125Iothalamate and 131I-hippuran clearances, sodium excretion and plasma renin activity (PRA) before and during indomethacin administration in an oral dose of 3 × 50 mg/day were studied in volunteers with a normal or reduced kidney function, as well on non-sodium-restricted as on sodium-restricted diet. Indomethacin induced a temporary sodium and water retention and a decrease in glomerular filtration rate. It also lowered PRA. The latter phenomenon did not depend on sodium retention and was present within 2 h after an oral dose of 50 mg. The results may be explained by indomethacin-induced inhibition of prostaglandin synthesis.
In 19 nephrotic patients on a dietary intake of 20 mEq sodium/24 hours, indomethacin caused an immediate decrease in glomerular filtration isate (GFR) and urinary protein excretion, an effect completely reversible upon withdrawal of the drug. As a consequence of lower protein excretion, there was eventually a rise in GFR. It is proposed that the therapeutic effect of indomethacin in nephrotic syndrome is caused by its inhibiting action on renal prostaglandin synthesis, thereby potentiating the effect of the renin-angiotensin system on the kidney. The difference between the decrease in GFR (mean 35%) and proteinuria (mean 55%) and the more selective proteinuria during indomethacin administration may be explained by quantitative and qualitative differences in protein leakage between outer cortical and inner cortical nephron populations.In patients with nephrotic syndrome, indomethacin may cause a reduction of urinary protein excretion (4, 11, 12, 13). Recently we have shown (15) that the glomerular filtration rate (GFR) decreases during administration of this drug to volunteers with a normal or reduced kidney function without proteinuria. The sodium and water retention and the larger decrease in GFR on a sodium-restricted diet support the hypothesis that these effects of indomethacin are the result of a potentiation of the renin-angiotensin system by the inhibitive action of indomethacin on prostaglandin synthesis ( I , 8, 9). These results in the non-proteinuric state raised the possibility that the decrease in proteinuria, which accompanies indomethacin administration in nephrotic syndrome, is caused by diminished glomerular filtration. This was tested in 19 patients with a nephrotic syndrome. It was observed that indomethacin induces a rapid decrease in proteinuria, invariably associated with an initial fall in GFR. Both effects were enhanced by a sodiumrestricted diet and immediately reversible when the drug was discontinued.We suggest that indornethacin influences protein excretion by changing intrarenal hemodynarnics.
PATIENTS AND METHODSNineteen patients with proteinuria of 5.0 g or more ( Fig. I ) and serum albumen concentrations of 3.0 g/lOO ml or less were studied. Eleven of them were males and eight females, with a mean age of 30 years (range 14-56).
SummaryPreliminary report of the results obtained with an indirect immunofluorescent technique applied to the study of renal biopsy specimens.Depositions of IgG, IgA, IgM, complement, fibrinogen and albumin were investigated in glomeruli of children with diffuse nephropathies and in adult controls. The localization of the protein precipitates was confirmed by comparing the immunofluorescent picture with the results of the P.A.S.M./ H.E. staining of the same sections.
A short episode of diffuse intravascular coagulation caused a range of severe kidney alterations in rabbits which did not die immediately with renal cortical necrosis. Histology resembled that of chronic pyelonephritis. The rabbits exhibited a steep but completely reversible rise in blood creatinine level, and ultimately no abnormalities of the urine. Blood pressure remained normal. It is supposed that comparable situations may arise in human pathology.
This case report describes a patient with malignant hypertension and phaeochromocytoma in whom blockade of angiotensin II receptors by the competitive antagonist 1‐sar‐8‐ala‐angio‐tensin II (Saralasin®) resulted in a partial correction of the elevated BP. Plasma renin activity was high and rose further during the blockade. Competitive inhibition of angiotensin II by Saralasin does not abolish the pressor effect of catecholamines. It was therefore interesting to observe that in this patient with phaeochromocytoma, independently, both α‐adrenergic receptor blockade and angiotensin II receptor blockade were effective in lowering BP.
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