Effect of indomethacin on glomerular permeability in the nephrotic syndrome

Tiggeler, R.G.W.L.; Hulme, B.; Wijdeveld, Paul G. A. B.

doi:10.1038/ki.1979.133

Cited by 56 publications

(20 citation statements)

References 79 publications

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“…In this respect, it is noteworthy that Arisz et al [11] demon strated an increase in the selectivity o f the remaining pro teinuria after indomethacin administration. Tiggeleret al [12] confirmed this observation by using polyvinylpyrrol idone molecules. It is also worth mentioning that during intrarenal infusion o f renin or angiotensin II in rats the permeability of the glomerular basement membrane for macromolecules, including polyvinylpyrrolidone, in creased.…”

Section: Discussionmentioning

confidence: 81%

Antiproteinuric Effect of Naproxen and Indomethacin

Vriesendorp¹,

Donker²,

Zeeuw

et al. 1985

Am J Nephrol

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In a double-blind crossover study in 10 salt-depleted nephrotic patients the reduction of proteinuria was significantly larger during indomethacin 50 mg three times daily than during naproxen 250 or 500 mg three times daily (72 vs. 44%, p < 0.05; 77 vs. 46%, p < 0.05, respectively). Both drugs induced similar reversible intrarenal hemodynamic changes, but indomethacin had more pronounced effects than naproxen. A common pathway, such as the reduction of the glomerular filtration rate and a reduction of the glomerular transcapillary hydraulic pressure, is likely to explain the observed phenomena and is most probably mediated by inhibition of intrarenal prostaglandin synthesis. If treatment with a nonsteroidal anti-inflammatory drug is considered in patients with the idiopathic nephrotic syndrome, indomethacin appears up to now the most effective agent in reducing urinary protein loss.

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Section: Discussionmentioning

confidence: 81%

Antiproteinuric Effect of Naproxen and Indomethacin

Vriesendorp¹,

Donker²,

Zeeuw

et al. 1985

Am J Nephrol

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“…Glomerular transport theory predicts that electrical interaction between polycations and a negatively charged membrane (albeit less negatively charged than normal) should result in facilitated and not in restricted transport (13,44). This paradox may be reconciled by the observation that cations bind preferentially to proximal tubule brush border (45,46 (48) have described an acute reduction in filtra-tion of large PVP and protein molecules in nephrotic patients receiving indomethacin. They have proposed that the respectively enhanced and depressed production of prostaglandins anticipated during the foregoing maneuvers may in some way modify the size-selective properties of the glomerular capillaries (48).…”

Section: Discussionmentioning

confidence: 99%

“…This paradox may be reconciled by the observation that cations bind preferentially to proximal tubule brush border (45,46 (48) have described an acute reduction in filtra-tion of large PVP and protein molecules in nephrotic patients receiving indomethacin. They have proposed that the respectively enhanced and depressed production of prostaglandins anticipated during the foregoing maneuvers may in some way modify the size-selective properties of the glomerular capillaries (48). Similarly, infusion of the polycation hexadimethrine into a rat was found by Hunsicker et al (40) to result in a transient but massive increase in urinary excretion of proteins, prominent among which was IgG.…”

Section: Discussionmentioning

confidence: 99%

“…The selective proteinuria typical of this disorder appears to be a consequence of a loss of glomerular polyanion. Conversely, as judged by nonselective proteinuria and selectively enhanced transport of very large dextran and PVP molecules, focal defects (or large pores) in the size-selective barrier appear to typify many nonminimal glomerulopathies of man, including diabetic nephropathy (28,35,41,48). We propose that either charge depletion alone, or charge depletion in combination with defects in the size-selective properties of the glomerular capillary wall, represent nonspecific responses to a variety of glomerular injuries, including that induced by glomerulonephritis.…”

Section: Discussionmentioning

confidence: 99%

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Mechanisms of proteinuria in human glomerulonephritis.

