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)

Random urine samples were obtained from 16 healthy subjects (nine men and seven women) before and after a 100 Km hill walk for the estimation of total protein, albumin, N-acetyl-beta-glucosaminidase (NAG), retinol binding protein (RBP) and creatinine. The excretion of total protein, albumin and NAG (expressed in relation to creatinine excretion) increased significantly after the walk. The relative clearance of protein and albumin also increased. In four subjects serial measurements were made for 4 days and the excretion of albumin and NAG on the fourth day were similar to the pre-walk values. We conclude that proteinuria of prolonged exercise is at least partly due to reduced tubular reabsorption.
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PMID:Protein excretion after prolonged exercise. 843 65

Brugia malayi-infected patients, endemic normals with high levels of specific antibodies and European controls were investigated for kidney disorders by noninvasive techniques. Groups of patients with filarial infections included asymptomatic, microfilaraemic cases (group 1), patients with filarial fever (group 2) and with obstructive filariasis (group 3). Several patients underwent a treatment course with diethylcarbamazine (DEC) when blood and urine samples were collected. Urine samples were investigated for proteinuria and analysed by SDS-PAGE to discriminate between proteinurias caused by tubular and glomerular disorders. In addition, urine levels of alpha-1 microglobulin, of the brush border antigen gp400 and of N-acetyl-beta-glucosaminidase (NAG) activity were determined as indicators of tubular disorders, the albumin content of the urines served as indicator of glomerular alterations. IgG rheuma factors were also determined in the serum as possible reasons for glomerulonephritis. Neither in the endemic normals nor in the European controls there was evidence for kidney disorders. Infected patients had significantly increased proteinuria compared to controls. There were no significant differences between the 3 groups of infected persons, although the mean protein levels were highest in cases with chronic disease and lowest in asymptomatic patients. Quantitative urine analyses and results of accompanying tests suggest predominantly tubular but generally relatively weak disorders in asymptomatic infections; abundant involvement of the kidney which involves both compartments of the organ in the course of filarial fever; and partly severe and probably chronically progredient kidney alterations, which predominantly affect the glomerula in symptomatic cases. IgG rheuma factors do not seem to play a role in filarial infection associated renal disease. DEC-treatment indeed did not significantly alter degree and character of the proteinuria, but relatively high albumin levels in the urine of treated persons yet suggest increased glomerular disorders in these cases. In conclusion, renal disease appears to be a common event in Brugia filariasis; involving both the tubular and glomerular compartment of the organ its pathogenesis is obviously complex and not only immune complex-mediated.
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PMID:Renal disease in lymphatic filariasis: evidence for tubular and glomerular disorders at various stages of the infection. 931 46

D-amino acid oxidase (DAO) is an enzyme released from the kidney, and a method for its enzymatic assay was developed by our group for urine specimens. A clinical evaluation of the test was performed for healthy individuals and patients with various types of nephropathy. 1) The normal reference interval was 0-10.0 micrograms/g Cr for randomly-collected urine. The intra-assay CV was 3.5-9.4%, and the inter-assay CV was 4.5-9.8%. 2) Urinary DAO index correlated well with changes in urinary microalbumin and N-acetyl-beta-glucosaminidase. 3) Chronic renal failure generally showed high levels of DAO, except for nephrotic syndrome, in which changes were minimal after the acute stage. In the nephrotic syndrome, urinary DAO was elevated in the acute stage with high proteinuria, but went down to almost normal as the proteinuria improved, although DAO changes did not correlate with the changes in the degree of proteinuria in lupus nephritis. 4) DAO changes were more sensitive than those of N-acetyl-beta-glucosaminidase or alpha 1-microglobulin in the clinical course of renal disorders. From these findings, DAO was judged to be very useful for monitoring the severity of renal dysfunction.
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PMID:D-amino acid oxidase activity in urine obtained from patients with renal disorders. 958 50

