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

Diabetes mellitus can lead, along the years of its course, to chronic renal failure in a high proportion of cases. An early risk-indicator of later diabetic nephropathy is the presence of microalbuminuria, but it usually takes about fifteen to twenty years to appear. Before that, no clinical signs can disclose the underlying alterations of glomerular basement membrane that will eventually bring forth overt nephropathy. The usefulness of the altered excretion of isoenzymes of amylase as an early marker of the glomerular charge selectivity was tested in 202 juvenile onset insulin-dependent diabetics, compared with 51 normal subjects matched for age and sex. The diabetic patients studied showed increased excretion of salivary amylase into urine. The salivary to pancreatic amylase ratio of concentrations in urine was always below 1 in normal subjects, and was increased over 1 in 33.2% of diabetics, although microalbuminuria was present only in 26.2% of patients. The excretion of other proteins was within reference values in the majority of cases, indicating that the kidney was not seriously affected in those patients. Moreover, the altered salivary to pancreatic amylase ratio in urine was more prevalent than microalbuminuria (36.6% vs 18%) in the first decade of the evolution of the diabetes. These results indicate that the ratio of excretions of both isoamylases into urine is a more sensible and earlier marker of altered glomerular charge barrier for anionic proteins.
 ...
PMID:Utility of filtration markers to monitor the quality of glomerular function. 128 36

We report the case of an elderly black woman with a 20-year history of insulin-independent diabetes mellitus (IDDM), chronic renal failure, hypertension, proliferative retinopathy, and classical histologic features of diabetic glomerulosclerosis on renal biopsy. Repeat determinations of urinary albumin excretion rates failed to disclose significant microalbuminuria. This presentation should remind the clinician that a small minority of patients with IDDM of long duration may have severe diabetic glomerulosclerosis and renal insufficiency without detectable microalbuminuria.
 ...
PMID:Diabetic glomerulosclerosis and chronic renal failure with absent-to-minimal microalbuminuria. 162 84

It is recognized that diabetic patients with nephropathy frequently have macrovascular disease leaving them at risk of ischaemic foot lesions. In order to assess non-vascular risk factors for foot ulceration 64 patients were stratified into four groups: microalbuminuria, albuminuria with creatinine clearance greater than 40 ml min-1, chronic renal failure (clearance less than 40 ml min-1), and a non-nephropathic diabetic control group. Vibration perception threshold was measured by biothesiometry, peroneal nerve conduction velocity by conventional methods, and dynamic foot pressure by pedobarography. Vibration perception threshold was elevated in all three groups when compared with age-matched normal and diabetic control groups. Mean vibration perception threshold was 20.8 +/- 8.6 (+/- SD) in the microalbuminuria group (p less than 0.001 compared with age-matched normal control group), 28.1 +/- 5.6 (p less than 0.001) in the albuminuria group, 38.9 +/- 9.4 (p less than 0.001) in the renal failure group, 14.8 +/- 5.2 in the diabetic control group and 12.3 +/- 2.9 in the normal control group. Peroneal motor conduction velocity was reduced in all three groups when compared with normal control subjects, microalbuminuria 38.6 +/- 4.2 m s-1 (p less than 0.001), albuminuria 38.0 +/- 6.1 m s-1 (p less than 0.01), renal failure 35.5 +/- 1.2 m s-1 (p less than 0.001), diabetic control 40.6 +/- 1.8 m s-1, and normal 43.1 +/- 2.3 m s-1.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Risk factors for non-ischaemic foot ulceration in diabetic nephropathy. 182 36

Angiotensin converting enzyme (ACE) inhibitors are well established in the treatment of hypertension and cardiac failure. Experimental studies in rats have suggested that these agents may protect renal function in chronic nephropathy by a mechanism other than simply lowering the systemic blood pressure. In human studies of incipient diabetic nephropathy, worsening of microalbuminuria was prevented during 3 years of ACE inhibition. ACE inhibitors reduce arterial blood pressure in chronic nephropathy, and may cause a fall in glomerular filtration rate. In diabetic nephropathy, proteinuria was reduced by 2 months' treatment with enalapril to less than half of the values obtained in a control group treated with metoprolol. Nonrandomised trials have suggested that ACE inhibitors may slow the deterioration of renal function, but no comparisons with other antihypertensive agents in prospective studies have been published to date. In chronic renal failure, ACE inhibitors may worsen anaemia and hyperkalaemia. Renovascular hypertension can be treated with ACE inhibitors, but the treatment may lead to a compromised renal function. The dosage of these drugs should be reduced in renal failure and therapy should be started cautiously in this setting, with close monitoring of blood pressure, renal function and plasma potassium.
 ...
PMID:Angiotensin converting enzyme (ACE) inhibitors and renal function. A review of the current status. 193 Jul 42

