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Albumin Excretion Rate (albumin + excretion_rate)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of Albumin Excretion Rate

  • urinary albumin excretion rate
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    Selected Abstracts

    Losartan modifies glomerular hyperfiltration and insulin sensitivity in type 1 diabetes

    DIABETES OBESITY & METABOLISM, Issue 6 2001
    S. Nielsen
    Aim: The effect of the angiotensin II receptor antagonist losartan on renal haemodynamics and insulin-mediated glucose disposal was examined in normotensive, normoalbuminuric type 1 diabetic patients using a double-blind, placebo-controlled, cross-over design. Methods: Diurnal blood pressure, glomerular filtration rate (GFR, determined using [125I]-iothalamate), renal plasma flow (RPF, determined using [131I]-hippuran) and urinary albumin excretion rate (UAE) were measured, and a hyperinsulinaemic, euglycaemic clamp with indirect calorimetry was performed in nine patients (age 30 ± 7 years (mean ±,s.d.), HbA1c 8.1 ± 1.1%) following 6 weeks' administration of either losartan 50 mg/day or placebo. Results: Diurnal blood pressure was significantly reduced after losartan compared with placebo (122/70 ± 11/8 vs. 130/76 ± 12/6 mmHg, p <,0.05). A significant decline in GFR (133 ± 23 vs. 140 ± 22 ml/min, p < 0.05) and filtration fraction (FF; GFR/RPF) (24.6 ± 3.5 vs. 26.2 ± 3.6%, p <,0.05) was observed in the losartan vs. placebo groups. RPF and UAE did not change. Isotopically determined glucose disposal rates were similar after losartan and placebo in the basal (2.61 ± 0.53 vs. 2.98 ± 0.93 mg/kg/min) and insulin-stimulated states (6.84 ± 2.52 vs. 6.97 ± 3.11 mg/kg/min). However, the glucose oxidation rate increased significantly after losartan vs. placebo in the basal state (1.72 ± 0.34 vs. 1.33 ± 0.18, mg/kg/min, p <,0.01) and during insulin stimulation (2.89 ± 0.75 vs. 2.40 ± 0.62 mg/kg/min, p <,0.03). Basal and insulin-stimulated non-oxidative glucose disposal tended to decrease after losartan; however, this was not significant. Endogenous glucose production and lipid oxidation were unchanged after treatment and similarly suppressed during hyperinsulinaemia. Glycaemic control, total cholesterol, high-density lipoprotein (HDL)-cholesterol and triglycerides were stable in both losartan and placebo groups. Conclusions: Losartan reduces blood pressure, glomerular hyperfiltration and FF, and improves basal and insulin-stimulated glucose oxidation in normotensive, normoalbuminuric type 1 diabetic patients. [source]

    Therapeutic targets in the management of Type 1 diabetes

    DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue S1 2002
    P. D. Home
    Abstract For historical reasons, diabetes has long been linked with blood and urine glucose control, partly because these were clearly linked to acute symptoms, and partly because glucose became measurable around 200 years ago. Today it is recognized that there is far more to diabetes than simply monitoring symptoms and blood glucose. Intensive management has an impact on the quality of life. Late complications have their own risk factors and markers. Monitoring and early detection of these risk factors and markers can lead to changes in treatment before tissue damage is too severe. Accordingly, professionals now find themselves monitoring a range of adverse outcomes, markers for adverse outcomes, risk factors and risk markers for microvascular and arterial disease, acute complications of therapy, and the care structures needed to deliver this. Adverse outcomes lend themselves to targets for complication control in populations, and markers of adverse outcomes (such as retinopathy and raised albumin excretion rate) in treatment cohorts. Surveillance systems will have targets for yearly recall and review of early complications. Metabolic (surrogate) outcomes can be monitored in individual patients, but monitoring is only of value in so far as it guides interventions, and this requires comparison to some intervention level or absolute target. Even for blood glucose control this is not easy, for conventional measures such as glycated haemoglobin have their own problems, and more modern approaches such as post-prandial glucose levels are controversial and less convenient to measure. In many people with type 1 diabetes targets for blood pressure, LDL cholesterol, and serum triglycerides will also be appropriate, and need to be part of any protocol of management. Copyright © 2002 John Wiley & Sons, Ltd. [source]

    HMG-CoA reductase inhibitors prevent bone loss in patients with Type 2 diabetes mellitus

