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)

We describe our observations concerning differences in two groups of young hypertensive patients according to their renin activities after ACE inhibition. Seventeen of these patients (age 26 +/- 7 years), so far untreated, were investigated prospectively for hormone levels (renin, aldosterone, vasopressin), microalbuminuria, renal haemodynamics (inulin and PAH clearance) and signs of organ damage (echocardiography, fundoscopy). Secondary forms of hypertension were excluded by routine methods, including angiography. We differentiated two groups of young hypertensive patients. Group 1 (n = 9) had a false positive captopril test with elevated renin activities after ACE inhibition with captopril (8.4 +/- 5 ng/ml per hour) compared to group 2 (renin activity: 2.2 +/- 1.3 ng/ml per hour) or an increase of greater than 400% of renin activity after ACE inhibition. Baseline renin activities and sodium excretion did not differ between the groups. Group 1 also showed significantly greater GFR, FF, and microalbuminuria, as well as signs of organ damage, with left ventricular hypertrophy and hypertensive changes in fundoscopy. There were no differences between the groups concerning mean arterial blood pressure and duration of hypertension. In conclusion, we were able to demonstrate that patients with highly stimulated renin activities showed signs of visceral organ damage and renal hyperfiltration compared to the normal renin activity group after ACE inhibition. Investigations of the renin-angiotensin-aldosterone system with ACE inhibitors might constitute a helpful indicator of renal changes and organ damages in young hypertensive patients.
Nephrol Dial Transplant 1992
PMID:Renal haemodynamics and organ damage in young hypertensive patients with different plasma renin activities after ACE inhibition. 131 92

To detect early renal involvement in young diabetic patients (IDDM), urinary protein excretion and renal function were examined in 110 patients aged 5.9-25.0 years. Clearances of inulin and PAH were determined as well as albumin (Alb), IgG, N-acetyl-beta-D-glucosaminidase (NAG) and creatinine (Cr) excretion rates (UV). The patients were grouped according to IDDM duration (2- less than 5, 5-10 and greater than 10 years) and albumin excretion rate (non-albuminuria less than 20, microalbuminuria 20-200, and albuminuria greater than 200 micrograms/min per 1.73 m2). Four patients had overt albuminuria, 17 microalbuminuria (equally distributed among the duration groups). Grouped according to albumin excretion rate, the mean GFR was increased in those without albuminuria but 'normalized' in patients with microalbuminuria/albuminuria. Grouped according to albumin excretion rate and the duration of the disease, the non-albuminuric patients with IDDM for greater than 10 years had a lower GFR than those with a shorter duration of IDDM. The patients with microalbuminuria/albuminuria and IDDM for less than 5 years had a reduced GFR. Patients with increased NAG excretion rate had lower Na excretion rate, lower fractional Na excretion and greater creatinine excretion than those with normal NAG excretion. Albumin excretion correlated with IgG excretion, but also with NAG excretion. Our results suggest that early albuminuria in IDDM is of both glomerular and tubular origin. The hyperfiltration declines with increasing albumin excretion but also with the duration of the disease.
Nephrol Dial Transplant 1992
PMID:Urinary protein excretion and renal function in young people with diabetes mellitus. 132 Feb 27

The present study was designed to investigate whether microalbuminuria at the onset of diabetic nephropathy might be partially due to the glycation of serum albumin. It is postulated elsewhere (Ghiggeri et al., Proc. Eur. Dial. Transplant. Assoc. 21 (1984) 633-636) that the glycation of serum albumin and the subsequent cationization may induce microalbuminuria. To investigate whether a relationship exists between the amount of glycated albumin in its cationized form and the development, and progression of diabetic nephropathy, the urinary excretion of glycated albumin was studied in diabetic patients. The diabetic patients (type I and II diabetes) were divided into groups according to their albumin excretion rates: group I diabetics had a normal albumin excretion (n = 30, x = 4.2 mg/12 h); group II diabetes displayed microalbuminuria (n = 17, x = 38.6 mg/12 h); group III diabetics displayed macroalbuminuria (n = 21, x = 582.5 mg/12 h). The fraction of glycated albumin in serum (Glyco Gel Test Kit) was 0.032 in group I, 0.042 in group II, and 0.038 in group III, all these values were significantly higher than the value for the controls (0.014%; n = 17, 2 alpha = 0.001) as measured with the Glyco Gel Test Kit. The concentration of glycated albumin in the urine of the controls and group I was below the detection limit. Urine in group II contained only a glycated albumin fraction of 0.0002 of total albumin, and the fraction for group III was 0.0008. Isoelectric focussing (IEF) and chromato-focussing revealed native albumin with an isoelectric point of 4.7-4.9, and anionic glycated albumin with a pI of 3.0-4.2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glycation of serum albumin and its role in renal protein excretion and the development of diabetic nephropathy. 149 58

