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)

The role of polymorphonuclear leucocytes (PMN) in the autologous phase of nephrotoxic nephritis (NTN) in the rabbit has been investigated. Depletion of circulating PMN by nitrogen mustard protected renal function and immunofluorescent examination showed reduction in glomerular fibrin deposition. Depletion of circulating PMN using a highly specific goat anti-PMN serum (APS) provided similar protection of renal function, highly significant reduction in proteinuria and histological and immunofluorescent examination showed reduced glomerular PMN infiltration, extracapillary cell proliferation and virtual absence of fibrin deposition. Although protection by nitrogen mustard may have been partly due to immunosuppression, no reduction in antibody response was detected in the APS-treated rabbits. The results implicate the polymorph as the principal injurious agent in this model of NTN, responsible directly or indirectly for both proteinuria and glomerular fibrin deposition.
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PMID:The role of polymorphonuclear leucocytes in the autologous phase of nephrotoxic nephritis. 76 16

The unilateral kidneys of rabbits were frozen in situ for 3 min at --160 C with liquid nitrogen. After freezing, proteinuria was observed in a few rabbits. Passive hemagglutination and Ouchterlony double diffucion tests confirmed the presence of circulation antibodies against renal extracts in the serum. Immunofluorescent studies showed deposits of IgG along the renal glomerulus and in the mesangium. However, light microscopy results showed no change in renal glomerulus and electron microscopy results showed no depositions in the glomerular basement membrane. During 5 months after freezing of the kidney, glomerulonephritis has not occurred clinically and pathologically.
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PMID:Cryoimmunologic investigations of the rabbit kidney. 84

Seventy-five patients with congenital nephrotic syndrome of Finnish type were identified in Finland in the period 1965-1973, giving an incidence of 12-2/10(5). A large placenta and proteinuria from birth are the hallmarks of the disease. About one-quarter of the patients had oedema and/or abdominal distension at birth and in all cases the full nephrotic syndrome was documented before 2 months. More than half of the patients died before 6 months and none lived longer than 2 years 3 months. A slight rise in blood urea nitrogen or serum creatinine levels occurred in 14 cases, but in none of these did a frank uraemia develop before death. Infection appeared to be the immediate cause of death in 31% of the cases; in 43% no cause of death other than congenital nephrotic syndrome could be shown. Thrombi in large vessels were found in 11 out of 58 necropsies.
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PMID:Congenital nephrotic syndrome of Finnish type. Study of 75 patients. 93 78

The present studies were designed to characterize the extent and pathogenesis of the glomerular lesions which occur in the viable portion of the kidney following partial renal infarction in rats. Control rats with two normal kidneys had a mean blood pressure of 112 mm Hg, minimal proteinuria and no glomerular pathology on light (LM), electron (EM) or immunofluorescence microscopy (IFM). Rats with two-thirds infarction of one kidney (stage II) became hypertensive, although less than 4% of the glomeruli from either kidney were abnormal. Rats with two-thirds infarction of one kidney and contralateral nephrectomy (stage III) developed proteinuria and hypertension whether fed a normal, low or high Na+ diet. By light microscopy 37% of glomeruli were abnormal 28 days after partial infarction and contralateral nephrectomy and thereafter the percent of abnormal glomeruli increased. Detectable amounts of immunoglobulin and complement (C3) were present in kidneys of stage II or III rats but were always accompanied by more extensive albumin and fibrin deposits. Basement membrane deposits characteristic of immune complexes were not seen on EM. Administration of antihypertensive medication to stage III rats significantly lowered blood pressure and reduced the number of abnormal glomeruli on LM; however, IFM abnormalities remained prominent. Platelet thrombi seen by EM and abundant glomerular fibrin deposits seen on IFM suggested that coagulation mechanisms may be prominent in the pathogenesis of the renal lesion. Heparin-treated stage III rats had significantly lower blood urea nitrogen concentrations, blood pressures and proportion of abnormal glomeruli although glomerular deposition of serum proteins was still present on IFM. These observations suggest that this glomerulopathy is initiated by an unknown agent(s) which increased capillary permeability. This lesion progresses via thrombotic mechanisms which are prevented by heparin administration.
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PMID:Pathogenesis of the glomerulopathy associated with renal infarction in rats. 94 Feb 76

TO STUDY THE POSSIBILITY THAT CEPHALOSPORINS AUGMENT THE NEPHROTOXICITY OF GENTAMICIN, GROUPS OF RATS WERE GIVEN FOUR HOURLY SUBCUTANEOUS DOSES OF: gentamicin (5 mg/kg), gentamicin plus cephalothin (100 mg/kg), gentamicin plus cefazolin (20 mg/kg), gentamicin plus cefazolin (50 mg/kg), gentamicin plus cephaloridine (50 mg/kg), or saline diluent for 15 days. Periodic measurements were made of urine volume, urine osmolality, urine protein excretion and lysosomal enzymuria, as well as blood urea nitrogen, creatinine clearance, and drug concentrations in renal cortex and medulla. Tissue was examined by light and electron microscopy. Enzymuria and proteinuria increased early in the course of all treatment groups, whereas urine osmolality declined. No distinct patterns of these variables were discernable among the groups. Gentamicin alone, gentamicin plus cephalothin, and gentamicin plus cefazolin (20 mg/kg) caused the same significant fall in glomerular filtrate rate from control values by day 15 (P < 0.05). Gentamicin plus cefazolin (50 mg/kg) and gentamicin plus cephaloridine failed to cause a decline in glomerular filtration rate compared with controls (P > 0.05). Gentamicin concentrations in renal cortex were 5 to 10 times higher than those in medulla in all groups. Cephaloridine and cefazolin (50 mg/kg) also displayed a gradient pattern in renal cortex, whereas cephalothin and cefazolin (20 mg/kg) did not. Cytosegrosomes with myeloid figures were characteristic ultra-structural changes seen in all groups; however, they tended to be smaller with less numerous myeloid bodies in the groups receiving gentamicin plus cephalothin, cefazolin (50 mg/kg), or cephaloridine. Cephalosporins did not augment gentamicin toxicity. High doses of cefazolin and cephaloridine protected kidneys from gentamicin nephrotoxicity. The protection may involve intracellular drug interaction within the renal cortex.
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PMID:Nephrotoxicity of cephalosporin-gentamicin combinations in rats. 94 79

