Edema formation in the majority of patients with the nephrotic syndrome can best be explained by an overfill mechanism. This is particularly true for those patients with diabetic nephropathy. The maintenance of a normal plasma volume in the setting of hypoalbuminemia is the result of a series of edema preventing factors that act both to oppose fluid filtration across the capillary wall and to return fluid back into the vascular tree. The single most important variable in determining whether these factors are sufficient to prevent edema formation is the degree of renal salt retention. The variability in renal salt retention explains the poor correlation between the presence or absence of edema and the serum albumin concentration. The precise derangement in renal salt excretion has not been precisely localized but appears to reside in the distal nephron. The exact mechanism underlying this defect is unknown.
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