    DIABETIC MEDICINE, Issue 9 2004
    A. Nakashima
    Abstract Aims It has been reported that 3-hydroxy-3-methylglutaryl co-enzyme A (HMG-CoA) reductase inhibitors increase bone mineral density (BMD) in vivo. We investigated the effect of HMG-CoA reductase inhibitors on BMD in patients with Type 2 diabetes mellitus. Patients and methods We selected 122 patients with Type 2 diabetes, who were not taking active vitamin D preparations. Their mean age was 67.3 ± 9.2 years. They were divided into a control group (n = 63) without HMG-CoA reductase inhibitor therapy and an HMG-CoA group (n = 59) who were treated with these drugs. The BMD of the distal one-third of the radius was measured by dual-energy X-ray adsorptiometry at baseline and after 2 years. Results There were no significant differences between the control and HMG-CoA groups at baseline with respect to age, gender, body mass index, duration of diabetes, haemoglobin A1c, fasting plasma glucose, adjusted calcium, serum phosphorus, alkaline phosphatase, albumin excretion rate and radial BMD. However, there was a significantly smaller annual decrease of the radial BMD in the HMG-CoA group. Multiple regression analysis with a forward elimination procedure revealed a positive correlation of the radial BMD Z-score with body mass index, while there was a negative correlation with alkaline phosphatase and albumin excretion rate. In addition, the annual rate of change of the radial BMD showed a positive correlation with HMG-CoA reductase inhibitor therapy. Conclusions These findings suggest that HMG-CoA reductase inhibitors may prevent bone loss in patients with Type 2 diabetes. [source]

    Factors predictive of nephropathy in DCCT Type 1 diabetic patients with good or poor metabolic control

    DIABETIC MEDICINE, Issue 7 2003
    L. Zhang
    Abstract Aims The study aim was to assess the time-related risk of developing diabetic nephropathy [albumin excretion rate (AER) , 40 mg/24 h] from baseline covariates in Type 1 diabetic patients with either good or poor metabolic control (MC). Methods Based on material from the Diabetes Control and Complications Trial study (n = 1441), patients were considered as under good or poor MC if their HbA1c mean level up to last visit fell in the lowest (, 6.9%) or highest (, 9.5%) quintile of the overall HbA1c distribution, respectively. Prevalence cases of nephropathy were excluded from the study. Survival analysis and Cox regression were applied to the data. Results Among patients with good MC (n = 277), 15% had developed nephropathy at the end of the study. Conversely, among patients with poor MC (n = 268), the proportion without the complication was 52%. When adjusting for MC, time to diabetic nephropathy was related to age (P < 0.0001), AER (P < 0.001), duration of diabetes (P < 0.005), body mass index (BMI) (P < 0.005), all at baseline, and to gender (P < 0.01). Patients with upper normal range AER levels, longer duration of diabetes and lower BMI were at higher risk, regardless of MC. The adverse effect of younger age on diabetic nephropathy was more marked in good than in poor MC. Although women tended to develop the complication more often under good MC, they appeared to be better protected under poor MC. Conclusions This study confirms occurrence of diabetic nephropathy under good MC and non-occurrence of the complication despite poor MC. It also demonstrates that some baseline covariates can affect, in a differential manner, time to diabetic nephropathy depending on MC. Diabet. Med. 20, 580,585 (2003) [source]

    Plasma lipids and urinary albumin excretion rate in Type 1 diabetes mellitus: the EURODIAB IDDM Complications Study

    DIABETIC MEDICINE, Issue 1 2001
    M. B. Mattock
    SUMMARY Aims To examine the relationship between increased urinary albumin excretion rate and fasting plasma lipids among male and female respondents to the EURODIAB IDDM Complications Study, and attempt to explain inconsistencies in previous reports. Methods A cross-sectional study of 3250 randomly selected Type 1 diabetic patients from 31 diabetes clinics in 16 European countries was carried out between 1989 and 1990. Plasma lipids and urinary albumin were measured centrally. The present analysis was confined to the subgroup of 2205 patients attending after a 10,12 h overnight fast. Mean age was 33 years (sd 10) and mean duration of Type 1 diabetes mellitus was 15 years (sd 9). Results The prevalence of microalbuminuria (24-h urinary albumin excretion rate 20,200 ,g/min) was 21.7% (95% confidence interval 19.9,23.5) and macroalbuminuria (24-h urinary albumin excretion rate >,200 ,g/min) 7.8% (6.6,9.0). In comparison to patients with normal urinary albumin excretion rate (< 20 ,g/min), and after controlling for age, sex, glycaemic control, duration of diabetes and current smoking, macroalbuminuria was associated with significantly (P < 0.01) increased fasting plasma triglycerides, cholesterol, LDL-cholesterol, cholesterol:HDL-cholesterol ratio and, in women, reduced HDL-cholesterol. In men and women with microalbuminuria, the only significant association was with increased plasma triglycerides. Conclusions These data confirm that there is an association between fasting plasma lipids and increasing urinary albumin excretion rate in European Type 1 diabetic patients. In microalbuminuric patients, however, the association was weaker than previously reported and partly explained by confounding factors. [source]

