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)

Twenty-eight patients with demonstrated chronic renal vein thrombosis were studied. In seven, only small venous channels were involved; in 21, both small and large veins were thrombosed. A constellation of findings occurred with such frequency in these patients that we believe it virtually diagnostic of renal venous obstruction. These findings include the nephrotic syndrome, great variability in proteinuria and glomerular filtration rate, pulmonary embolization, sterile pyuria, hematuria, hyperchloremic acidosis, decreased renal tubular threshold for glucose and increased fibrin degradation products. These findings are an indication for definitive angiographic and biopsy procedures. Prolonged anticoagulant therapy was generally very effective.
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PMID:Chronic renal vein thrombosis. 90 Jan 43

Reproducibility of reading "N-Multistix" dipsticks by a semi-automated urinalysis instrument (Ames' "Clini-Tek") has been described for artifically prepared samples. Glucose, ketone, urobilinogen, and nitrite showed high reproducibility (greater than 90%) for reading multiple samples at predetermined analyte concentrations. Determination of proteinuria showed the lowest proportion of false positives (2-3%) and false negatives (0%). Determination of hemoglobinuria and bilirubinuria by dipsticks were the least reproducible. Urobilinogen showed no interference from bilirubin in concentrations up to 32 mg/liter. Precision was high for results for quality-control capsules provided by the manufacturer.
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PMID:Evaluation of Ames' "Clini-Tek". 92 73

Administration of D-serine to rats induced acute necrosis of the proximal straight tubules, proteinuria, glucosuria, and aminoaciduria. Proteinuria and glucosuria developed at the onset of tubular necrosis and disappeared when the tubules were completely relined by new epithelium. Our findings suggest (1) that abnormal loss of protein and glucose in urine is due to diffusion of these substances from interstitium to tubular fluid across the denuded permeable basement membranes of the necrotic tubules, and (2) that tubular cells normally are a barrier to diffusion of certain solutes betweeen interstitial and tubular fluids. Amino-aciduria preceded the onset of tubular necrosis and increased excretion of some amino acids persisted after tubular repair. Thus, D-serine-induced aminoaciduria may be due to impaired reabsorption of amino acids by the injured proximal straight tubules, as well as by backward diffusion of amino acids from the interstitium.
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PMID:D-serine nephrotoxicity. The nature of proteinuria, glucosuria, and aminoaciduria in acute tubular necrosis. 120 37

The purpose of these experiments was to determine whether reported changes in substrate metabolism by isolated glomeruli from rats with aminonucleoside nephrosis could be explained by the glomerular changes associated with proteinuria or, alternatively, whether these metabolic changes and proteinuria were synchronous but causally unrelated events. Aminonucleoside of puromycin produced proteinuria within 7 days when injected intraperitoneally or subcutaneously. However, when aminonucleoside of puromycin as well as adenine were given, the onset of proteinuria was delayed until after day 7. A significant reduction in U-14C-glucose oxidation to CO2 was found at day 7 by glomeruli from rats given aminonucleoside of puromycin intraperitoneally but no significant changes were found with aminonucleoside of puromycin given subcutaneously on days 7 and 9 and aminonucleoside of puromycin + adenine given subcutaneously on days 7 and 9. Rats given daunomycin or adriamycin had developed proteinuria by day 14. U-14C-glucose oxidation to CO2 was significantly reduced on day 14 in glomeruli from rats given daunomycin but no significant changes were found on day 21 with daunomycin, or on days 14 and 21 with adriamycin. There was a reduction in pyruvic-acid carbon metabolism but not in glutamine-carbon oxidation 14 days after treatment with daunomycin. These results suggest that the observed changes in glomerular metabolism occur independently of, albeit synchronous with, the development of proteinuria. A causal relationship between these metabolic alterations and proteinuria therefore may be unlikely.
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PMID:Effects of aminonucleoside, daunomycin, and adriamycin on carbon oxidation by glomeruli. 124 18

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

The critical levels for monitoring cadmium health effects in 358 workers engaged in ore crushing/roasting (cadmium concentration in the workplace air 2.5-6.5 mg/m3), dry smelting (10.8-23.3 mg/m3), cadmium melting (0.01-0.16 mg/m3), and ingot making (2.8-4.7 mg/m3), were investigated. Exposure parameters such as blood and urinary cadmium were determined, together with biological parameters such as proteinuria, amino acids, glucose, beta 2-microglobulin, retinol-binding protein, albumin, plasma beta 2-microglobulin, creatinine clearance, tubular reabsorption of beta 2-microglobulin and phosphate, and blood and urinary levels of zinc, copper and lead. Factor analysis and stepwise regression analysis were then applied to the data to classify parameters and to find the main contributing parameter. Blood and urinary cadmium, urinary beta 2-microglobulin, retinol-binding protein and the ratio of urinary beta 2-microglobulin to albumin were also subjected to multiple correlation analysis, multiple regression analysis and the Chi-square test was applied to contingency tables. It is concluded, based on the data, that cadmium health effects may be assessed by using the following critical levels: blood cadmium: 10 micrograms/l, urinary cadmium: 10 micrograms/g creatinine; urinary beta 2-microglobulin: 2000 micrograms/g creatinine, urinary retinol-binding protein: 200 micrograms/g creatinine and a ratio of urinary beta 2-microglobulin to albumin of 0.001.
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PMID:Critical levels of blood and urinary cadmium, urinary beta 2-microglobulin and retinol-binding protein for monitoring cadmium health effects. 130 59