To elucidate the contribution of the renin-angiontensin system (RAS) to glomerular injury in salt-sensitive hypertension, we investigated the chronic effects of the angiotensin I-converting enzyme inhibitor cilazapril and the angiotensin II type 1-receptor antagonist (AT1a) TCV-116 in Dahl-Iwai rats. Dahl salt-sensitive (S) rats receiving 8% salt diet for 6 wk were simultaneously treated with cilazapril (n = 6), TCV-116 (n = 6), or saline (n = 14). The 8% salt diet markedly increased systolic blood pressure (SBP), urinary protein, and N-acetyl-beta-glucosaminidase (NAG) excretion compared with 0.3% salt-treated S (n = 6) or salt-resistant (n = 6) rats. Although neither cilazapril nor TCV-116 reduced the elevated SBP, TCV-116 significantly lowered urinary protein and NAG excretion. Histologically, 8% salt treatment in S rats induced progressive sclerotic and proliferative glomerular changes, which were ameliorated by both drugs. TCV-116 increased the glomerular diameter. Immunofluorescence demonstrated the increased level of type III collagen in the mesangium of 8% salt-treated S rats, which was completely reversed by TCV-116. Competitive RT-PCR of mRNA extracted from the glomeruli revealed that 8% salt treatment significantly increased the levels of proliferating cell nuclear antigen (PCNA) and platelet-derived growth factor B-chain and that TCV-116 significantly reduced the levels of PCNA and transforming growth factor-beta1 (TGF-beta1). Thus, although the chronic RAS-inhibition in salt-sensitive hypertension exerted a histologically renoprotective effect by both ways without lowering blood pressure, the RAS inhibition due to AT1a had more beneficial advantages of reducing proteinuria and attenuating the levels of glomerular TGF-beta1 and extracellular matrix.
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PMID:Effects of chronic inhibition of ACE and AT1 receptors on glomerular injury in dahl salt-sensitive rats. 984 88

To elucidate the role of nitric oxide (NO) and renin-angiotensin system (RAS) in the development of salt-sensitive hypertension, we investigated the pressor responses and renal histologic changes after long-term inhibition of endogenous NO synthesis in Dahl-Iwai salt-sensitive (DS) and salt-resistant (DR) rats under salt-re-stricted conditions that exaggerate RAS activation. Male DS and DR rats (6 weeks old) were fed with a low-salt (0.3%) diet for 5 weeks. NG-nitro-L-arginine (L-NA; dissolved in 60 mg/L deionized water), an arginine analogue acting as a NO-inhibitor, was also administered for 5 weeks. L-NA administration induced a gradual increase in systolic blood pressure (SBP) in both strains, and the pressor response in DS rats was apparently more enhanced relative to that in DR rats. Urinary nitrate plus nitrite (u-NOx) excretion was decreased by L-NA, with a significant negative correlation between SBP and u-NOx excretion in DS rats but not in DR rats. Plasma renin activity and urinary aldosterone level were significantly increased in L-NA-treated DS rats on week 5. Marked histologic changes with glomerular sclerosis and increased proteinuria and urinary N-acetyl-beta-glucosaminidase excretion were found in L-NA-treated DS rats but not DR rats. Competitive RT-PCR of mRNA extracted from the glomeruli revealed that angiotensin II type 1 receptor (AT1R) mRNA level was significantly lower in DS rats than in DR rats at week 2, and that L-NA administration significantly reduced glomerular AT1R level of DS rats at week 5, possibly because of downregulation. Our results showed that, even under sodium restriction, the pressor response and renal injury induced by chronic NO inhibition were markedly more enhanced in DS rats than in DR rats, which indicates that depletion of NO participates in both the development of hypertension and glomerular injury in DS rats through a potential activation of RAS irrespective of sodium loading. These data suggest that endogenous NO is an essential determinant of salt-sensitive hypertension in DS rats.
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PMID:The role of nitric oxide and the renin-angiotensin system in salt-restricted Dahl rats. 1128 Dec 41

