Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The value of microalbuminuria in predicting hypertensive complications in pregnant patients at high risk was tested in a prospective trial. A total of 276 patients were studied (142 in the study group vs 134 controls). Albumin was measured in 8-h overnight urine collection throughout pregnancy using 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 trimester compared with the first. Using logistic and linear regression models, the presence of microalbuminuria in the early third trimester was proven to be predictive of severe disease (odds ratio 2.1, confidence interval (CI) 1.26-3.53) 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, we believe severe disease can be predicted by detecting microalbuminuria in the early third trimester of pregnancy in high risk patients.
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PMID:Microalbuminuria as an early marker of severity in hypertensive pregnant women. 887 40

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

Fifteen out-patients with type I diabetes mellitus and microalbuminuria (mean +/- SEM: 95.4 +/- 13.9 micrograms/min), were administered the glycosaminoglycan sulodexide, with the aim of investigating its influence on the rate of albumin excretion. Sulodexide was given intramuscularly in a dose of 600 lipoproteinlipase releasing units/day for three weeks. Albumin excretion was measured before dosing, at weekly intervals during dosing and also during the subsequent follow-up period of six weeks. Sulodexide yielded a clear-cut and statistically significant lowering of albumin excretion after the first week of treatment (from 95.4 +/- 13.9 micrograms/min to 53.6 +/- 11.1 micrograms/min; p = 0.0055); albumin excretion was further decreased after three weeks of treatment (26.5 +/- 6.05 micrograms/min; p = 0.0007) and was maintained during the follow-up period, at the end of which the mean value was still significantly lower than at baseline (39.6 +/- 10.3 micrograms/min; p = 0.01). Sulodexide short-term administration did not influence the routine haematological, haematochemical and coagulative tests performed contemporaneously. Patients' compliance with treatment was very good and no adverse events were reported.
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PMID:A pilot study of the effect of the glycosaminoglycan sulodexide on microalbuminuria in type I diabetic patients. 916 56

We report a new automated fluorescence assay for determination of albumin in urine. The dye Albumin Blue 580 specifically binds to albumin with exhibition of strong red fluorescence. The albumin concentration is calculated from emission intensity at 616 nm (excitation at 590 nm) and a calibration curve. Two Cobas Fara programs cover working ranges of 2-200 and 1-50 mg/L with detection limits of 1.4 and 0.4 mg/L, respectively. Within-run CVs (n = 10) ranged from 1.7% (189 mg/L) to 8.9% (7.2 mg/L) for 2-200 mg/L and from 2.9% (43.3 mg/L) to 5.7% (2.3 mg/L) for the 1-50 mg/L range. A test of urine samples (n = 100) submitted to routine analysis gave results that agreed well with those by the Behring nephelometric assay: AB 580 = 0.922 (+/-0.010) BNA + 4.16 (+/-0.78). No interference was detected from other urine components, including several proteins and 46 drugs. The high specificity and sensitivity make the method ideal for determination of microalbuminuria. In addition, the method is fast, inexpensive, and well-suited for clinical laboratory application and thus may be used instead of immunoassays.
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PMID:Microalbuminuria and borderline-increased albumin excretion determined with a centrifugal analyzer and the Albumin Blue 580 fluorescence assay. 919 52

