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 effects of a single intravenous injection of 100 mg/kg puromycin aminonucleoside (PAN) on renal protein, electrolyte, and fluid excretion as well as inulin and lithium clearances in rats were investigated under basal conditions, after iso-oncotic blood volume expansion with bovine serum albumin (BSA) and during infusion of atrial natriuretic peptide (ANP). All treated rats developed severe proteinuria 7-28 days after injection. On day 17, the protein excretion of the PAN group was 1,050 +/- (SE) 118 micrograms/(min x kg body weight) compared with 42.3 +/- 3.9 micrograms/(min x kg body weight) in the control group. Hypoproteinemia, edema or ascites were not observed. The renal protein excretion increased dramatically after BSA infusion and even more during ANP infusion in the PAN group. The PAN-treated animals lost about 62% of the infused BSA during the time of the experiment. No significant changes in protein excretion were observed in the controls. Both groups had similar basal excretions of urine volume, sodium, chloride, and potassium and responded to the BSA and PAN infusions with comparable increases in these parameters. The glomerular filtration rate was slightly, but not significantly higher in the PAN group during the control periods. Increases after BSA and ANP occurred in both groups, reaching significance only in the control group. Proximal tubular function was slightly impaired in PAN-treated rats as judged from a lower increase of the fractional excretion of lithium after BSA. Mean arterial blood pressure was higher in the PAN group (136.2 +/- 2.4 vs. 127.0 +/- 2.2 mm Hg) and fell in both groups to a comparable degree after BSA infusion. A further fall in blood pressure occurred after ANP infusion. Plasma ANP immunoreactivity was not different between the groups and increased after BSA infusion. Our data demonstrate that severe glomerular lesion as indicated by proteinuria can be observed after PAN administration without impairment of distal tubular function as judged from sodium and fluid excretion, and therefore support the view that the sodium retention observed in nephrotic syndrome is due to a separate intrarenal defect rather than a consequence of protein loss.
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PMID:Severe proteinuria without impairment of sodium and volume excretion after puromycin aminonucleoside administration in rats. 252 52

In order to investigate the role of polymorphonuclear leukocytes (PMN) in the distribution of antigen in various organs and in the development of nephritis, chronic serum sickness-type nephritis was induced in both anti-rat PMN rabbit serum (APS)-treated and normal rabbit serum (NRS)-treated rats by preimmunization with bovine serum albumin (BSA) and subsequent daily intravenous administration of BSA for 4 weeks. Kinetic studies using radiolabeled BSA showed that accumulation of BSA after the first intravenous administration was reduced by APS treatment in the liver, lungs and spleen and increased in the circulation, but was not affected in the kidneys and glomeruli. Histological studies supported the above findings. After 4 weeks of BSA administration, the BSA accumulation in the kidneys and glomeruli was significantly less in APS-treated rats than in NRS-treated ones, while amounts of BSA in the circulation and other organs were not different between the two groups. Furthermore, APS treatment reduced proteinuria, PMN infiltration and IC deposition in the glomeruli. These observations indicate that PMN play a partial role in IC deposition in the glomerular capillary walls and subsequent destruction of glomerular permeability in chronic serum sickness-type nephritis.
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PMID:The role of polymorphonuclear leukocytes in rat chronic serum sickness-type nephritis. 253 32

Adriamycin (ADR) nephrosis and a model of unilateral ADR-induced proteinuria were produced in Sprague-Dawley (S.D.) rats to investigate the mechanism of sodium retention by the nephrotic kidney. Plasma volume, as measured by the dilution principle using radioiodinated serum albumin, was significantly higher in nephrotic animals than in control ones (NS: 69.61 +/- 15.02: control: 47.05 +/- 5.32 ml/kg: P less than 0.01). Similarly plasma levels of immunoreactive ANP (iANP) were significantly higher in nephrotic animals compared to controls (NS 104.22 +/- 36.41: control 59.94 +/- 20.88 pg/ml; P less than 0.05). Using the unilateral model we found a markedly reduced diuretic and natriuretic response to the infusion of synthetic rat atrial natriuretic peptide (ANP 1-28) in proteinuric kidney but not in contralateral kidney, despite a comparable increase in glomerular filtration rate. To explain the blunted diuresis and natriuresis in the presence of normal glomerular response to ANP, we investigated the possibility of an abnormality at post-glomerular level by studying ANP receptor density and affinity of the inner stripe of outer medulla and the inner medulla in ADR-and vehicle-treated rats. The inner stripe of outer medulla and the inner medulla receptor density and affinity were not significantly different in ADR rats as compared to animals given the vehicle alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blunted excretory response to atrial natriuretic peptide in experimental nephrosis. 255 49