In guinea-pig nephrotoxic nephritis induced by a sheep antibody there was minimal glomerular capillary deposition of C3 and accumulation of polymorphonuclear leucocytes (PMN) in the heterologous phase. The C4-deficient strain developed the same injury as normal Duncan-Hartley animals. Complement depletion with cobra venom factor, polymorph depletion with nitrogen mustard or anti-PMN serum and treatment with antihistamines provided no protection. The relationship between the dose of nephrotoxic antibody and the proteinuria was similar for gamma1 and gamma2 subclasses and the F(ab')2 fragment of gamma1 antibody. However, the F(ab') and F(ab) antibody fragments, though fixing on the glomerular basement membrane, did not cause proteinuria. It is concluded that the development of proteinuria in this system: is largely independent of the complement-polymorph system; is due to the fixation of the F(ab')2 fragment of the antibody molecule; and does not depend on an intact Fc piece.
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PMID:Guinea-pig nephrotoxic nephritis. I. The role of complement and polymorphonuclear leucocytes and the effect of antibody subclass and fragments in the heterologous phase. 110 14

To assess their potential value as early indicators of gentamicin-induced kidney damage, lysosomal hydrolases were measured in the 24-h urines of rats receiving 30 or 60 mg of gentamicin per kg per day for 15 days. Proteinuria, urine osmolality, blood urea nitrogen, and creatinine clearance were also measured. Kidney tissue was examined by both light and electron microscopy. Beta-galactosidase, beta-n-acetyl-hexosaminidase, and alpha-fucosidase were sensitive indicators and were significantly elevated above control values by day 3 at both doses (P < 0.01). Proteinuria, urine osmolality, and tests reflecting glomerular filtration rate were later indicators of nephron damage. Changes by light microscopy were detected on day 5. Necrosis was most prominent in the proximal convoluted tubules on day 10. Electron microscopy revealed numerous cytosomes with myeloid bodies within the proximal tubular epithelium on day 5. Lysosomal enzymuria appears to be an early manifestation of gentamicin nephrotoxicity and may possibly be related to the lysosomal abnormalities seen on electron microscopy.
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PMID:Enzymuria in gentamicin-induced kidney damage. 113 89

Twenty-two young cows died or were euthanatized after intoxication associated with ingestion of redroot pigweed (Amaranthus retroflexus) growing in marginal grass pasture. After several days of weakness and posterior incoordination, the cattle became recumbent but remained alert. Pertinent clinical laboratory findings included increased blood urea nitrogen content and marked proteinuria. At necropsy, perirenal edema and toxic tubular neprosis were seen.
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PMID:Perirenal edema and toxic nephrosis in cattle, associated with ingestion of pigweed. 118 28

The influence of diet and feed restriction on kidney function was studied in aging male albino rats. Rats were fed either a commercial feed (LB) or a modified human diet (MHD) from weaning until sacrifice at either 12 or 24 mo. of age. Restricted rats were fed for only 15 out of each 48 hours. Feed restriction during either the first, the second, or both years of life was beneficial in delaying age-associated changes in kidney function as indicated by decreased proteinuria, increased in vitro transport of paraaminohippuric acid, and reduced incidence and severity of renal lesions. Urinary creatinine and blood urea nitrogen levels were also favorably influenced by restriction. Most parameters were modified by diet as well as by restriction, with MHD being generally associated with improved kidney function. Improvement in kidney function may have been more related to a reduction in protein intake than to a reduction in caloric intake as a whole.
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PMID:Influence of diet and feed restriction on kidney function of aging male rats. 127 Jul 59

The perioperative and long-term risks for living kidney donors are of concern. We have studied donors at the University of Minnesota 20 years or more (mean 23.7) after donation by comparing renal function, blood pressure, and proteinuria in donors with siblings. In 57 donors (mean age 61 [SE 1]), mean serum creatinine is 1.1 (0.01) mg/dl, blood urea nitrogen 17 (0.5) mg/dl, creatinine clearance 82 (2) ml/min, and blood pressure 134 (2)/80 (1) mm Hg. 32% of the donors are taking antihypertensive drugs and 23% have proteinuria. The 65 siblings (mean age 58 [1.3]) do not significantly differ from the donors in any of these variables: 1.1 (0.03) mg/dl, 17 (1.2) mg/dl, 89 (3.3) ml/min, and 130 (3)/80 (1.5) mm Hg, respectively. 44% of the siblings are taking antihypertensives and 22% have proteinuria. To assess perioperative mortality, we surveyed all members of the American Society of Transplant Surgeons about donor mortality at their institutions. We documented 17 perioperative deaths in the USA and Canada after living donation, and estimate mortality to be 0.03%. We conclude that perioperative mortality in the USA and Canada after living-donor nephrectomy is low. In long-term follow-up of our living donors, we found no evidence of progressive renal deterioration or other serious disorders.
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PMID:20 years or more of follow-up of living kidney donors. 136 68


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