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)

Although the protein leak of early diabetic nephropathy is said to be purely a glomerular lesion, there is still controversy as to the existence of a tubular component. We have, therefore, assessed the urine of insulin-dependent diabetics for tubular proteinuria as a feature of early diabetic nephropathy. The urine of 25 patients with increased albumin excretion rate was analyzed by sodium dodecyl polyacrylamide gel electrophoresis. One patient showed high molecular weight proteinuria, 2 showed low molecular weight proteinuria and 2 patients showed both low and high molecular weight proteinuria. The urine was also analyzed for 3 tubular proteins by single radial immunodiffusion. No patient showed elevated beta-2-microglobulin, but alpha-1-microglobulin (A1M) (corrected for creatinine excretion) was elevated in 3 out of 25 patients including 2 of the 4 patients with a low molecular weight pattern. One of the patients with raised A1M also had raised retinol-binding protein concentration. We conclude that, in early diabetic nephropathy, proteinuria can have a proximal tubular, as well as a glomerular, component.
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PMID:Low molecular weight proteinuria in insulin-dependent diabetes. 374 42

Daily blood and 24-hour urine samples from 6 runners were studied for 2 days before and for 5 days after a 42.2 km. marathon footrace run in cool environmental conditions. Although the race caused muscle damage as shown by the increased post-race serum creatine kinase activity and C-reactive protein levels, renal function measured by urine flow rates, creatinine clearance and protein excretion was normal during the race. Sodium and fractional sodium excretion decreased during the race despite a maintained osmolar clearance, and remained low for the next 48 hours, whereas osmolar clearance decreased sharply for the remainder of the race day but it was significantly elevated on days 2 to 4 after the race. Creatinine clearance was increased significantly 24 hours after the race, and reached its peak 3 days after the race, while urine flow rates were elevated from days 2 to 5 after the race. Urea excretion was significantly decreased 3 to 5 days after the race, while creatinine excretion was increased significantly on day 3 after the race. Glomerular proteinuria occurred 24 hours after the race with no associated reduction in tubular reabsorption of the low molecular weight protein beta-2-microglobulin. This study shows previously unrecognized substantial delayed effects of prolonged exercise on renal function. The nature of these changes may reflect catabolic followed by anabolic processes in muscle as well as changes consequent on excess sodium retention and related fluid compartment shifts.
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PMID:The immediate and delayed effects of marathon running on renal function. 377 85

The effect of prolonged restoration of near-normoglycemia on the progression of diabetic nephropathy was evaluated in a controlled study in which 10 insulin-dependent (type 1) diabetic patients with clinical proteinuria were randomized to continue with conventional insulin treatment (CIT) or to undertake more intensive diabetic therapy using continuous subcutaneous insulin infusion (CSII). The patients, mean age 33 +/- 8 yr, mean duration of diabetes 15 +/- 4 yr, were studied before and during 12 months of either CIT or CSII therapy. Glycemic control was assessed by means of mean blood glucose (MBG) +/- Standard deviation (SD), urinary glucose excretion and glycosylated hemoglobin, while renal function was assessed by albumin, IgG and beta-2-microglobulin urinary excretion rates, serum creatinine and creatinine clearance. Blood glucose level, urinary glucose excretion and glycosylated hemoglobin fell significantly in the CSII group, while no differences were found in the CIT group after the 12 months observation period. Both groups showed a deterioration in all indices of renal function, as illustrated by an increase of protein excretion rates and of serum creatinine, and by a decline in creatinine clearance. Comparison of the rate of increase of urinary albumin and IgG excretion and of serum creatinine and of the rate of fall in creatinine clearance between CIT and CSII groups demonstrated that the rate of progression of diabetic nephropathy may be slowed by correction of hyperglycemia. Our study, with due reservations because of the small number of examined patients and differences in kidney function at the beginning of the trial shows that intensive diabetic care may play a role in the proteinuric stage of diabetes in slowing further destruction of residual glomerular structure and in delaying end stage renal failure.
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PMID:Effect of long-term near-normoglycemia on the progression of diabetic nephropathy. 388 4

Although the kidney is the critical organ limiting occupational exposure to soluble uranium compounds, there have been no adequate studies evaluating renal tubular dysfunction in chronically exposed workers. The present investigation evaluated kidney function among 39 uranium mill workers and 36 local cement plant workers of equivalent age, sex, and race. The uranium workers showed a significantly higher excretion of beta-2-microglobulin and five amino acids than the reference group. Although the levels of tubular proteinuria were mild, a dose-effect relation existed between the clearance of beta-2-microglobulin, relative to that of creatinine, and the length of time that the uranium workers had spent in the yellowcake drying and packaging area, the work area with the highest exposures to soluble uranium. Age did not account for this relationship. Glomerular function was significantly better among the uranium workers than among the referents, though this may have been the result of differences in the physical activity of the groups during the collection period. The data presented suggest reduced renal proximal tubular reabsorbtion of amino acids and of low molecular weight proteins, consistent with uranium nephrotoxicity.
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PMID:Renal toxicity in uranium mill workers. 389 Jan 63

