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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A large number of carboximides have been synthesized, tested and, in some cases, marketed as agricultural fungicidal agents. One carboximide fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) proved to be both highly efficacious as a fungicide and a nephrotoxin. The purpose of this study was to compare the acute nephrotoxic potential of three N-(3,5-dichlorophenyl)carboximide fungicides [NDPS, vinclozolin (VCLZ) and iprodione (IPDO)] to determine if nephrotoxic potential correlated with fungicidal efficacy among this class of structurally-related agricultural agents. Male Fischer 344 rats (4 rats/group) received a single intraperitoneal injection of a fungicide (0.4 or 1.0 mmol/kg) or vehicle (sesame oil, 2.5 ml/kg), and renal function was monitored at 24 and 48 h. NDPS (0.4 or 1.0 mmol/kg)-induced renal effects were characterized by marked diuresis, increased proteinuria, elevated blood urea nitrogen (BUN) concentration and kidney weights, decreased organic ion accumulation by renal cortical slices and proximal tubular necrosis. In contrast, IPDO and VCLZ (0.4 or 1.0 mmol/kg) administration resulted in only minor or no alterations in the renal function parameters studied and renal morphology. These results suggest that fungicidal efficacy does not correlate with acute nephrotoxic potential among the N-(3,5-dichlorophenyl)carboximide fungicides.
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PMID:Comparative acute renal effects of three N-(3,5-dichlorophenyl)carboximide fungicides: N-(3,5-dichlorophenyl)succinimide, vinclozolin and iprodione. 273 5

Severity and duration of renal injury produced by low levels of uranyl fluoride (UO2F2) were examined in the rat. Rats received multiple ip injections of UO2F2 (cumulative dose: 0.66 or 1.32 mg U/kg body wt). Renal injury was characterized histologically by cellular and tubular necrosis of pars recta of proximal tubule (S2 and S3), with less severe cellular injury to thick ascending limb of loop of Henle and collecting tubule. Injury was evident when renal uranium levels were between 0.7 and 1.4 micrograms U/g wet kidney and was most severe when renal uranium burden was between 3.4 and 5.6 micrograms U/g. Repair of injury was rapid, with complete restoration within 35 days after exposure. Associated with injury were abnormalities in renal function, including impaired tubular reabsorption, proteinuria, and enzymuria, which appeared temporally related, to variable degrees, to progression of renal injury. Thus, reversible renal injury occurs in the rat at levels of uranium in kidney below the present Nuclear Regulatory Commission standard of 3 micrograms U/g kidney for renal injury in humans.
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PMID:Reversible uranyl fluoride nephrotoxicity in the Long Evans rat. 276 62

N-(3,5-Dichlorophenyl)succinimide (NDPS) induces nephrotoxicity via one or more metabolites which arise from oxidation of the succinimide ring. The purpose of this study was to examine the nephrotoxic potential of N-(3,5-dichlorophenyl)-3-hydroxysuccinamic acid (3-NDHSA), a potential metabolite of NDPS and a positional isomer of N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (2-NDHSA), a known nephrotoxic metabolite of NDPS. Male Fischer 344 rats were administered a single intraperitoneal injection of 3-NDHSA (0.2 or 0.4 mmol/kg) or sesame oil (2.5 mmol/kg), and renal function was monitored at 24 and 48 h. Both doses of 3-NDHSA induced diuresis, increased proteinuria, glucosuria and hematuria, elevated blood urea nitrogen (BUN) concentrations and kidney weights, decreased organic ion accumulation by renal cortical slices, and induced proximal tubular necrosis. The characteristics of 3-NDHSA-induced nephrotoxicity were identical to NDPS-induced nephropathy, but were evident at lower doses with 3-NDHSA. These results demonstrate that 3-NDHSA is a nephrotoxicant which might contribute to NDPS-induced nephropathy.
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PMID:Acute nephrotoxicity induced by N-(3,5-dichlorophenyl)-3-hydroxysuccinamic acid in Fischer 344 rats. 278 90

Acute renal failure was diagnosed by clinical, necropsy and histological criteria in 39 flocks (20 low ground, 13 hill and six marginal upland) in areas served by six veterinary investigation centres. Forty-eight lambs of 12 different breeds or crosses were investigated. The mean age of affected lambs was 38 days (range seven to 84 days); 21 lambs (44 per cent) were aged seven to 28 days, while only eight (17 per cent) were older than two months. Mortality in clinically affected lambs was almost 100 per cent, with no response to various treatments. Histological examination showed that 40 lambs (83 per cent) had nephrosis, while the rest had toxic tubular necrosis, interstitial nephritis or tubular damage associated with oxalate crystal deposits. Only about half of the lambs had any evidence of enteric infections or enteropathy. Acutely ill lambs had azotaemia, haemoconcentration and proteinuria; some lambs had glycosuria or haematuria. Samples of plasma from 22 lambs with nephrosis were compared with similar samples from 82 incontact but asymptomatic lambs. The clinically affected group had significantly elevated plasma urea, creatinine, total protein, globulin, phosphorus and chloride concentrations and significantly reduced plasma calcium concentrations compared with healthy lambs. Affected lambs had a significant reduction also in the calcium:phosphorus ratio. No significant differences between groups was found in plasma concentrations of albumin, glucose, lactate, glycerol, creatine kinase, alkaline phosphatase, sodium, potassium or magnesium.
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PMID:Acute nephropathy in young lambs. 291 11