Myers¹,

Okarma²,

Friedman³

et al. 1982

J. Clin. Invest.

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A B S T R A C T We evaluated glomerular barrier function in 28 patients with glomerulonephritis. Neutral dextrans of graded size were used to characterize the size-selective properties of the barrier. Charge selectivity was characterized by electrofocusing excreted urinary proteins. A fractional IgG clearance (relative to freely permeable inulin), smaller or greater than 100 X lo-was used to distinguish patients with minor (group I, n = 13) and major (group II, n = 15) urinary IgG leakage, respectively. Fractional clearances of smaller dextrans (radii 20-50 A) were similar, but those of larger dextrans (radii 52-60 A) were elevated in group II relative to group I patients. A model of solute transport through a bimodal pore size distribution revealed the values for pore radius in the lower mode to approximate 51-55 A in both group I and group II patients. Pore radius in the upper mode, by contrast, was much larger in group II than in group I patients, approximating 87-97 vs. 72-77 A, respectively. Electrofocusing of urinary protein from group I patients revealed mostly albumin (isoelectric point 5.2). In group II patients, however, immunoglobulin excretion was copious. Moreover, the distribution of anionic, neutral, and cationic species (isoelectric points 5.5-8.5) in urinary and plasma eluates of IgG2 and IgG4 was similar. We conclude that when glomerulonephritis is associated with selective albuminuria, as in group I, there is an isolated reduction of electrostatic retardation of relatively small anionic proteins. Major urinary IgG leakage (group II), however, appears to result from the development in the glomerular membrane of a subpopulation of enlarged pores that are highly permeable towards proteins of large size and varying charge.

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“…In contrast, indomethacin administration to patients with the nephrotic syndrome results in a parallel decline in absolute urinary protein excretion and GFR (4,5).…”

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confidence: 99%

The Effect of Captopril on Urinary Protein Excretion in Puromycin Aminonucleoside Nephrosis in Rats

et al. 1985

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ABSTIL4ff. We investigated the effect of captopril, an orally active angiotensin converting enzyme inhibitor, on urinary protein excretion in puromycin aminonucleoside nephrotic rats. The administration of captopril(10 mg/100 g body weight) decreased proteinuria on days 10-14 following the administration of puromycin aminonucleoside (73.0 versus 125.0 rng, p c 0.01), without affecting glomerular filtration rate. The beneficial effect of captopril was not abolished by the continuous intravenous infusion of angiotensin I1 (10 pg/kg/h for 9 days) or subcutaneous injections of aprotinin (50,000 KIU/day for 3 days). Indomethacin, in moderate (5 mg/kg/day for 3 days) or high (10 mg/ kg/day) doses, abolished the captopril attenuation in urinary protein excretion. The salutory effect of captopril was characteized by a reduction in the fractional excretion of protein without compromising the glomerular filtration rate. No difference in renal ultrastructure was noted in captopril-treated versus control animals. Captopril was ineffective in reducing urinary protein excretion in rats with adriamycin-induced glomerulopathy. W e conclude that captopril acts to reduce proteinuria in renal disease states arising from depletion of the glomerular basement membrane polyanion. The mechanism of action is postulated to be an alteration in renal hemodynamics, namely increased blood flow and a decrease in the ultrafiltration coefficient, that are the consequence of increased intrarenal prostaglandin production. (Pediatr Res 19: 828-834, 1985) Abbreviations AI, angiotensin I AII, angiotensin I1 ACE, angiotensin converting enzyme BW, body weight FEpr, fractional excretion of protein G B M , glomeruiar basement membrane GFR, glomerular filtration rate ka ultrafiltration coefficient PAN, puromycin aminonucleoside Q A , renal blood flow Many vasoactive substances are capable of altering quantitative urinary protein excretion in normal and disease states.The

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Effect of indomethacin on glomerular permeability in the nephrotic syndrome

Cited by 56 publications

References 79 publications

Antiproteinuric Effect of Naproxen and Indomethacin

Antiproteinuric Effect of Naproxen and Indomethacin

Mechanisms of proteinuria in human glomerulonephritis.

The Effect of Captopril on Urinary Protein Excretion in Puromycin Aminonucleoside Nephrosis in Rats

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