Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-term follow-up is presented of 73 patients suffering from the haemolytic-uraemic syndrome 10 years after the acute initial illness. The patients were subdivided into three groups, according to the criteria proposed by Gianantonio and based on the duration of oliguria and/or anuria. Four out of 38 patients belonging to the first group (oliguria for less than 7 days) had a slightly increased blood pressure as the only sequela. Two patients out of group two (n = 29, oliguria for 7-14 days or anuria for less than 7 days) had a diminished GFR and a reduced concentrating capacity, some proteinuria, and mild hypertension. Five other patients had slight proteinuria (less than 500 mg/24 h) and one of them a mild hypertension. All six patients belonging to the third group (oliguria for more than 14 days or anuria for more than 7 days) had late sequelae: two started haemodialysis more than 10 years after the initial phase; three have a decreased GFR and concentrating capacity. The unique remaining patient with a normal GFR without hypertension has a decreased concentrating capacity. The importance of careful treatment in children with a decreased GFR 2 years after the initial phase is stressed.
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PMID:Haemolytic-uraemic syndrome: a 10-year follow-up study of 73 patients. 314 Jan 21

Wistar rats (10 and 55 days old) were administered a single dose of 0.6 mg cisplatinum (CP) 100 g body wt. intraperitoneally. Urinary volume, p-aminohippurate and total protein excretion were determined. Separation of urinary proteins was performed by sodium dodecylsulfate polyacrylamide gel electrophoresis. Significant symptoms of nephrotoxicity (oliguria, reduced PAH-excretion, heavy proteinuria, changes in urinary protein composition) were detected in adult rats 72 h after CP. At that time young rats did not show distinct signs of nephrotoxicity. Experiments on time dependence of nephrotoxicity showed that in young rats symptoms occurred already 6 h after CP-administration, and 72 h after CP the damage was nearly completely repaired. Pt-determination in serum, kidney tissue, and urine showed a shorter t1/2 in serum, lower concentrations in kidney tissue as well as higher Pt-concentrations in urine of young compared with adult rats.
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PMID:Nephrotoxicity and pharmacokinetics of cisplatinum in young and adult rats. 324 Mar 9

Growing male rats were fed dietary Pirimiphos-methyl at 0, 500, 1000 and 1500 ppm for 28 days and selected blood and urine constituents were measured at weekly intervals. Dietary intake of Pirimiphos-methyl induced an initial, transient hypoglycemia and a marked elevation in blood urea at all dosages. Though it did not produce any significant change in the urine output initially, marked oliguria was observed after 12 days of feeding. The alterations observed in urine constituents were: increased urea, proteinuria, transient increase in creatinine and significant increase in the excretion of glucuronic acid and ethereal sulfate at all intervals. However, since no pathological alterations were evident in the kidney, the anomalous urinary excretion of various body constituents might be due to the anticholinesterase action of the insecticide at the central nervous system.
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PMID:Toxicity of pirimiphos-methyl: II. Effect of dietary feeding on blood and urine constituents in albino rats. 338 34

On the basis of animal experiments and clinical findings, pyrazolones are found to have adverse renal effects. However, the latter are minor, very rare, and of practically no clinical relevance. In animals, pyrazolones induce proteinuria, oliguria, retention of substances excreted via the urine, and probably, in rare cases, papillary necrosis. Oliguria is rare in humans. A contribution of pyrazolone drugs in a specific case of papillary necrosis and in rare cases of acute interstitial nephritis is not proven, yet possible. Pyrazolone drugs induce renal injury less frequently than do the other classical analgesics.
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PMID:Does pyrazolone-induced renal injury exist? 346 82

TI-31 (TEI-3096; 6-p-chlorobenzyl-5H-2,3,6,7-tetrahydro-5,7-dioxothiazolo[3,2-a]pyr imidine) is a novel immunomodulator. Various nephritic changes observed in female NZB/NZW F1 (B/W) mice with aging were suppressed by TI-31 when administered orally 5 times per week for 16 weeks at doses of 2, 10, or 50 mg/kg. It suppressed proteinuria, oliguria, the decrease of erythrocyte count, and increase of serum urea nitrogen, immune complex and anti-double-stranded DNA antibody levels. The anti-nephritic effect of TI-31 was confirmed by histopathological evaluation. TI-31 (10 mg/kg) could improve both the elevated polyclonal B cell activation and the depressed antibody response to sheep red blood cells in B/W mice, in comparison with age- and sex-matched BALB/c mice, without any effect on the antibody response in these normal mice. These findings indicate that TI-31 may inhibit B/W nephritis by regulating the antibody production through a mechanism different from that of anti-inflammatory drugs or immunosuppressants.
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PMID:Inhibitory effect of TI-31 on autoimmune nephritis in NZB/NZW F1 mice through regulation of the immune response. 349 22

