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 protein synthesizing capacity of liver parenchymal cells isolated from 3-, 12-, 24-, 31- and 36-month-old rats was determined by the incorporation of 14C-leucine. Conditions for optimum protein synthesis included the use of an enriched medium (modified Waymouth's MB 752/1) and cell suspension concentrations ranging from 0.25 to 4 X 10(6) cells/ml medium. The cells were incubated with a dose of 6 micronmol leucine/ml medium for 2 h at 37 degrees C under an atmosphere of 95% O2 and 5% CO2. With parenchymal cells isolated from 3-month-old rats, a leucine incorporation rate of 14.4 nmol leucine/h/10(6) cells was found. The capacity of the parenchymal cells to synthesize protein decreased between 3 and 12 months, remained constant between 12 and 24 months and increased between 24 and 26 months. Degradation of newly synthesized proteins or reutilization of 14C-leucine did not occur during the incubation period. The ratio between albumin and total protein synthesis as a function of age was determined. This ratio did not change between 3 and 24 months but there was a significant increase between 24 and 36 months. The increase in total protein synthesis in late age may be due to a compensation by the liver for a more pronounced proteinuria, increased proteolysis or an accumulation of "altered" proteins.
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PMID:The effect of age on protein synthesis by isolated liver parenchymal cells. 87 90

To investigate the mechanism(s) of angiotensin II-induced proteinuria, polydisperse [3H]dextran (D) (radius = 18-42 A) was infused into seven Munich-Wistar rats before and during intravenous infusion of angiotensin II (AII), 0.35 microgram/kg per min. During AII infusion, UprotV rose approximately twofold, and the fractional clearances of D [(U/P)D/(U/P)In] increased significantly for dextrans with radii greater than 22 A. Single nephron filtration fraction increased, due to a measured rise in the glomerular transcapillary hydraulic pressure difference from 34 to 43 mmHg. Near constancy of single nephron glomerular filtration rate resulted, however, from the offsetting effect of a decrease in glomerular plasma flow rate from 83 to 60 nl/min. These measured hemodynamic changes were found, by the use of pore theory, to account to a large extent for the measured increases in (U/P)D/(U/P)In. In seven other rats, fractional clearances of polyanionic dex-ran sulfate (a more reliable marker of albumin filtration than D) were also found to increase significantly with AII, suggesting that the proteinuria induced by AII can be explained, in large part, by hemodynamic factors.
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PMID:Mechanism of angiotensin II-induced proteinuria in the rat. 87 19

Sixteen nephrotized rats and eight controls were submitted to a continuous sterol balance for two weeks. During the whole experiment (two months) the rats were pair-fed a balanced sterol-free diet and their proteinuria regularly measured as a parameter of the nephrotic state. Serum cholesterol and albumin were also measured at the end of the experiment. Liver and carcass (excluding intestine and central nervous system) as well as feces were submitted to sterol analysis by gas-liquid chromatography. Sterol losses were corrected for by adding radioactive cholesterol and cholic acid at the beginning of the methodological procedures. The results showed that while fecal sterol excretion was similar in the nephrotic group as compared to controls, a definite increase in serum, carcass, and liver cholesterol was observed in the nephrotic animals, indicating that a real enhancement of synthesis had occurred. The meaning of increased cholesterol hepatic content is discussed, as well as the possible relationship between enhanced protein and cholesterol hepatic synthesis.
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PMID:Origin of hypercholesterolemia in chronic experimental nephrotic syndrome. 89 13

Two patients reacting with transitory, massive proteinuria after diagnostic renal arteriography with a commonly used non-ionic contrast medium, metrizoate, are described. One of them developed temporary renal failure; the concentration of urinary albumin reached 330 g/g creatinine. It is suggested that intratubular precipitation of proteins, obstructing urinary flow, might be one factor in the development of her renal failure.
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PMID:Proteinuria following renal arteriography. Report of two cases. 89 76

In addition to molecular size, at least two other factors influence the transglomerular passage of macromolecules. The hemodynamic determinants of glomerular filtration rate affect macromolecule transport by altering the volume flux through the glomerular capillary wall and the profile of macromolecule concentrations along a glomerular capillary. The electrostatic properties of the glomerular capillary wall markedly restrict the passage of circulating polyanions, relative to neutral macromolecules of similar size. In the normal animal, the combined effects of these various mechanisms ensure that only very small quantities of plasma proteins are filtered. In experimental proteinuric conditions such as nephrotoxic serum nephritis and puromycin-induced nephrosis, reduction in the fixed negative charges on the glomerular capillary wall appears to be largely responsible for the increased transglomerular passage of anionic macromolecules such as albumin. Other evidence suggests that hemodynamic factors may contribute to proteinuria under certain circumstance. The possibility of an increase in number and/or radius of glomerular "pores" being responsible for proteinuria, perhaps the most intuitively obvious and widely held view, has yet to receive direct experimental support.
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PMID:Determinants of the transglomerular passage of macromolecules. 91 20