Insulin pens are pen-like devices for multiple injection of insulin. They can cut down the equipment necessary for a multidose regimen and thus make the therapy more convenient and flexible to help improve daily-life quality. It is of interest for us to known whether the average diabetic patients are motivated to achieve better metabolic control by means of insulin-pens. Seven insulin-dependent diabetic patients (male: 3, female: 4, age: 21-34 years) from the Veterans General Hospital participated in the study. None of them had diabetic proliferative retinopathy or proteinuria. They are initially treated with twice daily injection of mixtures of short- and intermediate-acting insulin (run-in period, 8 weeks). A multi-dose regimen with three premeal injections of short-acting insulin with insulin-pen plus one injection of long-acting insulin at bedtime was then used during the study period (12 weeks). Improved in metabolic control as assessed by HbAlc (7.6 +/- 0.9 vs 6.9 +/- 0.8%) and mean blood glucose (175.2 +/- 34 vs 152.3 +/- 28.1 mg/dl) in all patients was found. The frequency and severity of hypoglycemic episodes were not changed. In addition, all patients chose to continue multiple injection using insulin-pen, indicating a high acceptability of such device.
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PMID:Insulin-pen: preliminary report on its use for multiple injection regiment in insulin-dependent diabetic patients. 131 79

Points of agreement: (1) In IDDM, hypertension occurs in patients who have already developed nephropathy, probably in the microalbuminuric phase. (2) Hypertension is an important accelerator of the development of diabetic nephropathy. (3) Hypertension, obesity and NIDDM are often associated, and insulin resistance is commonly observed in all three states. (4) Antihypertensive therapy retards the development of diabetic nephropathy in IDDM and reduces proteinuria in NIDDM. (5) The choice of antihypertensive agent in the diabetic patient must be based upon the efficacy of the drug as well as avoidance of side effects including deleterious influence on glucose, insulin and lipid levels and renoprotection. (6) Carefully conducted long-term comparative trials between different classes of antihypertensive drugs in microalbuminuric IDDM and NIDDM patients are essential. Points of major controversy: (1) Detection of IDDM patients prone to the development of diabetic nephropathy can be performed by measuring specific parameters such as erythrocyte Na(+)-Li+ countertransport activity. (2) Insulin resistance is a pathogenic mechanism rather than purely an association with hypertension and obesity. (3) A certain class of antihypertensive agents--ACE inhibitors--confers a specific renoprotective effect in diabetic nephropathy, in addition to its effects upon systemic blood pressure. (4) Reduction of blood pressure should be considered in the normotensive microalbuminuric diabetic patient. (5) Microalbuminuria is a sufficient 'surrogate endpoint' for the progression of renal failure.
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PMID:Meeting report of the International Society of Hypertension Conference on Hypertension and Diabetes. 131 6

We report here the alterations of serum angiotensin-converting enzyme activity (S-ACE) and of active renin plasma concentrations (ARPC) in 41 insulin-dependent diabetes mellitus (IDDM) patients compared with those of 26 control subjects. The IDDM patients had S-ACE activity (54 +/- 16 I.E.) in the upper normal range (controls, 39 +/- 7). When the patients were subclassified according to their diabetic complications, a significant increase of S-ACE within the IDDM group compared to the controls was observed in patients with nephropathy (68 +/- 13, P less than 0.001) with persistent proteinuria and with retinopathy (63 +/- 14, P less than 0.001). A significant correlation was found between proteinuria and S-ACE (r = 0.98, P less than 0.001) and between retinopathy and S-ACE levels (r = 64, P less than 0.001). No correlation between blood pressure and S-ACE or between blood glucose and S-ACE was observed. The ARPC were within the normal range in the IDDM (21 +/- 9 ng/l) and in control (19 +/- 3) groups. No correlations between ARPC and blood pressure or blood glucose or the degree of diabetic complications were registered. These data show that S-ACE activity is elevated in IDDM patients with nephropathy-proteinuria and/or with retinopathy and the circulating renin may not represent the renal renin-angiotensin vascular system.
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PMID:Serum angiotensin-converting enzyme activity and active renin plasma concentrations in insulin-dependent diabetes mellitus. 133 Apr 63

To assess whether urinary N-acetyl-beta-D-glucosaminidase (NAG) could be used as a predictor of diabetic nephropathy, renal tubular enzymes such as NAG and gamma-glutamyl transpeptidase (gamma GTP), albumin, total protein and beta 2-microglobulin (BMG) in urine and/or serum were measured in various stages of diabetic nephropathy. As a predictor of diabetic nephropathy, urinary NAG was the most useful indicator among of them. Urinary gamma GTP had no clinical benefit on early detection of diabetic nephropathy although in cis-platin induced nephrotoxicity both urinary gamma GTP and NAG increased in parallel. Increase of urinary NAG appeared in diabetic patients prior to clinical proteinuria. With appearance of proteinuria, urinary NAG more increased. Urinary NAG correlated significantly with HbAlc and BMG in serum (sBMG). It is therefore needed for clinical application of urinary NAG as a predictor of diabetic nephropathy that control states of blood glucose in the patients should be considered. However, the results of sequential measurements of urinary NAG, sBMG and HbAlc in 78 diabetic patients for 18-month period showed that only urinary NAG was a responsible factor for elevation of sBMG known as an indicator of deterioration of renal function. These results indicate that renal tubular damage may already exist in early-stage of diabetic nephropathy, and that increase of urinary NAG activity is a useful predictor of diabetic nephropathy.
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PMID:[Clinical evaluation of N-acetyl-beta-D-glucosaminidase on prediction of diabetic nephropathy]. 135 Jul 71


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