Central role of vasopressin in sodium/water retention in hypo- and hypervolemic nephrotic patients: a unifying hypothesis.
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.
Sala
Carla
C
Institute of Cardiovascular Medicine, University of Milan and Interuniversitary Center for Clinical Physiology and Hypertension, Maggiore IRCCS Hospital, Milan, Italy. carla.sala@unimi.it
Bedogna
Valeria
V
Gammaro
Linda
L
Valvo
Enrico
E
Del Bo
Alberto
A
Morganti
Alberto
A
D001810:Blood Volume / Q000502:physiology*; D006801:Humans; D020896:Hypovolemia / Q000150:complications* / Q000503:physiopathology; D008954:Models, Biological; D009404:Nephrotic Syndrome / Q000150:complications* / Q000503:physiopathology; D014664:Vasodilation / Q000502:physiology; D014667:Vasopressins / Q000502:physiology*; D014883:Water-Electrolyte Imbalance / Q000209:etiology* / Q000503:physiopathology
D014667:Vasopressins