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  • Title: Renal sodium retention in the nephrotic syndrome.
    Author: Firth JD, Ledingham JG.
    Journal: Aust N Z J Med; 1991 Dec; 21(6):893-901. PubMed ID: 1818554.
    Abstract:
    Where do the experiments on rat kidneys exposed to puromycin leave us in attempting to evaluate further the pathophysiology of oedema in human nephrotic syndrome? They cannot be considered conclusive. The arguments favouring an intrinsic abnormality in the kidney as a major factor in sodium retention, rather than this being a secondary response to humoral and neural influences stimulated by changes in actual or perceived plasma volume, would be strengthened by experiments using another animal model of the nephrotic syndrome. But taken together with the longstanding clinical observations demonstrating the absence of any correlation between plasma oncotic pressure and diuresis or sodium retention, the work particularly of Dorhout-Mees and his colleagues on plasma volume, the frequent failure of infusions of salt-free albumin to induce natriuresis, and the profound resistance to intensive diuretic therapy in many nephrotics, the evidence for an important, probably predominant, role of intrinsic renal retention of sodium is strong. This is not to negate the importance of Starling forces in determining the distribution of the retained salt and water, nor to suggest that, on occasion at least, hypovolaemia, relative or absolute, may contribute to sodium retention. Certainly hypotensive shock due to hypovolemia in nephrotic patients untreated by diuretics has been observed often enough, particularly in children, and the risk of over-enthusiastic diuretic treatment resulting in tubular necrosis in the course of management of minimal change disease, is well recognised. An important role for leakage of plasma from the vascular compartment in the initiation of the oedema of the nephrotic state is certainly likely, but to consider this the major continuing mechanism is really not tenable.(ABSTRACT TRUNCATED AT 250 WORDS)
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