Nephropathy is a frequent complication of long term diabetes. Diabetic nephropathy is the major determinant of premature morbidity and mortality both in insulin-dependent (IDDM) and in non-insulin dependent-diabetes mellitus (NIDDM). There is good evidence that genetic predisposition plays a major role in development of diabetic nephropathy. This hypothesis is based on the observation that diabetic nephropathy clusters within families, both in IDDM and NIDDM. Components of the renin-angiotensin system (RAS) are plausible candidate genes to examine for a association with microalbuminuria and diabetic nephropathy. In this study we compared the distribution of PstI melting polymorphism at the ACE locus among NIDDM patients with diabetic nephropathy and in patients who, despite long duration of NIDDM, remain without this complication. The 220 NIDDM patients for whom DNA was available were classified into two groups according to their renal status: normoalbuminuric control subjects (n = 80) who are NIDDM patients with an A/C ratio < 2.5 and nephropathy cases (n = 140) who are NIDDM patients with A/C ratio > 2.5. Albumin excretion rate was assayed by radioimmunoassay. HbA1c was assayed using HPLC methods, creatinine--using Jaffe methods and DNA analysis using PCR reaction, and then after the amplification product was digested with PstI enzyme. The study revealed that PstI sequence differences ("+/= and -") in the ACE gene do not contribute to genetic susceptibility to diabetic nephropathy in NIDDM.
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PMID:[Is PstI polymorphism of the angiotensin I converting enzyme gene associated with nephropathy development in non-insulin-dependent diabetes mellitus (preliminary study)]. 949 4

Microalbuminuria has been associated with a cluster of metabolic and nonmetabolic risk factors, suggesting that it might indicate the presence of generalized microvascular damage in patients with essential hypertension. To explore whether microalbuminuria is associated with early target organ damage, two groups of essential hypertensive patients, with (n = 17) (HtAlb+) and without (n = 16) (HtAlb-) microalbuminuria, and a control group (C) of healthy normotensive subjects (n = 20) were studied. The study groups, selected among participants of a large epidemiologic trial, were carefully matched for several potentially confounding variables such as gender, age, duration of hypertension, and body mass index. Albumin excretion rate was evaluated by radioimmunoassay in three nonconsecutive timed overnight collections after 3 weeks of pharmacologic wash-out. Left ventricular mass was assessed by M-B-mode echocardiography, carotid wall thickness by a high resolution ultrasound scan, and renal vascular impedance by Doppler scan. Office as well as 24-h ambulatory pressure monitoring (Takeda TM-2420) were also evaluated. There was no difference between the two hypertensive groups for office and 24-h blood pressure levels except for a lower daytime/nighttime systolic blood pressure ratio in the group with microalbuminuria. Microalbuminuric patients showed signs of early organ damage as compared to normoalbuminuric patients and normal subjects, namely greater left ventricular mass indices (LVMI 167+/-7 g/m2 in HtAlb+; 139+/-9 g/m2 in HtAlb-; 118+/-5 g/m2 in C, P < .001) and increased wall thickness of common carotid arteries (intima plus media thickness 12.5+/-0.2 mm in HtAlb+; 11.7+/-0.3 mm in HtAlb-; 11.2+/-0.2 mm in C, P < .001) as well as higher intrarenal vascular resistance (mean resistive index 0.62+/-0.01 in HtAlb+; 0.59+/-0.01 in HtAlb-; 0.59+/-0.01 in C, P < .05). In conclusion, microalbuminuria is an early marker of diffuse target organ damage in essential hypertension and therefore can be useful to identify patients for whom more aggressive preventive strategies or additional treatment measures are advisable.
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PMID:Microalbuminuria is an early marker of target organ damage in essential hypertension. 960 81

Although Type 2 (non-insulin-dependent) diabetes mellitus (Type 2 DM) is more common in South Asians than in Europeans in the UK, very little is known about complications and their risk factors in South Asians. We sought microalbuminuria in a cross-sectional study of 583 European and 889 South Asian Type 2 DM clinic attenders to Ealing Hospital, London, over 1 year. Albumin/creatinine ratios were measured in early morning urines. Prevalence of microalbuminuria was greater in South Asians compared to Europeans (40% versus 33% in men, p = 0.003, and 33% versus 19% in women, p < 0.0001). Glycaemic control was worse and prevalence of hypertension, retinopathy and heart disease was higher in South Asians. Key risk factors for microalbuminuria in both ethnic groups were glycaemic control, diabetes duration, blood pressure, triglyceride and retinopathy, but none accounted for the higher microalbuminuria prevalence in South Asians. Age and sex adjusted odds ratio for microalbuminuria was 1.78 (95% CI 1.02, 2.82, p = 0.02) in South Asians versus Europeans. After adjustment for confounders, this became 2.07, 95% CI 1.13, 3.79, p = 0.02. We conclude that microalbuminuria is more common in South Asians with Type 2 DM than in Europeans and, although risk factor relationships appeared similar in both groups, and some risk factors were more prominent in South Asians, this cannot account for the high prevalence of microalbuminuria observed in South Asians.
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PMID:Comparison of prevalence and risk factors for microalbuminuria in South Asians and Europeans with type 2 diabetes mellitus. 970 71

