1967
DOI: 10.1159/000179587
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Methemoglobin-Induced Acute Renal Failure in the Rat

Abstract: Oliguric acute renal failure was induced in dehydrated rats by an intravenous injection of human methemoglobin. Oliguria was associated with a markedly reduced pressure in the proximal tubules and efferent glomerular vessels. Neither intratubular obstruction nor massive backdffusion of filtrate were considered to play a decisive role in the establishment of anuria. Tubular compressing interstitial edema was not histologically evident. The major factor leading to anuria was thought to be a reduction of glomerul… Show more

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Cited by 74 publications
(15 citation statements)
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“…In order to account for the nearly complete cessation of glomerular fil tration occurring in acute renal failure [17][18][19][20] in the presence of relatively intact RBF, the components of ultrafiltration pressure must be considered. Hemodynamically, changes in intrarenal arteriolar tone could affect single nephron glomerular filtration rate by altering glomerular capillary pressure [21], Considering this factor alone, a significant increase in afferent arteriolar resistance with attendant decrease in resistance of the efferent arteriole would be required to sufficiently reduce glomerular capillary pressure, so that net ultrafiltration pressure could fall close to zero in lhe presence of normal glomerular blood flow.…”
Section: Discussionmentioning
confidence: 99%
“…In order to account for the nearly complete cessation of glomerular fil tration occurring in acute renal failure [17][18][19][20] in the presence of relatively intact RBF, the components of ultrafiltration pressure must be considered. Hemodynamically, changes in intrarenal arteriolar tone could affect single nephron glomerular filtration rate by altering glomerular capillary pressure [21], Considering this factor alone, a significant increase in afferent arteriolar resistance with attendant decrease in resistance of the efferent arteriole would be required to sufficiently reduce glomerular capillary pressure, so that net ultrafiltration pressure could fall close to zero in lhe presence of normal glomerular blood flow.…”
Section: Discussionmentioning
confidence: 99%
“…The precise pathogenetic role of intratubular protein casts frequently found in distal tubules remains to be establish ed. Several lines o f evidence support the view that protein casts are not likely to be of primary pathogenetic importance for the developement of pigment nephropathy, since they do not in fluence intratubular pressure [21][22][23][24], Conver sely, other investigators [25][26][27][28] could demon strate elevations of tubular pressure. Thirdly, once stored intracellularly, hemoglobin seems to act cytotoxically via Fc-promotcd oxygenderived free radical generation [29][30][31][32].…”
Section: Introductionmentioning
confidence: 99%
“…[2][3][4][5] Phenazopyridine associated acute renal failure and AIN are rare but recognizable phenomena with phenazopyridine use in patients with renal dysfunction. 6,7 Few case reports have highlighted renal failure due to phenazopyridine overdose in patients with normal renal function [3][4][5][8][9][10][11][12][13][14][15][16][17][18] (Table 1). Various mechanisms have been postulated for phenazopyridine causing acute renal failure.…”
Section: Discussionmentioning
confidence: 99%
“…In rat models, phenazopyridine-induced methemoglobinemia has shown to cause interstitial edema, cast formation, tubular degeneration and regeneration. 1,3,9 Its overdose also causes dehydration, as a result of nausea and vomiting, leading to acute renal failure. 19 We hereby report biopsy proven case of AIN, solely related to phenazopyridine, without any evidence of methemoglobinemia or hemolytic anemia.…”
Section: Discussionmentioning
confidence: 99%