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)

Albumin; and alpha 1-, alpha 2-, beta-, and gamma-globulins were estimated by cellulose acetate electrophoresis in the serum and urine from rats with nephrotic syndrome (NS), 2, 4, 6, 8, 10, 12, 16, 20, and 30 days after a single injection of puromycin aminonucleoside (PAN). It was found that: (a) total serum protein level decreased on days 4-16, and total urine protein excretion rose on days 6-16; (b) serum albumin level fell on days 4-16, and urine albumin excretion increased on days 6-16; (c) serum alpha 1-globulin level rose on days 8-30, and urine alpha 1-globulin excretion increased on days 8-16; (d) serum alpha 2-globulin level remained essentially unchanged, and urine alpha 2-globulin excretion rose on days 4-10; (e) serum beta-globulin level decreased on days 4-20, and urine beta-globulin excretion increased on days 6-16, (f) serum gamma-globulin level diminished on days 6, 8, and 12, and urine gamma-globulin excretion rose on days 6-10. All serum protein fractions were excreted in the urine of nephrotic rats; these findings suggest that proteinuria is nonselective. The differences observed in the serum protein profiles, even when all protein fractions were lost in the urine, suggest an independent regulation of each protein fraction in PAN-nephrotic rats. In addition, the electrophoretic profile of serum proteins in PAN-nephrotic rats is different from previously reported patterns in human nephrosis and in rats with an acute-phase response.
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PMID:Electrophoretic analysis of serum and urinary proteins in rats with aminonucleoside-induced nephrotic syndrome. 846 81

Clinical and experimental data have indicated that heavy proteinuria in renal glomerular diseases is associated with the formation of tubulo-interstitial fibrosis and contributes to the progression of renal failure. Albumin in glomerular ultrafiltrate does not appear to cause this sequelae, rather than compounds that are associated with ultrafiltered plasma proteins. One such protein-bound factor could be insulin-like growth factor I (IGF-I). The present studies show that in nephrotic rats, IGF-I is ultrafiltered in conjunction with IGF-binding protein-2 and is present in proximal tubular fluid at 1.35 nM. Proximal tubular fluid from nephrotic rats autophosphorylates IGF-I receptors in cultured proximal tubular cells. Nephrotic, but not control, rat proximal tubular fluid increases the [3H]thymidine incorporation in cultured tubular cells, and neutralizing IGF-I-receptor antibodies partially inhibit this activity. Incubation of cultured proximal tubular cells with an extract that was prepared from nephrotic rat urine increases the secretion of collagen types I and IV. Secretion of the two collagens is in part ameliorated by neutralizing IGF-I-receptor antibody. In concert, these findings suggest that the IGF-I present in nephrotic rat tubular fluid is bioactive and may contribute to the development of tubulo-interstitial fibrosis in chronic nephrotic glomerular diseases.
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PMID:Bioactivity of glomerular ultrafiltrate during heavy proteinuria may contribute to renal tubulo-interstitial lesions: evidence for a role for insulin-like growth factor I. 869 Jul 82

Serum and urinary proteins from rats with nephrotic syndrome (NS) induced by puromycin aminonucleoside (PAN) were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Analysis was made on days 2, 4, 6, 8, 10, 12, 16, 20, and 30 after PAN injection. Data were compared with control rats (C). Rats developed proteinuria on days 4-30 and hypoproteinemia on days 4-16. Total protein concentration in serum and urine was similar on day 6. SDS-PAGE revealed that urinary albumin augmented on days 4-30 and serum albumin decreased markedly on days 4-20. Albumin concentration in serum and urine was similar on days 4-16. In addition, the study examined serum changes of 7 other proteins (designed as A, B, C, D, E, F, and G) which appeared or increased in urine, and whose molecular weights were higher (A, B, and C) or lower (D, E, F, and G) than that of albumin. In serum, protein A remained unchanged; protein B and G increased; proteins C, D, E, and F decreased. The qualitative pattern of urinary proteins remained essentially unchanged on days 4-30. During the intense proteinuria, the serum concentrations of protein B and albumin were similar and the urine concentrations of proteins C and D became comparable to that found in serum. These 7 serum proteins did not show the same behavior although all of them were excreted in urine. These data indicate that in PAN-nephrotic rats: (a) urinary proteins can be of low and high molecular weight, (b) serum proteins can be regulated independently of their urinary excretion and molecular weight, (c) the urine concentration of total protein and some specific proteins can reach values similar to that found in serum during the intense hypoproteinemia, and (d) the qualitative pattern of urinary proteins was unrelated to the magnitude of proteinuria.
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PMID:Time course analysis of serum and urinary proteins by SDS-PAGE in experimental nephrotic syndrome. 872 56