We examined whether the ACE gene insertion/deletion (I/D) polymorphism modulates renal disease progression in IDDM and how ACE inhibitors influence this relationship. The EURODIAB Controlled Trial of Lisinopril in IDDM is a multicenter randomized placebo-controlled trial in 530 nonhypertensive, mainly normoalbuminuric IDDM patients aged 20-59 years. Albumin excretion rate (AER) was measured every 6 months for 2 years. Genotype distribution was 15% II, 58% ID, and 27% DD. Between genotypes, there were no differences in baseline characteristics or in changes in blood pressure and glycemic control throughout the trial. There was a significant interaction between the II and DD genotype groups and treatment on change in AER (P = 0.05). Patients with the II genotype showed the fastest rate of AER progression on placebo but had an enhanced response to lisinopril. AER at 2 years (adjusted for baseline AER) was 51.3% lower on lisinopril than placebo in the II genotype patients (95% CI, 15.7 to 71.8; P = 0.01), 14.8% in the ID group (-7.8 to 32.7; P = 0.2), and 7.7% in the DD group (-36.6 to 37.6; P = 0.7). Absolute differences in AER between placebo and lisinopril at 2 years were 8.1, 1.7, and 0.8 microg/min in the II, ID, and DD groups, respectively. The significant beneficial effect of lisinopril on AER in the II group persisted when adjusted for center, blood pressure, and glycemic control, and also for diastolic blood pressure at 1 month into the study. Progression from normoalbuminuria to microalbuminuria (lisinopril versus placebo) was 0.27 (0.03-2.26; P = 0.2) in the II group, and 1.30 (0.33-5.17; P = 0.7) in the DD group (P = 0.6 for interaction). Knowledge of ACE genotype may be of value in determining the likely impact of ACE inhibitor treatment.
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PMID:Effect of angiotensin-converting enzyme (ACE) gene polymorphism on progression of renal disease and the influence of ACE inhibition in IDDM patients: findings from the EUCLID Randomized Controlled Trial. EURODIAB Controlled Trial of Lisinopril in IDDM. 972 42

In a randomized, double-blind, placebo-controlled study, we investigated in normotensive type 2 diabetics with microalbuminuria the effect of ramipril, an ACE inhibitor, on urine albumin excretion and serum lipids. A total of 1,882 patients were screened for urine microalbumin consecutively by dipstick test, Rapi Tex-Albumin test and RIA. The final 28 normotensive and microalbuminuric patients were assigned to receive either ramipril (1.25 mg/d, n = 16) or placebo (n = 12) for 12 weeks. Throughout the study, both groups had no changes in blood pressure, fasting plasma glucose, HbA1C, serum creatinine and electrolytes and no difference in creatinine clearance. At week 12 only the placebo group showed the significant increment of urine albumin excretion and triacylglycerol (30.6 +/- 38.3 to 39.0 +/- 19.7 and 167 +/- 64 to 208 +/- 77 mg/dl, respectively) but the decrement of HDL-cholesterol (46 +/- 16 to 35 +/- 6 mg/dl). During a 3 month period, increased urine albumin excretion was observed in normotensive type 2 diabetes with microalbuminuria who received only placebo. We conclude that ramipril may arrest the progression of albumin excretion and had favorable effects on serum lipids. Ramipril was safe and well-tolerated without untoward side effects during the study period.
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PMID:Impediment of the progressions of microalbuminuria and hyperlipidemia in normotensive type 2 diabetes by low-dose ramipril. 973 24


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