PATHOGENESIS OF EDEMA FORMATION IN THE NEPHROTIC SYNDROME

The development of edema in the nephrotic syndrome has traditionally b een viewed as an underfill mechanism. According to this view, urinary loss of protein results in hypoalbuminemia and decreased plasma oncoti c pressures a result, plasma water translocates out of the intravascul ar space and results in a decrease in intravascular volume. In respons e to the underfilled circulation, effector mechanisms are then activat ed that signal the kidney to secondarily retain salt and water. While an underfill mechanism may be responsible for edema formation in a min ority of patients, recent clinical and experimental findings would sug gest that edema formation in most nephrotic patients is the result of primary salt retention. Direct measurements of blood and plasma volume or measurement of neurohumoral markers that indirectly reflect effect ive circulatory volume are mostly consistent with either euvolemia or a volume expanded state. The ability to maintain plasma volume in the setting of a decreased plasma oncotic pressure is achieved by alterati ons in transcapillary ex change mechanisms known to occur in the setti ng of hypoalbuminemia that limit excessive capillary fluid filtration. The intrarenal mechanism responsible for primary sodium retention is not yet known, but may involve tubular resistance to the natriuretic e ffect of atrial natriuretic peptide.