The value of microalbuminuria in predicting hypertensive complications in pregnant patients at high risk was tested in a prospective trial. A secondary aim was to compare the urinary albumin excretion rate between high risk hypertensive pregnant patients (study group) and pregnant patients at high risk of other complications, normal pregnant subjects, and nonpregnant subjects. Over the last 5 years, 276 patients were studied (142 in the study group v 134 controls). Albumin was measured in an 8-hour overnight urine collection throughout pregnancy using a radioimmunoassay technique. The pregnant women in both the study and control groups demonstrated a statistically significant increase in albumin excretion rate in the second and third trimesters compared with the first. Mean albumin excretion rate values were significantly higher in the study group (P = 0.0001). Using logistic and linear regression models, the presence of microalbuminuria in the early third trimester was proven to be predictive of hypertensive complications (odds ratio, 2.1; confidence intervals, 1.26 to 3.53) and birth weight (R2 = 0.7, P < 0.05) in the study group. Intrauterine growth retardation and neonatal outcome were less predictable. With the introduction of radioimmunoassays and in light of these significant clinical results, we believe that high-risk patients in whom abnormal proteinuria develops usually have a microalbuminuric phase weeks earlier, and this test has some predictive value for severe disease. In addition, the accepted definition of gestational proteinuria should be reconsidered.
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PMID:Microalbuminuria as an early predictor of hypertensive complications in pregnant women at high risk. 876 17

Proteinuria is an adverse feature in patients with renal disease, possibly due to toxicity of albumin to proximal tubular cells. Albumin is reabsorbed from tubular fluid by receptor-mediated endocytosis. The mechanism of regulation of the endocytosis is unknown. The large quantities of G proteins in proximal tubular cell apical membranes suggests that they may have a regulatory role in endocytosis. 125I-labeled albumin uptake was measured in opossum kidney (OK) cells. This is a saturable process with high-affinity [apparent dissociation constant (Kd) = 24.3 mg/l] and low-affinity (Kd = 15.9 g/l) components. The endocytic uptake of gold-albumin into OK cells was confirmed by electron microscopy. 125I-albumin endocytosis in OK cells was inhibited by pertussis toxin, but cholera toxin had no effect. Pertussis toxin also inhibited uptake of [3H]inulin. OK cells were stably transfected with a cDNA for the G protein subunit G alpha i-3 and transfectants were screened by immunoblotting. Several G alpha i-3-overexpressing clones were detected. OK cells overexpressing G alpha i-3 demonstrate increased 125I-albumin uptake, which is abolished by pertussis toxin, in both a concentration- and time-dependent manner. These results suggest that albumin endocytosis in OK cells is regulated by the G protein G alpha i-3.
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PMID:Albumin endocytosis is regulated by heterotrimeric GTP-binding protein G alpha i-3 in opossum kidney cells. 877 Jan 67