Rats were injected with various amounts of bovine albumin (0.5, 1.0 and 1.75 g/24h), inducing thereby proteinuria ranging from 100 to 400 mg/24h. The glomerular oxygen uptake, dry weight and glucose-6-phosphate dehydrogenase (G-6-PHD) activity were measured on the 4th day of proteinuria and in a group of control animals. Oxygen uptake increased of +60%, expressed per glomerulus and of +25% when expressed per milligram dry weight and this increase was not different between the 3 groups of rats. Glomerular dry weight increased significantly in the 3 series. There was an highly significant relationship between glomerular dry weight and oxygen uptake, combining the 3 series together. G-6-PDH increased as expected from previous experiments and this increase was more marked for the more marked proteinuria. The relationship between G-6-PDH and QO2 was of borderline statistical significance (p=0.05). The glomerular hypertrophy, oxidative hyperactivity and increase in G-6-PDH activity are probably related to transcellular transport of protein.
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PMID:Glomerular metabolism in protein-load proteinuria. 91 75

Mental retardation in combination with proteinuria and a slight hyperlipoproteinemia was found in three brothers. The increased urinary protein excretion was dominated by albumin and the low molecular weight proteins retinol-binding protein (RBP) and beta2-microglobulin, indicating the presence of proximal tubular dysfunction. However, there was no glucosuria, phosphaturia or amino aciduria and the renal concentrating and acidification capacities were normal. A kidney biopsy in one of the patients revealed morphologic evidence of glomerular damage but a normal tubular structure. A mild hyper-beta-lipoproteinemia was found in the patients but not in their healthy siblings. The cause of this syndrome, hitherto not described, is unknown.
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PMID:Low molecular weight proteinuria and slight hyperlipoproteinemia in three mentally retarded brothers. 93 5

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

No differences were found at the 30th week of pregnancy in total body water, serum sodium, potassium, chloride and osmolality, plasma volume, total protein concentration, intravascular protein mass, serum albumin concentration, intravascular albumin mass, and urinary estriol and pregnanediol in 94 primigravidae who remained normotensive, 35 who developed mild preeclampsia, and 23 who developed severe preeclampsia (i.e. hypertension and significant proteinuria in the third trimester). In twin pregnancies no differences were found between 13 primigravidae who remained normotensive and nine who subsequently developed proteinuria and hypertension.
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PMID:Changes preceding the development of preeclamptic toxemia. 95 65

The rate of progression of nephropathy was studied in 6 young male diabetics with intermittent proteinuria (Albustix) and in 10 young male diabetics with constant proteinuria by measuring glomerular filtration rate (GFR), renal plasma flow (RPF), and urinary albumin excretion by exact techniques. Albumin excretion was elevated in both the recumbent and the erect position in patients with intermittent proteinuria. GFR and RPF were at the same level as in diabetics without proteinuria, and no deterioration in renal function was noted during a mean control period of 32 months. In the patients with constant proteinuria the fall rate during a mean period of 33.6 months for GFR and RPF was 0.91 ml/min/month +/- 0.68 (S.D.) and 4.38 ml/min/month +/- 3.23 (S.D.) respectively. Initial fall rate in GFR correlated well with long-term fall rate, both of which were studied in 7 patients. In the same patients there was a positive correlation between the fall rate in GFR and diastolic blood pressure as well as albumin clearance. In 8 patients with constant proteinuria and mean blood pressure of 159/101 mmHg, antihypertensive treatment was started with propranolol alone or combined with hydralazine and furosemide. During a treatment period of 47 days blood pressure was reduced to 143/93 mmHg, and in the same period urinary albumin excretion was reduced significantly from a mean value of 3547 mug/min to 2414 mug/min (P less than 0.01). Further control studies will clarify whether end-stage of renal insufficiency will be postponed by antihypertensive treatment.
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PMID:Progression of nephropathy in long-term diabetics with proteinuria and effect of initial anti-hypertensive treatment. 95 56


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