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 authors applied a new method for biochemical determination of proteinuria selectivity by means of ceruloplasmin clearance, used as a protein with high molecular weight as well as those of haptoglobulin and albumin -used as proteins with low molecular weight. The investigation was carried out among 94 patiens with different glomerulopathies. The equivalence of both the biochemical methods was confirmed statistically. In 58 of the examined patients, proteinuria selectivity is determined simultaneously and by the JgG clearance and trasferrin-accoringing to the method of Cameron et al. (with immunodiffused plaques) and immunoelectrophoresis and by the clearance of alpha2-macroglobulin and transferrin. Nd. statistically significant and authenical differences were established between the proteinuria selectivity determined by the relationship between the clearances of ceruloplasmin and albumin, of ceruloplasmin and haptoglobulin (biochemically determined) and of Jg G and transferrin (determined with the aid of immunodiffused plaques and immunoelectropphoresis). All that gives ground the authors to consider the results from the biochemical and immunochemical methods rather similar. That fact, the low prime cost and the possibility the biochemical methods to be put into practice in well equipped clinical laboratories emphasize their importance for the everyday nephrologist practice as well.
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PMID:[Proteinuria selectivity in patients with glomerular nephropathy determined by a biochemical route]. 122 22

Lymphocytes from N.S. patients, in culture and stimulated by PHA or Con A, release a lymphokine which increases vascular permeability; this factor is not present in normal subject and in control supernatants. Pharmacological and biological properties of this factor are similar to the guinea pig S.R.F. (PICK, TURK, MAILLARD). Modifications observed with meclofenamate, DTTC and addition of N.H.S. suggest that it could be an activator of the kinin system. Physicochemical studies show that it is a protein migrating as albumin. We have also recently demonstrated (unpublished data) the relationship of this factor with proteinuria: injections of active supernatants in rats renal artery is immediately followed by increase in proteinuria from 0,8 mg/h to 3,5 mg/h. Up to date, lymphokines have been studied in animals but seldom in human. Our results show that in human, variations in lymphokine production may be present. Pathogenic implications are now under study.
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PMID:Lymphokine 'skin reactive factor' (SRF) and the nephrotic syndrome. 123 73

This is a study of the changes, both in serum and urine, of a wide enzymatic pattern whose origin is well known to be the renal parenchyma (LDH, LAP, AP and lysozyme), in the course of two experimental prototype lesions induced in rats. Simultaneously a similar enzymatic study was carried out in a group of patients with nephropathies. The experimental lesions were a toxic tubular dysfunction using a mercury salt and an immune glomerulonephritis of two types: by foreign proteins (human albumin) and by rabbit nephrotoxic serum. In all these cases, there has been a convincing evidence, both direct (histological and inmunofluorescent) and indirect (marked proteinuria), of the induced lesions which were similar to the experimental models reported in the literature. The isolated enzymatic changes we observed in serum made us conceed less value to this pattern in comparison to the urinary one which proved to be more important in our study. It was possible to define the following urinary enzymatic patterns for each of the experimental groups: a) The acute toxic tubular dysfunction has a marked rise in the activity of LDH and LAP, and less so in the activity of AP and lysozyme. The retarded tubular lesion has a moderate rise in LAP. b) The glomerular lesion has a moderate and exclusive rise in the activity of LDH and LAP. Likewise the clear similarity between each experimental group and its clinical equivalent was demonstrated as refers to the urinary enzymatic pattern.
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PMID:[Renal enzymology: experimental patterns and clinical symptoms]. 123 86

Angiotensin-induced proteinuria was examined at the glomerular-tubular level in rats. Ultra-micro-disc electrophoresis was employed to determine albumin concentration of rat proximal tubular fluid samples under control conditions and during the infusion of 0.15 mug/min X 100 g body weight angiotensin II using micropuncture techniques. Under control conditions proximal tubular albumin concentration was 1.32 +/- 0.79 (SD) mg/100 ml (n = 71). There was no correlation between albumin concentration and (TF/P)-inulin ratio indicating an albumin reabsorption in the proximal tubule parallel to fluid reabsorption under control conditions. During angiotensin infusion using re-collection techniques, there is an average increase of 26 times in tubular albumin concentration, indicating an increase in albumin filtered. There was no change in GFR, SNGFR, transit time, (TF/P)-inulin ratio, an increase in urine flow rate, sodium excretion, protein excretion, mean arterial blood pressure during angiotensin infusion. Since effective glomerular filtration pressure was not increased during angiotensin it is concluded that angiotensin-induced proteinuria is due to an increase in filtered protien mediated by a change in glomerular permeability to proteins.
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PMID:Effect of angiotensin on glomerular filtration of albumin. 123 90