High doses of intravenously and intramuscularly administered oxytetracycline were believed to be responsible for acute renal failure in a dehydrated cow. Signs of renal disease included oliguria, perirenal edema, marked azotemia, moderate proteinuria, tubular casts in urinary sediment, and inability to concentrate urine. Concurrent intravenous administration of fluids and diuretics (mannitol and furosemide) resulted in reestablishment of normal urine production. Because of its nephrotoxic potential, oxytetracycline should be used cautiously and at recommended dosages in ruminants that have prerenal azotemia or otherwise reduced renal function.
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PMID:Acute renal failure associated with administration of excessive amounts of tetracycline in a cow. 369 19

We describe an animal model of generalized sepsis, induced in the sheep by cecal perforation, which reproduces the high systemic flow and peripheral vasodilation seen in early human sepsis. Despite volume loading, animals demonstrate a fall in glomerular filtration rate, oliguria, low fractional sodium excretion, maintained urine osmolarity, and increased plasma renin activity. Histologically, kidneys show no consistent abnormality; overall the findings suggest volume contraction or hypoperfusion. This is contradicted, however, by maintained blood pressure and pulmonary capillary wedge pressure, increased cardiac output, and reduced peripheral resistance. Increased Fc lysozyme and low molecular weight proteinuria suggest tubular damage. These paradoxical observations are currently unexplained.
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PMID:The renal response produced by nonhypotensive sepsis in a large animal model. 374 63

The effects of treatment with either cysteine (2 X 150 mg/kg) or diethylmaleate (0.7 ml/kg) on renal function and response to the nephrotoxicant hexachloro-1,3-butadiene (HCBD) were examined. Cysteine caused oliguria, blocked the polyuric and glucosuric effects of HCBD and attenuated the reduction of urine osmolality. Diethylmaleate (DEM) decreased urine osmolality; further decreases of urine osmolality were not seen after HCBD. DEM pretreatment increased HCBD-induced proteinuria. HCBD-induced elevation of plasma creatinine concentration was not affected by either of the pretreatments whereas the plasma urea nitrogen concentration was greater in the DEM-pretreated group. The latter may represent an effect of DEM on non-filtration handling of urea. The results suggest that cysteine and diethylmaleate each have effects on kidney function which alter the response of the nephron tubule to a subsequently administered toxic agent.
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PMID:Effects of cysteine and diethylmaleate pretreatments on renal function and response to a nephrotoxicant. 374 Nov 49

Sheep were drenched with a single toxic dose of dried and milled Isotropis forrestii in water. Intoxication resulted in early onset of glycosuria, enzymuria and proteinuria. Terminal gross lesions included pale kidneys and perirenal oedema. Histologically and ultrastructurally the renal lesions were typical of primary nephrotoxicosis, with extensive proximal tubular epithelial necrosis. The tubular damage was sufficient to cause acute primary renal failure, characterised by oliguria, azotemia and failure of urinary concentrating mechanisms.
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PMID:The nephrotoxicity of Isotropis forrestii in sheep. 376 96

Nineteen patients with severe renal failure due to multiple myeloma and with Bence Jones proteinuria greater than 1 gm/day were randomly assigned to group I or group II. Corticosteroids and cytotoxic drugs were given to all cases. The 9 patients of group I were also treated by peritoneal dialysis and the 10 patients of group II by plasma exchange and hemodialysis. Only 1 patient of group I, who was not oliguric at the onset, showed partial recovery from renal failure after 3 months of therapy, while 9 patients of group II (3 of whom were oliguric) had significant decrease in Bence Jones proteinuria and rapid improvement from the renal failure. In our experience, plasma exchange is more effective than peritoneal dialysis for reducing Bence Jones proteinuria and recovering from renal failure, even when there is oliguria.
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PMID:Plasma exchange therapy in rapidly progressive renal failure due to multiple myeloma. 405 8


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