    Urinary L-FABP and anaemia: distinct roles of urinary markers in type 2 diabetes

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2010
    M. Von Eynatten
    Eur J Clin Invest 2010; 40 (2): 95,102 Abstract Background, Urinary liver-type fatty acid binding protein (L-FABP) and kidney injury molecule (KIM)-1, novel urinary biomarkers of renal tubulointerstitial function, have previously been associated with acute ischaemic kidney injury. We studied the clinical significance of urinary L-FABP, KIM-1 and N -acetyl-,-glucosaminidase (NAG) as potential markers of renal function and chronic ischaemic injury in patients with diabetic nephropathy. Material and methods, A total of 130 type 2 diabetes patients with early diabetic nephropathy and 40 healthy controls were studied. Urinary L-FABP, KIM-1, NAG, albumin excretion rate (AER) and creatinine clearance were obtained from 24-h urine samples, and correlated with measures of red blood cell count, renal function and metabolic control. Results, Urinary L-FABP was significantly increased in diabetes patients compared with healthy controls [8·1 (interquartile 0·6,11·6) vs. 2·4 (0·5,3·6) ,g/g creatinine, P < 0·001] and correlated with AER (r = 0·276, P = 0·002), creatinine clearance (r = ,0·189, P = 0·033) and haemoglobin levels (r = ,0·190, P = 0·030). In multivariable linear regression analysis, haemoglobin (, = ,0·247, P = 0·015) and AER (, = 0·198, P = 0·046) were significant predictors of urinary L-FABP. Prevalent anaemia was independently associated with a 6-fold risk for increased tubulointerstitial kidney damage (upper vs. lower two L-FABP tertiles: OR, 6·06; 95% CI: 1·65,22·23; P = 0·007). Urinary KIM-1 was not significantly associated with kidney function, AER, or measures of red blood cell count while urinary NAG was associated with parameters of glucose control and renal function. Conclusions, Different urinary biomarkers may reflect distinct pathophysiological mechanisms of tubulointerstitial damage in early diabetic nephropathy: Urinary L-FABP could be a novel biomarker for chronic intrarenal ischaemia. [source]

    Effect of activin A on tubulointerstitial fibrosis in diabetic nephropathy

    NEPHROLOGY, Issue 3 2009
    XIAO-JUN REN
    SUMMARY Aim: The effect of activin A on tubulointerstitial fibrosis in diabetic nephropathy (DN) using streptozotocin (STZ)-induced diabetic rats and high glucose-cultured HK-2 cells was investigated. Methods: Male Wistar rats were randomized into a normal control group (NC) and diabetes mellitus group (DM). Diabetes was induced by i.p. injection of STZ. Six rats were respectively killed 4, 8, 12 and 16 weeks after model establishment in each group. The changes of kidney weight/bodyweight (KW/BW), urine albumin excretion rate (AER) and creatinine clearance rate (Ccr) were determined. The morphology of tubulointerstitium was observed by light microscopy. Further biochemical analysis was provided using immunohistochemistry and real-time polymerase chain reaction. The different parameters in high glucose-cultured HK-2 cells were monitored by western blotting or enzyme-linked immunosorbent assay (ELISA) and the intervention of rh-follistatin on them was investigated. Results: Compared with the NC group, there was marked enlargement in the levels of KW/BW, AER, Ccr and interstitial fibrosis index, and the production of P-Smad2/3 and fibronectin in the DM group from 8 to 16 weeks. Activin ,A, mainly located in tubular epithelial cells, was significantly higher in the DM group than that in the NC group throughout the study periods. Follistatin was abundant in the NC group, but was diminished gradually in the DM group. High glucose may facilitate the synthesis of activin ,A, transforming growth factor (TGF)-,, P-Smad2/3 and fibronectin in HK-2 cells while rh-follistatin inhibited them except TGF-,. Conclusion: Activin A is involved in tubulointerstitial fibrosis in DN by inducing the production of fibronectin through Smad signal pathway. [source]

    Methylenetetrahydrofolate reductase and methionine synthase reductase gene polymorphisms and protection from microvascular complications in adolescents with type 1 diabetes