The renal selectivity properties towards albumin were evaluated in ten diabetic patients with arterial hypertension before and after the pharmacological normalisation of blood pressure, and were compared to 12 subjects with essential hypertension. While all patients of the control group were normoalbuminuric during hypertension, six of the diabetic group were microalbuminuric when hypertensive and became almost normoalbuminuric after blood pressure pharmacological control. All microalbuminuric diabetic patients presented altered properties of renal selectivity as epitomised by a non-preferential urinary excretion of glycosyl albumin (GA) (urinary GA/serum GA less than or equal to 1). At variance the selectivity properties were normal in normoalbuminuric diabetic patients and in essential hypertension. It was concluded that in diabetes mellitus arterial hypertension is associated with microalbuminuria when the renal properties of selectivity are altered, but does not implicate any proteinuric effect in those cases where the GBM function is preserved.
Nephrol Dial Transplant 1990
PMID:Hypertension and renal selectivity properties in diabetic microalbuminuria. 212 64

A novel enzyme-linked immunosorbent assay (ELISA [Dialbumin]) for rapid office measurement of microalbuminuria was evaluated and its performance compared with that of a commercially available radioimmunoassay (double-antibody albumin). Urine samples containing between 0.75 and 1800 micrograms/ml of albumin were obtained from 31 diabetic patients and assayed by both methods. A comparison of the paired values obtained from the two methods gave a correlation coefficient of greater than 0.99. The Dialbumin assay, which used detachable eight-well strips (1 strip/sample), 10-min incubation, tap water wash, and a 2-min color development step, was read on both an ELISA reader and a hand-held analytical device (Acc-U-Dial) designed specifically for this test. The findings of this study indicate that the Dialbumin assay, used in conjunction with the Acc-U-Dial device, affords a rapid, convenient, and sensitive method for quantitative determination of a broad range (0.3-1280 micrograms/ml) of urinary albumin levels in the office setting.
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PMID:Evaluation of new rapid office test for microalbuminuria and its comparison to fully quantitative radioimmunoassay. 220 4

We examined ten patients with type I diabetes mellitus and ten age- and sex-matched healthy controls. Median duration of diabetes was 7 years (range 0.5-24). None of the diabetic patients had hypertension, microalbuminuria, or proliferative retinopathy. Maximal specific binding capacity for angiotensin II to thrombocytes was significantly increased in diabetics (Bmax 11.9 +/- 1.6 sites per cell vs 7.0 +/- 0.9 in controls; P less than 0.01). In contrast, maximal binding for atrial natriuretic factor tended to be lower in type I diabetics (8.84 +/- 1.25 sites per cell vs 16.8 +/- 2.97; P less than 0.07). There was no difference of apparent dissociation constant (KD) for either receptor. Angiotensin II values (RIA) were greater in diabetics (16.2 +/- 1.5 pg/ml vs 8.5 +/- 1.4 in controls; P less than 0.02) and concentrations of atrial natriuretic factor (RIA) were not significantly different. The data suggest increased angiotensin II binding despite high angiotensin II concentrations in non-nephropathic type I diabetic patients. These findings may be relevant when considering the evolution of hypertension and microangiopathy lesions.
Nephrol Dial Transplant 1989
PMID:Specific binding of angiotensin II and atrial natriuretic factor in non-nephropathic type I diabetes mellitus. 252 55

Urinary enzymes were determined in a controlled study including 28 type I diabetes mellitus patients. Fifteen patients had persistent microalbuminuria and were compared to 13 normoalbuminuric patients with comparable age and sex distribution. All patients had normal renal function as measured by serum creatinine. Human intestinal alkaline phosphatase (hIAP), a specific marker of the proximal tubular S3 segment, was elevated in the urine of microalbuminuric patients while human tissue non-specific alkaline phosphatase (hTNAP), indicating effects mainly at the S1-S2 segments, was not. Urinary hIAP was correlated with serum glycated haemoglobin. These results suggest that tubular alterations are present at an early stage of diabetic nephropathy, especially at the S3 segment, and that hIAP may have promise as an early marker.
Nephrol Dial Transplant 1994
PMID:Human urinary intestinal alkaline phosphatase as an indicator of S3-segment-specific alterations in incipient diabetic nephropathy. 808 50