The aim of this study was to evaluate the circadian blood pressure variations in subjects with or without microalbuminuria (Urinary Albumin Excretion (UAE) between 30 and 300 mg/24 h. Forty-nine non-insulin dependent diabetic subjects with essential arterial hypertension and without proteinuria (UAE < 300 mg/24 h) were consecutively recruited. Systolic (SBP) and Diastolic Blood Pressure (DBP) have been measured using a SpaceLabs 90207 ambulatory blood pressure monitor, every 15 minutes during daytime (7:00 a.m. to 22:00 p.m.) and every 30 minutes during nighttime (22:00 p.m. 7:00 a.m.). UAE has been measured by nephelometry on three 24 h urine collections. The group with microalbuminuria (n = 16) was not different from the group with normoalbuminuria (n = 33) for age, sex ratio, body mass index, known diabetes duration, proportion of anti-hypertensive treatment, serum creatinine and HbA1c. Daytime blood pressures (SBP/DBP: 144 +/- 15/83 +/- 8 vs 137 +/- 13/84 +/- 9 mmHg) and nighttime DBP (75 +/- 7 vs 74 +/- 9 mmHg) were comparable between both groups. In contrast, the nighttime SBP was higher in subjects with microalbuminuria than in those without (139 +/- 17 vs 129 +/- 17 mmHg; p = 0.016). If dippers are the subjects with a nocturnal blood pressure reduction (SBP and/or DBP) below 4%, there is a relationship between "non dippler" subjects and those with microalbuminuria (Chi-squared test = 5.67; p = 0.017). In conclusion, hypertensive non-insulin dependent diabetic subjects with microalbuminuria have a loss of nocturnal blood pressure decrease.
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PMID:[Decrease of nocturnal blood pressure in type II diabetic subjects with microalbuminuria]. 894 75

The integrity of the blood-retinal and blood-glomerular vascular barriers were investigated simultaneously in diabetic individuals to determine whether or not the early forms of diabetic retinopathy and nephropathy are temporally related. The blood-retinal barrier was assessed by the technique of vitreous fluorophotometry. Twenty-four hour urinary excretion of albumin was determined by radioimmunoassay before fluorescein measurement. Posterior vitreous fluorescein leakage was greater in the study cohort than in the control population after diabetes had been present 11-20 years (p < 0.05) and 21 years or more (p < 0.01). Albumin excretion was also increased in the diabetic subjects (p < 0.001) and correlated to duration of diabetes (r = 0.51, p < 0.005). Hypertension raised midvitreous fluorescein levels (p < 0.05), but it had no effect on posterior vitreous values. Hypertension was an independent predictive factor for urinary albumin excretion (p < 0.05). Partial correlation analysis showed that vitreous fluorescence and urinary protein were not significantly correlated when controlled for duration of diabetes and for age. Early proteinuria did not predict retinal vascular leakage, nor did increased fluorescein leakage predict renal decompensation in the diabetic subjects. The data suggest that during the early stages of retinal and renal abnormalities associated with insulin-dependent diabetes, the eye and kidney follow different temporal courses to abnormal function.
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PMID:Early retinal and renal abnormalities in diabetes. 920 98

