldosterone Axis in Refractory Hepatic Ascites. Characterization of The Response of the Axis to Both the Acute and Long Term Effects of Peritoneuvenous Shunting

Campbell

Grieg

Blendis

1989

Canadian Journal of Gastroenterology

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Twenty-two patients with refractory asc1tes secondary to chronic liver disease undergoing pcritoneovenous shunting (PVS) were studied und er strict metabolic conditio ns, preoperatively and for the first 8 h postoperatively. Fourtren subjects were restudied under similar metabolic conditions three months post-l 1 VS. Thirteen of the 22 patients (59%) had an immediate dramatic natriuresis and entered negative sodium balance (group A), the remaining nine patients !41.,.o) remained in positive sodium balance during the first 8 h post-PVS (group B) Group B was characterized preoperatively by significantly higher mean plasma rcnin activity (P· 0.01) and scrum aldosterone levels (P, 0.01) compared to group A Yet, plasma renin activity and aldosterone levels in both groups were similar at 8 h following shunting. At three mo nths post-PVS in the 14 patients restudied , mean plasma renin activity and seru m aldosterone levels were not significantly elevated above the normal range. Yet the patients still demonstrated continued sodium retention on a 20 mEq sodi um diet, mean sodium excretion 10.5 ± 2.8 mEq/day. The close correlation of sc rum aldosteronc with plasma renin activity and the parallel suppressio n acutely post-PVS, indicate that the level of plasma renin activity is a major determinant of serum aldosterone in re fractory ascites. However, the find ing of no rmal preoperative values for plasma renin acti vity and aldosterone in certai n patients, combined with the failure of group B subjects to enter negative sodi um balance despite acute normalization of aldosterone, would indicate that facto rs other than activation of the renin-aldosterone axis contribute to the sodium retention of chro nic liver disease. This conclusion is supported by the late results which document persistent sodium retentio n three months following PVS , despite normalization of aldosterone and presumably normalization of any deficit in effective plasma volume. Can J Gastroenterol 1989;3(3):103·110 (Pour resume voir page 104)

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Section: Individual Natriuretic Response To Pvssupporting

confidence: 86%

Renin-Aldosterone Axis in Refractory Hepatic Ascites. Characterization of The Response of the Axis to Both the Acute and Long Term Effects of Peritoneuvenous Shunting

Campbell

Grieg

Blendis

1989

Canadian Journal of Gastroenterology

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“…The group of preascitic cirrhotics demonstrated moderately reduced values of plasma renin activity (PRA) and aldosterone and significantly increased endogenous dopaminergic function (Table 2), all indicative of a certain degree of expansion of the extracellular fluid volume, as already reported (27,(32)(33)(34)(35)(36)(37)(38). In particular, the increased endogenous dopaminergic tone, demonstrated by the higher than normal incremental responses of plasma aldosterone after metoclopramide administration, is a reliable and Digestive Diseases and Sciences, Vol.…”

Section: Discussionsupporting

confidence: 62%

“…In other words, in preascites GFR appeared to rise and PRA to drop, while in ascitic patients GFR appeared to have dropped to within the normal range and PRA was high. This peculiar observation is substantially supported by a long series of previous papers addressing the same topic: in preascitic cirrhosis PRA have been found to be significantly (35)(36)(37)(44)(45)(46) or slightly (47,48) reduced regardless of sodium intake, whereas most ascitic patients, as a group, display clear-cut secondary hyperaldosteronism (45,(49)(50)(51)(52); glomerular hyperfiltration occurs in compensated cirrhotics (53)(54)(55) and disappears once clinical decompensation supervenes (9,56).…”

Section: Discussionmentioning

confidence: 64%

Loss of Tubuloglomerular Feedback in Decompensated Liver Cirrhosis: Physiopathological Implications

Sansoè

Silvano²,

Mengozzi

et al. 2005

Dig Dis Sci

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In healthy subjects, arterial pressure reduction or renal ischemia produces renal artery dilatation through autoregulation and tubuloglomerular feedback (TuGF). Patients with decompensated cirrhosis have reduced kidney perfusion pressure but show renal vasoconstriction instead of autoregulation-mediated vasodilation. This study investigates the consequences of kidney autoregulation loss on renal perfusion, glomerular filtration rate, and tubular handling of electrolytes in both compensated and ascitic nonazotemic cirrhotic patients. Forty-two consecutive patients with diuretic-free liver cirrhosis (32 with preascitic and 10 with ascitic disease) and 10 controls were submitted to the following determinations: (a) basal plasma renin activity and aldosterone levels; (b) endogenous dopaminergic activity measured as incremental aldosterone responses during metoclopramide administration; and (c) renal clearances of sodium, potassium, inulin, para-aminohippurate and lithium. Compared with the other groups, ascitic patients showed lower renal plasma flow (P < 0.01) and lithium clearance (P < 0.05), a higher filtration fraction (P < 0.01), and secondary aldosteronism. Controls and preascitic patients displayed tubuloglomerular feedback (the mechanism increasing the glomerular filtration rate when a reduced sodium load reaches the distal tubule), as demonstrated by negative correlations between fractional excretion of lithium (an expression of fractional delivery of sodium to the distal nephron) and glomerular filtration rate (respectively, r = -0.73, P < 0.03, and r = -0.48, P < 0.01). Conversely, patients with ascites showed a positive correlation between lithium fractional excretion and glomerular filtration rate (r = 0.64, P < 0.05). Reduction in renal perfusion, increased filtration fraction, and TuGF derangement, as found in decompensated patients, are indicative of prevalent postglomerular arteriolar vasoconstriction, with ensuing stimulation of proximal tubular sodium reabsorption.

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“…The amount of endogenous renin substrate varies from sample to sample and changes in various physiological and pathological conditions (Sealey et al, 1982, Wilkinson et al, 1979, Rasmussen et al, 1981.…”

Section: Discussionmentioning

confidence: 99%

Plasma Active Renin Concentration in Children.

et al. 1989

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In normal children aged one month to 16 years, the plasma active renin concentration (PARC) was measured with a renin immunoradiometricassay (IRMA) kit, and was compared with plasma renin activity (PRA).The IRMA for renin was found to be independent of the amount of renin substrate and not affected by the dilution of plasma samples, and was therefore proved to be a simple and reliable method. PRA measured in non-diluted plasma samples correlated well with PARC. In the age-related change, PARC in infants was significantly higher than that in older children. In infants, PARC was markedly higher in the crying state than that in the non-crying state.

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Changes in plasma renin activity in cirrhosis: a reappraisal based on studies in 67 patients and "low-renin" cirrhosis.

Abstract: SUMMARY The generally held views that plasma renin activity (PRA) is increased in cirrhosis and

Cited by 59 publications

References 19 publications

Renin-Aldosterone Axis in Refractory Hepatic Ascites. Characterization of The Response of the Axis to Both the Acute and Long Term Effects of Peritoneuvenous Shunting

Renin-Aldosterone Axis in Refractory Hepatic Ascites. Characterization of The Response of the Axis to Both the Acute and Long Term Effects of Peritoneuvenous Shunting

Loss of Tubuloglomerular Feedback in Decompensated Liver Cirrhosis: Physiopathological Implications

Plasma Active Renin Concentration in Children.

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