Using a complex stimulating mixture containing ADP, epinephrine and collagen, a significantly (p less than 0.002) enhanced platelet aggregability, expressed as platelet sensitivity factor (PSF) was noted in platelet rich plasma of patients with proteinuria (PSF = 472 +/- 125), as against normal weight normolipidemic control subjects (PSF = 32.76 +/- 2.67). A significantly negative correlation (r. -0.579; p less than 0.001) was found between serum albumin concentration and the logarithmic values of platelet sensitivity factor. Plasma von Willebrand factor activity expressed as a percentage of normal was also significantly (p less than 0.001) higher in proteinuric patients (287% +/- 25.8) than in control subjects (99% +/- 5.02), but this hemostatic variable did not correlate with the logarithm of platelet sensitivity factor. Platelet aggregability was higher in hyperlipidemic nephrotic patients than in proteinuric patients with normal serum lipids, while renal failure led to a decrease of platelet function. The raised plasma levels of von Willebrand factor noted in proteinuric patients were not influenced by either hyperlipidemia or by chronic renal failure. It is concluded that changes affecting platelet function in the nephrotic syndrome are produced by other mechanisms than these leading to an increase of endothelia-derived von Willebrand factor. Both changes may, however, contribute to the thrombotic tendency of nephrotic patients.
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PMID:Plasma von Willebrand factor antigen and activity and platelet aggregability in patients with proteinuria. 261 81

Of 55 patients with adult onset minimal change glomerulopathy (MCG) studied at our center between 1971 and 1986, five (9%) had an association with the use of nonsteroidal antiinflammatory drugs (NSAIDs). All of the patients were female, and their mean age at the time of diagnosis was 57.4 +/- 11 (SD) (range 47 to 71) years. They had received NSAIDs for an average of 6.9 +/- 6.4 (range, 3 to 18) months before developing proteinuria. The presenting 24-hour urine protein was 11.3 +/- 10.2 (range, 2.1 to 24) g and all patients were hypoalbuminemic (serum albumin less than 3.5 g/dL) with edema. Two patients presented with acute renal insufficiency (serum creatinine greater than or equal to 1.3 mg/dL). Histologically, three patients had MCG associated with interstitial nephritis, and two had no evidence of interstitial disease. All five patients achieved a complete remission after discontinuing the NSAIDs. The remission occurred within 15 days for 80% of patients. A mean follow-up of 6.4 +/- 3.9 (range, 1.3 to 10.5) years was obtained on the patients. At the time of last follow-up, all patients had remained in complete remission, and all patients had normal renal function. Our experience confirms that MCG may present with or without interstitial nephritis. Once the NSAID is discontinued, a complete remission can be expected.
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PMID:Minimal change glomerulopathy associated with nonsteroidal antiinflammatory drugs. 259 82

We studied the long-term effect of an angiotensin converting enzyme (ACE) inhibitor, captopril, on the progression of chronic renal failure and on the rate of urinary protein excretion. When compared with standard triple therapy, captopril slowed the progression of renal failure. Captopril was also able to reduce the proteinuria of non-diabetic glomerular origin. This reduction was not dependent on the presence or absence of arterial hypertension but was limited by the presence of low serum albumin levels, and only occurred in patients with proteinuria in excess of 3 g/24 h.
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PMID:Effects of angiotensin converting enzyme inhibitors on the progression of renal failure and proteinuria in humans. 269 57

The effects of injected native and cationized bovine serum albumin (BSA- and BSA+ respectively) were evaluated in rats which subsequently received anti-BSA. Thrombocytopenia, low creatinine clearance (Ccr), increased proteinuria, capillary swelling, mild tuft necrosis and BSA+ deposits in glomeruli resulted within 24 h of BSA+ injection. Later BSA+ produced mesangial expansion glomerular capillary wall (GCW) thickening and deposits of BSA+ accompanied by rabbit anti-BSA and rat anti-BSA which correlated well with small mesangial, subendothelial and subepithelial electron-dense granular accumuli. These latter enlarged considerably after the injection of anti-BSA. BSA- controls showed minimal or no lesions. The disappearance from the blood (t1/2) of a single dose of immune complexes (IC) prepared with chromatography-purified, radioiodinated anti-BSA - BSA- and BSA+ was determined in another group of rats. The t1/2 of BSA- anti-BSA was 42.8 h (95% confidence: 39.8-46.2) while that of BSA+ anti-BSA was 52.5 h (48.1-57.8). These results suggested that serum sickness glomerulitis developed only in rats injected with BSA+, due to in situ IC which presumably grew by accretion of foreign anti-BSA. Circulating IC may have developed and colocated with the latter, with dissociation and recombination at these sites. It is postulated that the functional-immunomorphological changes and the slow removal of cationized IC reported herein could be explained by the highly positive net charge of the injected antigen.
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PMID:Glomerulitis induced by cationized bovine serum albumin in the rat. 270 65

