Blood Volume and Sodium Retention in the Nephrotic Syndrome: A Controversial Pathophysiological Concept

Mees, E. J. Dorhout; Geers, Anton B.; Koomans, Hein A.

doi:10.1159/000183155

Cited by 60 publications

(22 citation statements)

References 63 publications

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“…Tradi tionally, it has been proposed that renal sodium and water retention is a consequence of the hypoalbuminemia that attends massive urinary losses of protein [148,149], According to this theory, lowered plasma oncotic pressure permits extracellular fluid to be translo cated from the vascular to the interstitial compartment. The ensuing reduction of 'effective' plasma volume is then postulated to result in a series of neurohormonal adaptations that promote renal sodium retention [148][149][150]. Among these adaptations may be suppression of the basal levels of ANP.…”

Section: Studies In Nephrotic Syndromementioning

confidence: 99%

Effects of Water Immersion on Atrial Natriuretic Peptide Release in Humans

Epstein

Norsk²,

Loutzenhiser³

1989

Am J Nephrol

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Water immersion (WI) to the neck induces prompt increases in central blood volume, central venous pressure, and atrial distension. Since atrial distension is a major stimulus for atrial natriuretic peptide (ANP) release, WI constitutes a unique model to investigate the physiological importance of ANP in humans. All studies to date demonstrate that ANP increases during the 1st h of WI in hydrated subjects, rising 2.5- to 3-fold by the end of the 2nd or 3rd h. During recovery from WI, ANP returns promptly to prestudy levels. Although distension of the atria probably constitutes the major stimulus for ANP release during WI, other mechanisms may coexist. In normal hydrated subjects undergoing WI, the increases in ANP correlate with the magnitude of the natriuresis, suggesting that ANP constitutes an important determinant of renal sodium handling in humans. It is simplistic, however, to consider the Wl-induced augmentation of ANP to be the sole, or even the prepotent, mediator of the resultant natriuresis. Rather ANP should be considered as one of several hormonal, neural, and hemodynamic factors acting in concert in an integrated matrix to modulate volume homeostasis. Clearly, the results of several recent studies utilizing WI demonstrate that this maneuver constitutes an important investigative model to delineate further the role of ANP in subserving volume homeostasis in normal humans and in disorders of deranged volume regulation.

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Section: Studies In Nephrotic Syndromementioning

confidence: 99%

Effects of Water Immersion on Atrial Natriuretic Peptide Release in Humans

Epstein

Norsk²,

Loutzenhiser³

1989

Am J Nephrol

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“…These hormonal findings are more compatible with volume expansion or a hyporeninemic hypoaldosterone state rather than hy povolemia. In this regard, expanded plasma volumes have been reported in nephrotic patients [2]. In some studies, however, such volume expansion has been asso ciated with a diminution in renal function [1], It is also unclear whether no correction [2], correction for dry weight [3] or wet weight [4] is the most appropriate way to express plasma volume measurements in patients with nephrotic syndrome as compared to normal subjects.…”

Section: Introductionmentioning

confidence: 99%

Role of Aldosterone in the Sodium Retention of Patients with Nephrotic Syndrome

et al. 1990

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The role of aldosterone in the abnormal sodium retention in patients with nephrotic syndrome has been debated. In fact, studies using a converting enzyme inhibitor to lower plasma aldosterone have rejected such a role. We therefore studied 5 nephrotic patients and 6 control subjects by using the more specific aldosterone antagonist, spironolactone. After withdrawal of diuretics 5 days prior to the study, the nephrotic patients and control subjects were placed on a high-sodium diet (285 ± 6 mEq/day) for 8 days. After 4 days, spironolactone 200 mg p.o., b.i.d., was given for the remaining 4 days. Plasma renin activity and plasma aldosterone levels were similar in both nephrotic patients and control subjects before the study, after sodium loading and after spironolactone had been given. After 4 days of high sodium intake control subjects were in sodium balance, but the nephrotic patients were in a positive sodium balance (approx. 80 mEq/day; p < 0.01). On days 3 and 4 of spironolactone, the nephrotic patients exhibited an increase in urinary sodium excretion (205 ± 20 vs. 312 ± 13 mEq/day; p < 0.005) but not the control subjects (279 ± 16 vs. 286 ± 13 mEq/day; NS). It is therefore concluded that aldosterone is a significant contributor to the sodium retention in patients with nephrotic syndrome.

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“…In a number of reports we have put emphasis on the fact that in patients with the nephrotic syndrome (NS) the blood volume is normal and that 'hypovolemia' is found only occasionally [1][2][3]. This situation raises two prob lems.…”

Section: Introductionmentioning

confidence: 99%

“…Various studies, recently reviewed [2], have brought evidence that the sodium retention in the NS is indeed due to the primary renal disease rather than to intravascu lar hypovolemia. For example, in rats with unilateral nephrosis the fall in sodium excretion was limited to the diseased kidney [4].…”

Section: Introductionmentioning

confidence: 99%

Lowered Protein Content of Tissue Fluid in Patients with the Nephrotic Syndrome: Observations during Disease and Recovery

Koomans¹,

Kortlandt²,

Geers³

et al. 1985

Nephron

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To find out why most patients with the nephrotic syndrome maintain a normal blood volume despite a reduced plasma colloid osmotic pressure (COP), we measured the transcapillary (plasma-tissue fluid) COP difference in 12 patients with the nephrotic syndrome, as well as in 6 patients during complete (n = 3) and partial (n = 3) recovery. Subcutaneous nylon wicks were used to collect tissue fluid. The albumin content was also measured. The albumin content and COP were lowered in both plasma and tissue fluid in the nephrotic phase, and rose gradually during recovery. During these changes the transcapillary COP difference only rose slightly: from 6.2 ± 1.7 mm Hg when the plasma COP was below 10 mm Hg (n = 11) to 8.7 ± 1.5 mm Hg when the plasma COP exceeded 20 mm Hg (n = 12). These observations indicate that in hypoproteinemia preservation of the intravascular volume is strongly dependent on maintenance of the difference in oncotic pressure across the capillary wall.

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Blood Volume and Sodium Retention in the Nephrotic Syndrome: A Controversial Pathophysiological Concept

Cited by 60 publications

References 63 publications

Effects of Water Immersion on Atrial Natriuretic Peptide Release in Humans

Effects of Water Immersion on Atrial Natriuretic Peptide Release in Humans

Role of Aldosterone in the Sodium Retention of Patients with Nephrotic Syndrome

Lowered Protein Content of Tissue Fluid in Patients with the Nephrotic Syndrome: Observations during Disease and Recovery

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