The nephrotic syndrome

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        The nephrotic syndrome is characterized by albuminuria, edema, hypoalbuminemia and hypercholesterolemia; frequently, it is accompanied by a depression of the basal metabolic rate. It occurs most often in the course of chronic glomerulonephritis but may exist independently, as in lipoid nephrosis. Rarely, it is associated with secondary syphilis, leptospiral infections, amyloid disease, Kimmelstiel-Wilson syndrome or nephrotoxic poisons.
        The term “nephrosis” was originally applied by Müller to degenerative lesions of the kidney primarily involving the renal tubules. The nephrotic state, however, occurs also with inflammatory diseases of the kidney. Furthermore, the significance of the tubular lesion in the etiology of the syndrome is open to question for it has been quite clearly shown that, in some instances at least, the tubular change may be the result and not the cause of albuminuria. It is obvious that some disturbance of the glomerular filter or in the serum proteins must be predicated to allow for the increased supply of protein presented to the tubules.
        It was originally suggested by Epstein that the low serum albumin in the nephrotic state might result solely from urinary loss of serum proteins and that edema formation could be adequately explained on the basis of the Starling hypothesis of lowered osmotic pressure in hypoalbuminemia. But there is evidence that the Epstein hypothesis does not afford a complete explanation for the formation of edema. Thus diuresis may occur spontaneously without any increase in the low serum albumin levels. Excess protein intake usually does not restore the blood level of albumin even when positive nitrogen balance is established and body protein is stored.
        It is now plain that leakage of albumin through the kidneys does not alone explain the manifestations of the nephrotic state, which evidently involves much more profound metabolic disturbances. Other factors evidently are at work. There is a renal defeet in the handling of the sodium ion by the kidnev. Adrenal cortical hormones conceivably might play a part in water and sodium balance; and the role of the anti-diuretic hormone of the posterior pituitary gland has yet to be properly evaluated. The significance of hypercholcsterolcmia and lowered basal metabolic rate in the nephrotic state is not known, nor is it understood why the alpha globulins apparently are increased and the gamma globulins decreased in the blood.
        Measures directed against the clinical abnormalities present in the nephrotic syndrome include diet high enough in protein to assure nitrogen balance; excessive feeding of protein accomplishes nothing more than restoration of body protein and may actually injure the renal tubules, Sodium intake is kept to less than 0.5 Gm. daily because more tends to promote edema. At this level, water may be taken freely; otherwise it. too, should be restricted. Of the diuretics, urea and mercurials are most often effective, but neither can be relied upon. Efforts to promote diuresis by increasing the osmotic pressure of the circulating plasma have been unsatisfactory. Therapy with hypertonic glucose, acacia, human plasma or serum fall into this category. Salt-tree for human albumin may be highly effective hut has serious limitations. Thyroid extract rarely produces diuresis. In children, intercurrent infections, particularly pneumococcic peritonitis, respond promptly to penicillin. Syphilitic nephrosis also yields rapidly to treatment with penicillin.
        Prognosis depends on the underlying disease. In lipoid nephrosis and chronic glomerulonephritis the duration of the nephrotic state cannot be predicted. In the former, however, the outcome is almost uniformlv good today since formerly fatal infectious complications may now be adequately handled. Patients in the nephrotic phase of chronic glomerulonephritis. however, (and these comprise by far the largest proportion of cases) still face the ultimate fate of patients with the underlying disease.
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