    PEDIATRIC DIABETES, Issue 4pt2 2008
    Esko J Wiltshire
    Abstract:, Folate status has been associated with endothelial dysfunction in adolescents with type 1 diabetes, and elevated total plasma homoocyst(e)ine (tHcy) is a risk for vascular disease in the non-diabetic population. Polymorphisms in genes involved in folate and homocysteine metabolism are implicated in vascular disease. We aimed to determine whether polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) genes are risk factors for early microvascular disease in a large group of adolescents with type 1 diabetes. Four hundred and eighty adolescents were screened annually for retinopathy and microalbuminuria for a median of 4 yr. Molecular analysis for the polymorphisms 677C,T, 1298A,C in MTHFR, and 66A,G in MTRR was performed. The MTRR 66GG genotype reduced the risk for elevated albumin excretion rate (AER) (OR 0.47, CI 0.25, 0.88, p = 0.018) and showed a trend to reduced risk for microalbuminuria (OR 0.27, CI 0.06,1.21, p = 0.09). Survival without elevated AER was increased with the MTRR 66GG genotype (12.4 vs. 9.7 yr, p = 0.04) and with the MTHFR 1298CC genotype (15.2 vs. 10.2 yr, p = 0.007). Conversely, survival without retinopathy was reduced with the MTHFR 677TT and MTRR 66GG combined genotype (6.2 vs. 10.2 yr, p = 0.015). The MTRR 66GG and MTHFR 1298 CC genotypes may confer protection against early nephropathy, possibly because they are associated with lower tHcy. The MTHFR 677 TT was only related to earlier onset retinopathy in combination with MTRR 66GG. [source]

    Low risk of overt nephropathy after 24 yr of childhood-onset type 1 diabetes mellitus (T1DM) in Norway

    PEDIATRIC DIABETES, Issue 5 2006
    Torild Skrivarhaug
    Aim:, To estimate the risk of diabetic nephropathy and associated risk factors in a nationwide cohort of childhood-onset type 1 diabetes mellitus (T1DM) and 19,30 yr of diabetes duration. Methods:, Patients diagnosed with childhood-onset T1DM (<15 yr) from 1973 through 1982, who previously (1989,1990) participated in a clinical examination to assess diabetic complications, were invited for a new examination in 2002,2003. Of 355 eligible patients, 299 participated (84.2%), and complete urine samples for evaluation of albuminuria were obtained from 295 patients, with a mean age of 33 yr (range 20.9,44.0) and mean diabetes duration of 24 yr (range 19.3,29.9). Persistent microalbuminuria and overt nephropathy [albumin excretion rate (AER) 15,200 ,g/min and AER > 200 ,g/min, respectively] in at least two out of three consecutive overnight urine samples were defined as diabetic nephropathy. Results:, Overt nephropathy was found in 7.8% [95% confidence interval (CI) 4.7,10.9] and persistent microalbuminuria in 14.9% (95% CI 10.8,19.0) of the subjects. Hemoglobin A1c (HbA1c) (p = 0.001), systolic blood pressure (BP) (p = 0.002), total cholesterol (p = 0.019), and C-reactive protein (CRP) (p = 0.019) were associated with diabetic nephropathy. Significant predictors in 1989,1990 for the development of diabetic nephropathy in 2002,2003 were HbA1c (p < 0.001), AER (p = 0.007), and cholesterol (p = 0.022). Conclusions:, In a subgroup of patients diagnosed with childhood-onset T1DM in 1973,1982, 7.8% had overt nephropathy after 19,30 yr of diabetes duration, which is low compared with studies from other countries. HbA1c, systolic BP, total cholesterol, and CRP were each independently associated with diabetic nephropathy. [source]

    The accuracy of cystatin C and commonly used creatinine-based methods for detecting moderate and mild chronic kidney disease in diabetes

    DIABETIC MEDICINE, Issue 4 2007
    R. J. MacIsaac
    Abstract Background, The accuracy of measuring serum cystatin C levels for detecting various stages of chronic kidney disease (CKD) in diabetes is still unclear. Methods In a cross-sectional study of 251 subjects, a reference glomerular filtration rate (GFR) was measured using 99cTc-DTPA plasma clearance (iGFR). Multivariate analysis was used to identify independent clinical and biochemical associations with serum cystatin C and iGFR levels. The diagnostic accuracy of cystatin C and commonly used creatinine-based methods of measuring renal function (serum creatinine, the MDRD four-variable and Cockcroft,Gault formulae) for detecting mild and moderate CKD was also compared. Results, In the entire study population the same five variables, age, urinary albumin excretion rates, haemoglobin, history of macrovascular disease and triglyceride levels were independently associated with both cystatin C and iGFR levels. A serum cystatin C level cut-off > 82.1 nmol/l (1.10 mg/l) had the best test characteristics as a screening tool for detecting moderate CKD (< 60 ml/min per 1.73 m2) when compared with creatinine-based methods. At the upper threshold for mild CKD (< 90 ml/min per 1.73 m2), cystatin C also had greater diagnostic accuracy than creatinine, but had similar diagnostic accuracy when compared with creatinine-based formulae for predicting renal function. Conclusions, This study suggests that the clinical and biochemical parameters associated with serum cystatin C levels are closely linked to those associated with GFR and highlights the potential usefulness of screening for moderate or mild CKD in subjects with diabetes by simply measuring serum cystatin C levels. [source]