The underfill and overflow hypotheses are usually held as mutually exclusive mechanisms for explaining sodium/water retention in nephrotic syndrome, but neither of them is entirely convincing. In this paper, we will briefly summarize the experimental and clinical evidence in favor of and against each hypothesis. Based on our personal observations, we propose a unifying hypothesis in which underfill and overflow are subsequent stages of the disease. In the transition, a central role is played by vasopressin, which is secreted in the two phases, respectively, by a volume and an osmotic stimulus; therefore, persistent sodium/water retention is maintained through the vascular and tubular effects of this peptide. In addition, we propose that vasodilation and sodium/water excretion could ensue when both stimuli for vasopressin release fade away, leading to the resolution of the syndrome.

Central role of vasopressin in sodium/water retention in hypo-and hypervolemic nephrotic patients: a unifying hypotesis / C. Sala, V. Bedogna, L. Gammaro, E. Valvo, A. Del Bo, A. Morganti. - In: JN. JOURNAL OF NEPHROLOGY. - ISSN 1121-8428. - 17:5(2004), pp. 653-657.

Central role of vasopressin in sodium/water retention in hypo-and hypervolemic nephrotic patients: a unifying hypotesis

C. Sala
Primo
;
A. Del Bo
Ultimo
;
A. Morganti
2004

Abstract

The underfill and overflow hypotheses are usually held as mutually exclusive mechanisms for explaining sodium/water retention in nephrotic syndrome, but neither of them is entirely convincing. In this paper, we will briefly summarize the experimental and clinical evidence in favor of and against each hypothesis. Based on our personal observations, we propose a unifying hypothesis in which underfill and overflow are subsequent stages of the disease. In the transition, a central role is played by vasopressin, which is secreted in the two phases, respectively, by a volume and an osmotic stimulus; therefore, persistent sodium/water retention is maintained through the vascular and tubular effects of this peptide. In addition, we propose that vasodilation and sodium/water excretion could ensue when both stimuli for vasopressin release fade away, leading to the resolution of the syndrome.
Atrial natriuretic peptide; Intravascular volume; Nephrotic syndrome; Renin-angiotensin system; Sodium/water retention; Systemic vasoconstriction; Vasopressin
Settore MED/09 - Medicina Interna
2004
Article (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/27878
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