Immune complexes in serum, urinary excretion of albumin and beta-2-microglobulin were determined in patients with infectious mononucleosis, both during the acute stage of the disease and one month later. At the first examination immune complexes were detected in 8 out of 12 patients, using both the ClqBA and the PP-Lc methods, but had disappeared in all after one month. Urinary excretion was initially increased for albumin in one of 9 and for beta-2-microglobulin in 5 of 9 patients. A significant fall in excretion was noted for beta-2-microglobulin during the acute phase (0.486 to 0.190 ng/min (medians), p less than 0.01) whereas albumin excretion did not change significantly (9.0 to 4.0 micrograms/min). Excretions were normal in all patients after one month. The magnitude of proteinuria was not correlated to the serum level of immune complexes. Serum beta-2-microglobulin was initially increased in 8 of 9 patients, but normal after one month (3.8 to 2.2 mg/l, p less than 0.01). There was a significant correlation between levels of beta-2-microglobulin in serum and urine (rho = 0.833, n = 9, p less than 0.01). 51Cr-EDTA clearance was the same during the acute illness and one month later. It is concluded that the abnormalities in urinary protein excretion do not seem to be related to the presence of circulating immune complexes in infectious mononucleosis and that the elevated urinary beta-2-microglobulin excretion is most likely due to increase production.
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PMID:Urinary excretion of albumin and beta-2-microglobulin, glomerular filtration rate and immune complexes in serum during infectious mononucleosis. 618 60

The pattern of proteinuria found in patients during the administration of methotrexate (MTX) or aminoglycosides (AG) and in cadmium or Balkan nephropathy was investigated using the technique of sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE). As renal tubular dysfunction increased, measured by the urinary concentration of 4 low molecular mass (LMr) proteins, SDS-PAGE bands appeared in the following order of molecular mass (Mr): 59, 44, 31, then below 31 000. The presence of bands less than 31 000 was not an early indicator of drug-induced renal damage. Tubular proteinuria could be monitored more easily by the serum and urinary measurement of any one of the LMr proteins: alpha-1-microglobulin (alpha 1m), retinol-binding protein (RBP), beta-2-microglobulin (beta 2m), except alpha-1-acid glycoprotein (AGP), than by SDS-PAGE.
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PMID:Comparison of tubular proteinuria, using sodium dodecyl sulphate polyacrylamide gel electrophoresis, in patients during methotrexate or aminoglycoside treatment or with cadmium or Balkan nephropathy. 646 14

Circulating immune complexes (CIC) were detected in 8 of 15 patients with fever due to non-renal infections. Elevated urinary albuMin and beta-2-microglobulin excretion rates were found during the febrile period compared to the levels two days after normalization of the temperature. No relationship could be demonstrated between CIC and the excretion rates of albumin and beta-2-microglobulin or the albumin/beta-2-microglobulin ratio. Thus we have not been able to confirm the hypothesis that the glomerular type of proteinuria is caused by immune complexes.
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PMID:Patterns of proteinuria and circulating immune complexes in febrile patients. 675 48

To evaluate the effect of improved metabolic control on kidney function, urinary excretion rate of beta-2-microglobulin, lysozyme, and gamma-glutamyltransferase were evaluated in nine poorly controlled, newly diagnosed diabetic patients before and during treatment. In six poorly controlled insulin-dependent nephropathic diabetic patients, besides the parameters cited above, urinary albumin excretion rate and IgG/transferrin clearance ratio were further investigated to estimate the permeability and the selectivity of glomerular barrier during conventional treatment and after improvement of the metabolic control by a glucose-controlled insulin infusion system (GCIIS). The improved glycemic control resulted in a significant reduction of urinary beta-2-microglobulin and lysozyme excretion in all diabetic patients. Significant decreases of urinary albumin excretion and of IgG/transferrin clearance ratio (indicating a more selective proteinuria) during strict metabolic control were also observed in nephropathic diabetic patients. The reduction of urinary beta-2-microglobulin and lysozyme excretion indicates that a tubular reabsorptive dysfunction, reversible with the amelioration of glycemic control, can be observed in poorly controlled, newly diagnosed and in insulin-dependent nephropathic diabetic patients during conventional treatment. In the latter patients, the permeability and the selectivity properties of glomerular barrier also improved during GCIIS.
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PMID:Kidney function after improved metabolic control in newly diagnosed diabetes and in diabetic patients with nephropathy. 692 32

The pattern of urinary protein excretion was followed for 2 to 19 months in 15 children with the congenital nephrotic syndrome of the Finnish type. The duration of the disease and the renal histopathological changes were correlated with the urinary total protein and albumin excretion, the sieving coefficients of five proteins, the selectivity angle based on relative clearances of four proteins, and the excretion of beta-2-microglobulin. Total urinary protein excretion increased with time; in general, the proteinuria was of glomerular type and highly selective. With advancing histological lesions selectivity declined corresponding to the increases in individual sieving coefficients, and there were signs of secondary tubular impairment as shown by increased beta-2-microglobulin excretion. Of the histopathological changes, tubular atrophy correlated best with the various measures of proteinuria. The findings support the concept of a primary glomerular disease with secondary tubular injury.
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PMID:Proteinuria in congenital nephrotic syndrome of the Finnish type. 698 18

Forty-five patients with uncomplicated rheumatoid arthritis and 45 control individuals were subjected to immunochemical investigation of the urinary excretion of renal tubular basement membrane antigen (TBM), renal tubular epithelial antigen (RTE), and beta-2-microglobulin. Tubular proteinuria occurred significantly more frequently in patients treated with gold salts than in those not treated (P less than 0.05). Large amounts of RTE and TBM were detected only in the urine of patients who received gold salt therapy. However, the amounts of these proteins in urine did no correlate with the total dose of gold. These results indicate that renal tubular damage frequently occurs in patients with rheumatoid arthritis who are treated with gold salts; the tests outlined are useful in detecting renal tubular disorders developing during gold salt therapy and have certain advantages over routine urinalysis.
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PMID:Renal tubular dysfunction as a complication of gold therapy in patients with rheumatoid arthritis. 703 44


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