The pathophysiology of edema formation in the nephrotic syndrome.
The mechanism of edema formation in the nephrotic syndrome has long been a source of controversy. In this review, through the construct of Starling's forces, we examine the roles of albumin, intravascular volume, and neurohormones on edema formation and highlight the evolving literature on the role of primary sodium absorption in edema formation. We propose that a unifying mechanism of sodium retention is present in the nephrotic syndrome regardless of intravascular volume status and is due to the activation of epithelial sodium channel by serine proteases in the glomerular filtrate of nephrotic patients. Finally, we assert that mechanisms in addition to sodium retention are likely operant in the formation of nephrotic edema.
Division of Hospitalist Medicine, Department of Medicine, Columbia University Medical Center-Allen Hospital, New York, NY 10032, USA. jr55@columbia.edu
Eric C
EC
Siddall
Jai
J
Radhakrishnan
D000818:Animals; D001810:Blood Volume; D002199:Capillary Permeability; D004487:Edema / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D006874:Hydrostatic Pressure; D034141:Hypoalbuminemia / Q000209:etiology / Q000503:physiopathology; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology*; D008954:Models, Biological; D009404:Nephrotic Syndrome / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D018377:Neurotransmitter Agents / Q000378:metabolism; D011507:Proteinuria / Q000209:etiology / Q000503:physiopathology; D012084:Renin-Angiotensin System; D012307:Risk Factors; D012709:Serum Albumin / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D018377:Neurotransmitter Agents; D012709:Serum Albumin; D012964:Sodium