This review has demonstrated that there is a considerable amount of information in the medical literature concerning hydrocarbon-associated kidney effects. The existing data lends itself to a variety of divergent interpretations. Ravnskov has stated that "glomerulonephritis should be recognized legally as an occupational disease," yet there is no mention of hydrocarbon exposure in the differential diagnosis of glomerulonephritis in two standard American textbooks of internal medicine. Two recently published textbooks of occupational medicine state without reservation that "studies have linked hydrocarbon exposure to glomerulonephritis" and base this conclusion on the previously cited studies of Beirne and Brennan, Zimmerman, and Ravnskov. Based on this review, the following conclusions have been reasonably substantiated: 1. Massive exposure to petroleum distillates on rare occasions may cause acute renal failure due to tubular necrosis. This appears to be a reversible lesion which, depending on the level of exposure, the medical care and support available, and pre-existing renal function, may be without chronic sequelae. 2. Case reports linking Goodpasture's syndrome and other types of glomerulonephritis to hydrocarbon exposure are based on circumstantial evidence and cannot be used to establish a causal association. 3. The evidence from the eight case-control studies of hydrocarbon exposure and glomerulonephritis is inconclusive. Six of the eight published case-control studies show a positive association between hydrocarbon exposure and glomerulonephritis, but four of the six studies have methodologic flaws that could explain the observed effect. The findings in the one positive study that is methodologically acceptable were not replicated in a subsequent study utilizing a similar design. 4. Studies of hydrocarbon-exposed occupational cohorts have generally revealed a lower than expected risk of death from renal causes. As with most historical cohorts, the specific exposures, intensities and durations of exposure have been poorly defined. Effects of mortality that may occur among highly exposed subsets of these occupational cohorts may be diluted by a relatively large proportion of workers with minimal or no exposure to the class of hydrocarbons in question. 5. Studies of renal biochemistry and renal function effects have been uniformly negative in groups of workers from several industries with relatively high exposures of long duration to a variety of hydrocarbon solvents. The statistically significant differences in proteinuria and cell excretion observed in one of the studies should not be confused with clinical significance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A review of the non-neoplastic kidney effects of hydrocarbon exposure in humans. 304 37

Although a variety of renal lesions may occur in acquired immune deficiency syndrome (AIDS), a rare but aggressive form of focal and segmental glomerulosclerosis with capillary collapse has been considered a possible component of this disorder. It is manifested by heavy proteinuria and progression to renal failure in a short time. We studied renal biopsies from nine patients with HIV infection and the above clinical features and compared the renal tissues to biopsies from HIV-positive individuals with immune complex glomerulonephritis and to biopsies from patients with heroin abuse nephropathy. The HIV-associated nephropathy was characterized by a combination of lesions: focal and segmental glomerulosclerosis, often in an early stage of evolution and with prominent degenerative changes of visceral epithelium; tubular necrosis without identifiable nephrotoxic or hemodynamic etiology; interstitial edema; large plasma protein-containing tubular casts in all segments of the nephron associated with marked tubular dilatation; and widespread tubuloreticular structures in vascular endothelium. In contrast, neither the sclerosing glomerular changes nor the tubulointerstitial abnormalities were present in HIV-infected patients with immune complex glomerulonephritis. Similarly, the tubular and interstitial changes and widespread tubuloreticular structures were absent in heroin-abuse nephropathy. The lesions of HIV-associated nephropathy occurred in patients with AIDS, AIDS-related complex, and in individuals clinically asymptomatic for HIV infection. Their morphological features in asymptomatic patients are sufficiently specific to allow for accurate diagnosis of HIV infection.
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PMID:HIV-associated nephropathy. A unique combined glomerular, tubular, and interstitial lesion. 307 May 50

Electrolyte and renal hemodynamic imbalance, acute interstitial nephritis with nephrotic-range proteinuria, papillary necrosis, tubular necrosis, and vasculitis are complications after intake of nonsteroidal anti-inflammatory drugs (NSAID). We report on 2 cases of biopsy-proven granulomatous interstitial nephritis with rapidly progressing renal insufficiency. Patient 1 was on ketoprofen for 7 months and indomethacin for 10 weeks before admission to hospital. The medication was not discontinued and renal insufficiency progressed to end-stage renal failure. Renal function did not respond to steroid and tuberculostatic treatment. Patient 2 was on diclofenac for 6 months and indomethacin for 7 weeks before admission to hospital. These drugs were withdrawn at diagnosis and renal function rapidly improved. We conclude that granulomatous interstitial nephritis may be a complication of NSAID medication indicating a cell-mediated immunologic disorder. False diagnosis (sarcoidosis, tuberculosis) may lead to end-stage renal disease (case 1). Discontinuation of medication obviates further therapy (case 2).
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PMID:Granulomatous interstitial nephritis after nonsteroidal anti-inflammatory drugs. 307 Nov 48