Sensitive and specific biomarkers are needed to detect early kidney injury. The objective of the present work was to develop a sensitive quantitative urinary test to identify renal injury in the rodent to facilitate early assessment of pathophysiological influences and drug toxicity. Two mouse monoclonal antibodies were made against the purified ectodomain of kidney injury molecule-1 (Kim-1), and these were used to construct a sandwich Kim-1 ELISA. The assay range of this ELISA was 50 pg/ml to 5 ng/ml, with inter- and intra-assay variability of <10%. Urine samples were collected from rats treated with one of three doses of cisplatin (2.5, 5, or 7.5 mg/kg). At one day after each of the doses, there was an approximately three- to fivefold increase in the urine Kim-1 ectodomain, whereas other routinely used biomarkers measured in this study [plasma creatinine, blood urea nitrogen (BUN), urinary N-acetyl-beta-glucosaminidase (NAG), glycosuria, proteinuria] lacked the sensitivity to show any sign of renal damage at this time point. When rats were subjected to increasing periods (10, 20, 30, or 45 min) of bilateral ischemia, there was an increasing amount of urinary Kim-1 detected. After only 10 min of bilateral ischemia, Kim-1 levels on day 1 were 10-fold higher (5 ng/ml) than control levels, whereas plasma creatinine and BUN were not increased and there was no glycosuria, increased proteinuria, or increased urinary NAG levels. Thus urinary Kim-1 levels serve as a noninvasive, rapid, sensitive, reproducible, and potentially high-throughput method to detect early kidney injury in pathophysiological studies and in preclinical drug development studies for risk-benefit profiling of pharmaceutical agents.
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PMID:Urinary kidney injury molecule-1: a sensitive quantitative biomarker for early detection of kidney tubular injury. 1617 63

We investigated the prevalence of CKD and factors associated with CKD in HIV-infected patients who were under stable medical control. We retrospectively abstracted the medical records of 748 HIV-infected outpatients(659 males and 89 females). Their mean age was 44.9+/-11.7 (range; 21 to 79) years. The following parameters were reviewed: urinalysis including proteinuria and microscopic hematuria, urinary N-acetyl-beta-glucosaminidase (NAG) level as a marker of tubular damage, serum creatinine level, estimated glomerular filtration rate calculated based on the Modification of Diet in Renal Disease formula (eGFR), CD4 count in peripheral blood, HIV-RNA copies in serum, use and vintage of highly active antiretroviral therapy (HAART), and use of anti-hypertensive drugs (AHTD). Stages of CKD were determined based on the K/DOQI stages of kidney disease. Chronic renal failure (CRF) was defined as an eGFR value of less than 60 mL/min/1.73 m2. The chi-square test was used to evaluate differences in the prevalence of dichotomous variables. Multivariable logistic regression analysis was applied to assess independent contributors to existence of CRF, proteinuria, and tubular damage. Proteinuria was positive in 50.0 % and hematuria was positive in 11.3 %. Both were positive in 8.41%. Tubular damage (> 11 U/L of urinary NAG levels) was positive in 42 out of 112(37.5 %). Prevalence of CKD and CRF was 87.8 % and 16.2 %, respectively. Stages of CKD were: stage 5D, 4 patients (0.53 %); stage 5, 0 patients (0%); stage 4, 3 patients (0.40 %); stage 3, 114 patients (15.2 %); stage 2, 487 patients (65.1%); stage 1, 49 patients (6.6%); and non-CKD, 91 patients (12.2 %). Statistically, use of HAART, urinary NAG level, and age were significant contributors to proteinuria. Proteinuria, age, and use of AHTD were strong predictors for CRF. Tubular damage was related to HAART vintage, age, and TG levels. In addition, HAART vintage of more than 2.5 years was statistically associated with the existence of tubular damage in HIV-infected patients. Prevalence of CKD in stable HIV-infected patients was unexpectedly high in our hospital. Aged patients with a long HAART vintage who have proteinuria and hypertension are predisposed to the development of CRF through tubular damage.
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PMID:[Prevalence of chronic kidney disease (CKD) and significant contributors to CKD in HIV-infected patients]. 1854 81


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