Proteinuria was studied experimentally in pigs with renal damage induced by maleic acid, potassium dichromate and by 5/6 nephrectomy. The methods used were: analysis of total protein, immunochemical quantitation of a porcine low molecular weight (alpha-PLMW) protein, agarose gel electrophoresis, and gel chromatography of concentrated urine samples. The urinary clearance of the alpha-PLMW protein in normal pigs was considerably higher than LMW protein clearance in normal man. No increase was seen after surgery. The induction of proximal tubular damage resulted in an increased excretion of, above all, high molecular weight proteins (greater than or equal to albumin) but also of low molecular weight proteins. The highest increase in alpha-PLMW clearance was seen immediately after 5/6 nephrectomy, and the increased alpha-PLMW excretion in pigs with proximal tubular dysfunction was better correlated to creatinine clearance than to the degree of phosphaturia or glucosuria. The results suggest different renal handling of plasma proteins in pigs and humans.
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PMID:Proteinuria in pigs with experimentally induced renal damage. 123 91

Severe plasma deficiencies of clotting factors IX and XII developed in a 59-year-old woman with a nephrotic syndrome secondary to a laminated membranous glomerulopathy. Both these clotting factors were subsequently identified in the patient's urine. Chromatographic analysis of the urine revealed that the bulk of clotting activity attributed to factors IX ann XII was in early eluting gel filtration fractions containing predominately alpha-2 globulin and albumin. The unprecedented finding of two coagulation proteins in the urine is attributed to the marked proteinuria present in this case.
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PMID:Urinary loss of clotting factors due to hereditary membranous glomerulopathy. 125 29

Thirty-four patients with primary generalized amyloidosis (PGA) and 14 with multiple-myeloma-related amyloidosis (MRA) were studied. The commonest clinical manifestations in PGA were nephrotic syndrome, hepatomegaly and congestive heart failure, and in MRA, low back pain, plasmacytoma and rheumatoid-arthritis-like syndrome. Eight patients with PGA had limited clinical expression of the disease, such as involvement of only kidneys, joints, parotid glands or gastrointestinal tract; in one patient amyloidosis was limited to lymph nodes. Low serum concentrations of total protein and albumin were common. M components were detected in the serum of 91% of patients with PGA and 92% of patients with MRA: 70% of the M components in PGA and 25% of those in MRA had lambda light chains. Bence Jones proteinemia was detected in 56% of the patients with PGA and in 77% of those with MRA. The serum concentration of immunoglobulins was decreased substantially in more than two thirds of the patients with PGA. Proteinuria (greater than 250 mg/24 h) was observed in 78% of patients with PGA and in 93% of patients with MRA. Bence Jones proteinuria was noted in 75 and 77% of patients, respectively. Plasmacytic infiltration of the bone marrow was found in 90% of the patients with PGA. The mean survival time of the patients with PGA was 28 months and of those with MRA, 29 months from the time of diagnosis.
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PMID:Clinical and laboratory findings in primary generalized and multiple-myeloma-related amyloidosis. 126 76

To investigate whether perchloroethylene (PCE) can induce renal disturbances and to compare morphological alterations with functional data, two groups of 12 male and female Fischer-344 mature rats were treated daily with PCE (500 mg/kg body wt in corn oil, p.o.) for 4 weeks. Sex- and age-matched control groups received corn oil only. Weekly, the urinary excretion of albumin (Alb), alpha 2 mu-globulin (alpha 2 mu) and retinol-binding protein (RBP) was measured in 24-hr urine samples using immunoassays specific for rat proteins. N-acetylglucosaminidase (NAG) activity was measured by a colorimetric assay. Electrophoretic analysis of proteinuria included SDS-PAGE and isoelectric-focusing of Alb purified from serum and urine. Weekly histopathology comprised light and electron microscopy. In the male rat, a trend toward progressive albuminuria (up to 15 times the pair-fed controls) was observed, together with transient increases in alpha 2 mu and NAG; RBP showed a twofold increase at the end of treatment. Histopathology failed to demonstrate glomerular changes, whereas it displayed alpha 2 mu accumulation and mild lesions in the S2 segment of proximal tubules. Thus, in the male rat, the selective damage to S2 was associated with "glomerular" proteinuria, the alpha 2 mu cortical content being closely correlated with albuminuria (n = 9, r = 0.92, P < 0.001). In the female rat, only minor, although statistically significant (P < 0.05), increases were recorded for Alb, whereas urinary alpha 2 mu reached up to four times the control values. As a whole, these findings suggest that PCE, like other hydrocarbons, selectively affects the tubular segment S2 in the rat. A competition with alpha 2 mu for tubular uptake could explain enhanced albuminuria. Owing to the species specificity of alpha 2 mu, caution should be exercised in extrapolating these findings to man.
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PMID:Rat model of perchloroethylene-induced renal dysfunctions. 128 47