A single large dose of butylated hydroxytoluene (BHT, 1000 mg/kg) in male Fischer 344 rats produced some renal damage, reduced accumulation of p-aminohippuric acid in renal slices, proteinuria and enzymuria, in addition to hepatic damage. Further, prior administration of phenobarbital (80 mg/kg, i.p., daily for 4 days) in the high-dose BHT-treated male rats produced renal damage accompanied by slight tubular necrosis. The renal damage was confirmed by biochemical and histological changes. These changes were dose dependent, with a maximum at 24 h after BHT administration, but had returned to the normal range by 48 h. Female rats, on the other hand, were less susceptible to BHT-induced renal and hepatic damage than male rats. The results indicate sex differences in BHT-induced renal or hepatic damage.
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PMID:Nephrotoxicity of butylated hydroxytoluene in phenobarbital-pretreated male rats. 339 47

Previous studies have demonstrated that N-(3,5-dichlorophenyl)succinimide (NDCPS) is the most nephrotoxic compound among the N-(mono- or dichlorophenyl)succinimides. The purpose of this study was to examine the nephrotoxic potential of the different N-(3,5-dihalophenyl)succinimides (NDHPS) to determine the importance of the halogen species for NDHPS-induced nephrotoxicity. Male Fischer 344 rats were administered a single intraperitoneal injection of an NDHPS (0.4, 0.8, or 1.0 mmol/kg) or vehicle (2.5 ml/kg), and renal function was monitored at 24 and 48 h. NDCPS or N-(3,5-diiodophenyl)succinimide administration produced the greatest nephrotoxic response. Nephrotoxicity was characterized by diuresis, increased proteinuria, glucosuria, increased kidney weight and blood urea nitrogen (BUN) concentration, decreased accumulation of p-aminohippurate (PAH) and tetraethylammonium (TEA) by renal cortical slices and proximal tubular necrosis. N-(3,5-Dibromophenyl)succinimide injection produced mild nephrotoxicity, while N-(3,5,-difluorophenyl)succinimide administration did not result in nephrotoxicity. These results indicate that the halogen species can influence the nephrotoxicity produced by the NDHPS. In addition, nephrotoxic potential did not correlate with fungicidal efficacy, which suggests that the nephrotoxic and fungicidal mechanisms of these compounds might be different.
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PMID:Nephrotoxicity of N-(3,5-dihalophenyl)succinimides in Fischer 344 rats. 356 Feb 57

N-(3,5-Dichlorophenyl)succinimide (NDPS), an experimental agricultural fungicide, has been shown to be a selective nephrotoxin in Sprague-Dawley and Fischer 344 rats. Previous studies have demonstrated that a toxic metabolite contributes to or is responsible for acute NDPS-induced nephrotoxicity. The purpose of this study was to investigate the role of glutathione in NDPS-induced renal effects. In 1 set of experiments, male Sprague-Dawley or Fischer 344 rats received a single intraperitoneal (i.p.) injection of NDPS (0.4 or 1.0 mmol/kg) or sesame oil (2.5 ml/kg). Rats were killed at 1, 3, 6 or 24 h, and reduced (GSH) and oxidized (GSSG) glutathione concentrations determined in liver and renal cortex. In both rat strains NDPS (0.4 or 1.0 mmol/kg) administration produced small decreases in GSH concentrations (1 and 3 h) but moderate increases in GSSG concentrations (1 and 3 h) in liver and kidney. At 24 h both GSH and GSSG concentrations were increased, particularly in kidney. In a second set of experiments, rats were pretreated with the glutathione depletor diethyl maleate (DEM) (0.4 ml/kg, i.p.) 1 h prior to NDPS (0.2, 0.4 or 1.0 mmol/kg, i.p.) or sesame oil (2.5 ml/kg, i.p.) administration, and renal function monitored at 24 and 48 h. DEM pretreatment attenuated the increase in urine volume (24 and 48 h), proteinuria, glucosuria, hematuria and elevated blood urea nitrogen (BUN) concentration produced by NDPS (0.4 or 1.0 mmol/kg) in both Sprague-Dawley and Fischer 344 rats. NDPS-induced increases in kidney weight also were generally prevented by DEM pretreatment. Proximal tubular necrosis produced by NDPS administration was reduced by DEM but not prevented. Pretreatment with the cysteine conjugate beta-lyase inhibitor amino-oxyacetic acid (0.5 mmol/kg, i.p.) 1 h prior to NDPS (0.4 or 1.0 mmol/kg) markedly attenuated all NDPS-induced effects on renal function and morphology. These results suggest that glutathione does not play a protective role against NDPS-induced renal effects and that a glutathione or cysteine conjugate of NDPS might contribute to NDPS-induced nephrotoxicity.
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PMID:Role of glutathione in acute N-(3,5-dichlorophenyl) succinimide-induced nephrotoxicity in Sprague-Dawley and Fischer 344 rats. 360 74


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