Low-protein diets in nondiabetic renal failure may slow the progressive loss of renal function in some patients, but few studies have detailed the nutritional consequences of these diets in patients with diabetic nephropathy. We studied 7 patients with insulin-dependent diabetes mellitus and chronic renal insufficiency [mean +/- SEM creatinine clearance (S, U): 28.3 +/- 6.5 ml/min (0.47 +/- 0.11 ml/s x 1.73/A)] for 15 weeks who were prescribed a diet of 0.6 g protein/kg ideal body weight. Midarm muscle circumference (24.1 +/- 1.8 at onset vs. 24.5 +/- 1.5 cm at completion), triceps skinfold thickness (21.6 +/- 3.1 vs. 21.0 +/- 1.5 mm), body weight (71.8 +/- 4.1 vs. 71.2 +/- 4.6 kg), and serum albumin [3.0 +/- 0.1 vs. 3.2 +/- 0.1 g/dl (30 +/- 1 vs. 32 +/- 1 g/l)] remained stable. Based on urinary nitrogen excretion, diet diaries overestimated the degree of dietary protein restriction; there was good adherence to the diet as evidenced by a reduction in urinary urea nitrogen (average 32%). Blood glucose control was maintained despite increased carbohydrate intake. On average, creatinine clearance did not change significantly, but proteinuria diminished slightly (1.8 +/- 0.2 vs. 1.5 +/- 0.6 g/day). These results indicate that 0.6 g/kg/day protein diets did not cause protein depletion in insulin-dependent diabetic patients. Longer-term studies are indicated to assess more fully the efficacy of these dietary regimens in reducing proteinuria or benefiting diabetic nephropathy.
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PMID:Protein-restricted diets in diabetic nephropathy. 271 Feb 67

Low-protein diets are being increasingly used as a treatment for early nephropathy associated with diabetes. Recent research studies have shown a decrease in proteinuria while serum albumin levels and weight have been maintained. A level of 0.6 g protein/kg ideal body weight has been suggested. In structuring these diets, fat should be restricted to approximately 30% of calories, with the remainder supplied as carbohydrate calories after the protein content has been calculated. In some persons, simple sugars need to be included to avoid excessive amounts of high-bulk, high-fiber carbohydrate foods. Insulin and oral agent dosages may need adjustment to compensate for increased glucose levels. Self-monitoring of glucose levels can provide valuable feedback for medication adjustment. Intensive dietary education is needed with these patients, as the diet is sometimes radically different from diets previously used. A hypothetical patient is described and diet calculations provided using the ADA Exchange Lists with accompanying menus.
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PMID:Implementation of low-protein diets for treatment of persons with early diabetic nephropathy. 271 93

Lecithin:cholesterol acyltransferase (LCAT) and lysolecithin acyltransferase (LAT) are two activities carried out by the same plasma enzyme, but require different apoprotein activators. The LCAT reaction takes place primarily on high density lipoproteins (HDL) and is activated by serum albumin, whereas LAT takes place on low density lipoproteins (LDL) and is inhibited by albumin. In nephrotic syndrome (NS), the levels of serum albumin are reduced, whereas the LDL levels are increased, and therefore, the ratio of LAT/LCAT activities should be increased. To test this hypothesis, we estimated the lipid levels and the two enzyme activities in experimental NS induced in rats by the injection of anti-Fx1A antibody (passive Heymann nephritis). As found in other nephrotic conditions, the plasma lipid levels rose progressively as the proteinuria increased and the serum albumin concentration declined. In addition, the ratio of LAT/LCAT activities increased by about fourfold after nine days of induction of nephritis. The LCAT activity correlated positively and the LAT activity negatively with serum albumin levels. The esterified cholesterol correlated positively with LCAT activity in normal rats but negatively in nephrotic animals, indicating that most of the cholesteryl esters in NS may be non-LCAT derived. The free cholesterol/lecithin ratio, a known risk factor for atherosclerosis, increased significantly in nephrotic rats. Furthermore, since the increase in the LAT activity produces more disaturated lecithins, another putative risk factor, the cumulative risk of coronary heart disease may be increased in long-term NS.
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PMID:Plasma lipids and acyltransferase activities in experimental nephrotic syndrome. 277 94


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