Administration of captopril, a scavenger of oxygen derived radicals as well as an inhibitor of angiotensin converting enzyme, has been an efficient way of treating diabetic proteinuria. In the present study, we evaluate whether captopril can ameliorate diabetic proteinuria as an effect on oxidative stress in streptozotocin- induced diabetic rats (STZR). At four weeks after the injection of streptozotocin (50 mg/kg, i.v.), STZR (n = 5) exhibited microalbuminuria. The rate of urinary albumin excretion was 0.5 +/- 0.1 and 2.6 +/- 0.3 mg/24hr in age-matched control rats (CR; n = 5) and STZR, respectively. Compared to CR, STZR also showed an extremely increased rate of urinary lipid peroxides (LPO) excretion, an index of oxygen derived radicals generation. The respective values for CR and STZR were 0.6 +/- 0.3 and 6.9 +/- 0.6 mumol/24 hr. Significant amelioration of urinary albumin and LPO excretion rate by the treatment of insulin (2 U/day) suggests that these are associated with the diabetic state induced by streptozotocin rather than a direct effect of streptozotocin. Chronic administration of captopril, which did not cause any discernible effect on CR, significantly reduced the urinary albumin excretion rate and decreased LPO excretion in STZR. The urinary albumin excretion rate was significantly correlated with the LPO excretion rate (p = 0.0004). These results suggest that oxidative stress can be responsible for diabetic microalbuminuria, and captopril could diminish the lipid peroxidation and ameliorate the microalbuminuria in diabetic rats.
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PMID:Amelioration of diabetic microalbuminuria and lipid peroxidation by captopril. 129 45

According to international consensus, microalbuminuria is defined as an elevated urinary albumin excretion rate (UAER) of 20-200 micrograms/min, which is below the proteinuric range. Nephropathy is a major complication in IDDM, seen in about 30% of patients after many years of diabetes. Increasing microalbuminuria is an excellent marker of subsequent nephropathy in these patients. End-stage diabetic nephropathy is also important in NIDDM, but in most Western countries this serious complication eventually develops in only 5 to 10% of cases, whereas the majority of patients die before this from cardiovascular disease. In completely healthy individuals there is no clear correlation between age and UAER, at least up to about 70 years of age. The mean excretion rate is around 5 micrograms/min, with a considerable range, but excretion only rarely exceeds 15 micrograms/min. In population studies among middle-aged and elderly individuals, higher values are seen. In newly diagnosed NIDDM about 40% of patients show an excretion rate above 15-20 micrograms/min. There is a significant but not precise correlation between albumin excretion rate and glycemic control, and usually UAER is reduced by standard antidiabetic treatment. In a considerable number of patients, high values cannot be reduced. In the course of NIDDM about 20-30% of patients show microalbuminuria. In patients with known diabetes, microalbuminuria is related not only to subsequent diabetic proteinuria, but even more strongly to early death, mainly from cardiovascular disease. Even slight microalbuminuria (15-40 mg/l in early morning urines) is clearly associated with increased mortality. In subjects with newly detected elevated blood glucose (by screening) microalbuminuria also predicts early mortality. The mechanisms are not established, but several arteriosclerosis-related risk factors are seen more frequently in patients with microalbuminuria, e.g. lipid abnormalities, elevated systolic blood pressure (BP), hemostatic measures, as well other markers of cardiovascular disease. Usually there is a significant but not precise correlation between BP and UAER in groups of patients throughout the course of diabetes. New studies document that also in the elderly background population microalbuminuria is a significant risk factor for early death, maybe even stronger than the established risk markers, which thus may be confounded with the presence of microalbuminuria.
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PMID:Microalbuminuria in non-insulin-dependent diabetes. 129 5


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