Proteinuria and nephropathy have been found to cluster in families of non-insulin-dependent diabetic (NIDDM) Pima Indian, and in Caucasian insulin-dependent diabetic (IDDM) patients. No information is at present available for Caucasian NIDDM patients. The aim of the present study was to determine whether micro-macroalbuminuria (AER+) is associated with albumin excretion rate abnormalities in diabetic and non-diabetic siblings of probands with NIDDM and AER+. We identified 169 Caucasian families with one NIDDM proband (the patient with longest known NIDDM duration) (101 families with only NIDDM siblings, 33 families with both NIDDM and non-NIDDM siblings and 35 families with only non-NIDDM siblings). Of the probands 56 had AER+ [Prob-NIDDM-(AER+)], 78 had AER-[Prob-NIDDM-(AER-)], 74 siblings of Prob-NIDDM-(AER+), and 113 siblings of Prob-NIDDM-(AER-) also had NIDDM. Data on albuminuria and retinopathy from multiple sibling pairs when the size of the sibship was more than two was adjusted according to a weighting factor. The odds ratio for AER+, in siblings of Prob-NIDDM-(AER+) adjusted for age, hypertension, glycated haemoglobin A1c and other confounding variables was 3.94 (95% confidence intervals: 1.93-9.01) as compared to siblings of Prob-NIDDM-(AER-). The 74 siblings of Prob-NIDDM-(AER+) had higher prevalence of proliferative retinopathy than siblings of Prob-NIDDM-(AER-) (14 vs 2%; p < 0.01). We also identified 66 non-diabetic siblings of 41 NIDDM probands with AER+ and 36 non-diabetic siblings of 27 NIDDM probands with AER-. Albumin excretion was two times higher, although still within the normal range, in the non-diabetic siblings of Prob-NIDDM-(AER+) than in siblings of Prob-NIDDM-(AER-) [median = 13.5 (range 0.5-148) vs 6.6 (range 1-17) micrograms/min (p < 0.05)]. In conclusion higher rates of albumin excretion aggregate in Caucasian families with NIDDM. Proliferative retinopathy is more frequently observed in families showing a clustering of AER+ and NIDDM. These findings suggest that familial factors play a role in the pathogenesis of renal and retinal complications in NIDDM.
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PMID:Clustering of albumin excretion rate abnormalities in Caucasian patients with NIDDM. The Italian NIDDM Nephropathy Study Group. 924 3

There is a lack of information about renal responses in heart and kidney transplant patients after intense physical exercise. Eleven heart and ten kidney transplant recipients, as well as two control groups of healthy subjects, were given a maximum exercise test on a bicycle ergometer. One control group was also given a moderate load corresponding to the peak load of the kidney transplant group. Blood and urine samples were collected before and after exercise and assayed for lactate, creatinine, total protein, and albumin. The glomerular filtration rate remained stable at the end of exercise in the transplant patients, while there was a slight (17%) decrease in the control group. Albumin excretion rates after maximum exercise attained a mean of 237 micrograms.min-1 in the control group and a mean of 45 and 16 micrograms.min-1, respectively, in the heart and kidney groups. Postexercise proteinuria seemed to be related to the absolute intensity of the event, but kidney transplant patients showed a reduced effect as compared to heart transplant patients. We conclude that short-term, maximum exercise in heart and kidney transplant recipients is not detrimental to kidney function.
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PMID:Renal responses to exercise in heart and kidney transplant patients. 924 44

Currently, neither the American Diabetes Association nor the Kidney Foundation consider the results of a positive dipstick urine test for protein, a semi-quantitative measurement, in the final evaluation of diabetic nephropathy. Instead, they require a quantitative test. The object of this study was to assess whether a positive semi-quantitative test could accurately substitute for a quantitative one to evaluate renal disease. We determined the proportion of urine samples dipstick positive for protein that had an albumin:creatinine ratio of 30 microg/mg or more, the recommended value for the diagnosis of microalbuminuria (incipient nephropathy). Albumin:creatinine ratios were measured in urine samples from 19 diabetic and 51 nondiabetic patients in which the dipstick test for protein was positive. Twelve of 24 (50%) urine samples trace positive for protein by a dipstick method had albumin:creatinine ratios of 30 microg/mg or more, whereas 42 of 46 (91%) urine samples greater than or equal to 1+ for protein exceeded that ratio. The results were similar in the two groups of patients. The positive predictive value for a test result more than or equal to 1+ for protein was 91%. We conclude that in contrast to the recommendations of the American Diabetes Association and the National Kidney Foundation, dipstick positive proteinuria of more than or equal to 1+ can substitute for an albumin:creatinine ratio. An algorithm for this more cost-effective approach to the diagnosis of diabetic nephropathy is suggested.
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PMID:Relationship between dipstick positive proteinuria and albumin:creatinine ratios. 1023 10


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