A cohort of 227 untreated essential hypertensive patients from north-western Italy was studied in order to evaluate the prevalence of micro- and macroalbuminuria and their relationship with other cardiovascular risk factors. Albuminuria was evaluated as the albumin to creatinine ratio (Alb/Cr) in three non-consecutive first morning samples. The prevalence of microalbuminuria and macroalbuminuria was 10% and 2.2%, respectively. Albuminuric patients showed higher blood pressure, serum creatinine, triglycerides and uric acid as well as a greater prevalence of retinopathy. Stepwise multiple regression analysis demonstrated that only a small part of variations in albuminuria was explained by changes in blood pressure. Duration of disease did not seem to influence microalbuminuria. The presence of hypertensive retinopathy was associated with greater albuminuria, longer duration of hypertension, and higher prevalence of major ECG changes, but not with higher blood pressure levels. Microalbuminuria, rather than a consequence of elevated blood pressure levels, seems to be a marker of a syndrome featuring, among other characteristics, essential hypertension. Furthermore, microalbuminuria must be considered as an independent cardiovascular risk factor.
Nephrol Dial Transplant 1995
PMID:Prevalence of micro- and macroalbuminuria and their relationship with other cardiovascular risk factors in essential hypertension. 852 98

This study was conducted to determine whether circulating levels of lipoprotein (a), an independent risk factor of macrovascular disease, are increased in non-insulin-dependent diabetes mellitus (NIDDM) patients with microalbuminuria who have an increased risk of cardiovascular mortality. Apolipoprotein (a) [apo(a)] levels and phenotypes, and other circulating lipid levels were determined in 227 Chinese NIDDM patients with varying stages of diabetic nephropathy. None was on lipid-lowering therapy. Apo(a) levels in normoalbuminuric (geometric mean 166 U/L; 95% confidence intervals 137, 200; n = 105) and microalbuminuric patients (162; 132, 209; n = 77) were similar to values in controls (166; 143, 193, n = 168). Albuminuric patients, however, had higher apo(a) levels than both normoalbuminuric patients and controls (242; 184, 317; n = 45; P < 0.05). The overall size range of the apo(a) phenotypes and the frequency of having at least one small isoform, i.e. < 700 kDa, were similar among the four groups of subjects. A positive correlation was found between log apo(a) and log plasma creatinine levels (P < 0.01). Compared to normoalbuminuric patients, both microalbuminuric and albuminuric patients were older (P < 0.01) and had higher HbA1c (P < 0.01), greater BMI (P < 0.05) and longer disease duration (P < 0.05) compared to normoalbuminuric patients. Nevertheless, using multiple linear regression analysis, it was found that the presence of nephropathy conferred an independent influence on increasing total cholesterol (P < 0.001), triglyceride (P < 0.001) and apoB (P < 0.01), and decreasing HDL cholesterol (P < 0.05) levels even when only the normoalbuminuric and microalbuminuric groups were analysed. The prevalence of macrovascular disease was significantly increased in microalbuminuric and albuminuric patients (45.1 and 48.7% respectively vs 20.2% in normoalbuminuric patients, P < 0.01). It is concluded that circulating apo(a) levels were not increased in Chinese NIDDM patients with microalbuminuria. However, atherogenic changes in other lipid and lipoprotein levels may contribute to an increased risk of macrovascular disease in these patients.
Nephrol Dial Transplant 1996 Nov
PMID:Apolipoprotein (a) levels and phenotypes in NIDDM patients with microalbuminuria and albuminuria. 894 83

In white Europeans, renal size and function decline with age. This phenomenon has long been attributed to nephrosclerosis, i.e. primary vascular lesions associated with glomerular obsolescence, tubulointerstitial lesions and fibrosis. The part played by ageing and by pre-existing hypertension is still a matter of debate. Nephrosclerosis is a diagnosis of exclusion when no renal histology is available. As renal biopsy is rarely carried out in an elderly patient with atrophic kidneys, a long history of hypertension and only microalbuminuria or no proteinuria, the diagnosis of nephrosclerosis is generally overestimated. Even when renal histology is available, only subtle differences in vascular lesions have been claimed to distinguish those due to ageing from those due to hypertension. At any rate, meticulous control of blood pressure is certainly the most efficient means of protecting the renal vessels from further deterioration. Atheromatous renal disease has more recently been recognized as a major cause of progressive renal failure in the elderly. Renal artery stenoses due to atheromatous plaques might well be the cause of 10-15% of end-stage renal failure in whites aged > 50 and be the fourth cause of uraemia in this age group. Such stenoses are usually bilateral and developing. Present imaging methods, such as duplex ultrasound scanning and renal scintigraphy, are valuable means of diagnosis. Renal angioplasty can halt the the pace of renal insufficiency, or even durably improve it in nearly half of the cases. Finally, aorto-renal atheroma is a common and underestimated cause of cholesterol embolism. Minor, spontaneous forms thereof are indistinguishable from nephrosclerosis. Massive embolism entails a dismal prognosis, in terms of both renal function and patient survival. In conclusion, renal vascular lesions in the elderly remain a major concern. Improving non-invasive diagnostic procedures and applying preventative as well as curative measures should significantly reduce the incidence of end-stage renal disease is such patients.
Nephrol Dial Transplant 1996
PMID:Renal vascular lesions in the elderly: nephrosclerosis or atheromatous renal disease? 905 35


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