It is well known that 30 to 50% of patients with Type I Diabetes develop nephropathy and that chronic renal failure, it's final pathway, is the main cause of death. Assessment of urinary albumin becomes an essential tool for identifying the population at risk of developing nephropathy, to study its physiopathologic mechanisms and to evaluate the response to therapeutic trials. The present article is a preliminary report on the study of urinary albumin excretion rate (AER) in a pediatric population with Type I Diabetes and its relation to teh duration of the disease. A RIA technique with double antibody was developed for albumin assessment, with a displacement range of 1 to 300 ng/tube. Urine samples were collected during short periods with water load as suggested by Mogensen. Thirty nine children (30 patients and 9 controls) free of renal disease and with normal blood pressure were studied. Patients were divided according to duration of the disease in: Group I: less than 5 years, Group II: 5 to 10 years and Group III: more than 10 years. Results (mean +/- SD) in micrograms/min/1.73 m2 were: Control Group (n = 9) 4.30 +/- 2.53, GI: (n = 12) 10.44 +/- 9.47, GII (n = 10) 8.03 +/- 7.27 and GIII (n = 8) 8.56 +/- 4.26. The mean value of the Control Group (+3 SD) 12 micrograms/min/1.73 m2, was considered as the upper normal limit. Thus, 16.6%, 40%, and 12.5% of children in Groups I, II and III had microalbuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Diabetic nephropathy in children: study using the amount of urinary albumin]. 263 Aug 69

Persistent Albustix-positive proteinuria and subsequent chronic renal failure are frequently encountered in insulin-dependent diabetes mellitus (IDDM). Rates of decline of renal function may be modified by treatment of accompanying hypertension, but studies of the effects of long-term continuous subcutaneous insulin infusion (CSII) on deterioration of renal function provide no statistically significant evidence of benefit of near-normoglycemia. However, short-term studies in IDDM subjects with negative Albustix tests but subclinically raised levels of albumin excretion rate (AER) have shown that treatment with CSII significantly reduces this microalbuminuria. The prospective, controlled 8-mo Kroc Collaborative Study therefore offered the opportunity of examining more protracted effects of CSII-induced metabolic correction upon microalbuminuria. Twenty-four-hour urine collections obtained at baseline, 4, and 8 mo were available from 59 Albustix-negative patients. Beta 2-microglobulin excretion was normal. The 39 normoalbuminuric (AER less than 12 micrograms/min) patients did not differ from the 20 microalbuminuric (AER elevated between 13.2 and 192.6 micrograms/min) with respect to distributions of age, sex, and duration of diabetes. In both the normoalbuminuric and the microalbuminuric groups studied at 4 and 8 mo, percent glycosylated hemoglobin (%HbA1) and mean blood glucose were significantly decreased during CSII compared with baseline values, whereas no change occurred in the group continuing their conventional insulin therapy (CIT). AER did not differ between CIT and CSII treatments in the normoalbuminuric group. AER fell significantly in the CSII-treated microalbuminuric patients at 4 (P less than 0.05) and 8 (P less than 0.01) mo but showed no consistent change in the CIT microalbuminuric group.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Eight-month correction of hyperglycemia in insulin-dependent diabetes mellitus is associated with a significant and sustained reduction of urinary albumin excretion rates in patients with microalbuminuria. 401 22

To investigate the role of vitronectin in the progression of diabetic nephropathy, plasma concentrations of vitronectin were measured by enzyme-linked immunosorbent assay in patients with diabetes mellitus and compared with normal control subjects. In diabetic patients with normoalbuminuria and microalbuminuria, plasma concentrations of vitronectin were significantly higher than those of control subjects. Plasma concentrations of vitronectin in diabetic patients with chronic renal failure were significantly lower than those with normal renal function. There was a significant positive correlation between plasma concentration of vitronectin and blood platelet counts. In the early stage of diabetic nephropathy, vitronectin may be increased caused by synthesis from activated platelets. With progression of diabetic nephropathy, plasma vitronectin may be decreased because of accumulation in sclerotic glomeruli and arteriosclerotic lesions. In conclusion, the plasma concentration of vitronectin appears to be an important marker for the progression of diabetic nephropathy.
 ...
PMID:Changes in plasma concentrations of vitronectin in patients with diabetic nephropathy. 752 68

Patients with diabetes mellitus are at increased risk of coronary, cerebral, and peripheral vascular disease, and frequently have abnormal plasma lipid levels. Glycaemic control, environmental factors and inherent genetic potential may affect lipoprotein metabolism. Quantitative alterations in the concentrations of major lipids and lipoproteins have been extensively studied in both insulin-dependent diabetes mellitus and non-insulin-dependent diabetes mellitus. However several recent findings indicate the possible presence of structural and functional abnormalities that may impair the lipid metabolism transport system in diabetic patients. These include glycation of several major or minor apolipoproteins, apo E phenotype frequency, free cholesterol or triglyceride enrichment of VLDL and LDL. Moreover lipoprotein (a) which is an independent risk factor for coronary heart disease may be increased in diabetic patients with poor glycaemic control or with microproteinuria. Patients with microalbuminuria or chronic renal failure show atherogenic changes of lipoprotein pattern. New epidemiological evidence indicates that hypertriglyceridaemia is an important predictor of coronary heart disease mortality in subjects with impaired glucose tolerance or diabetes. Postprandial lipaemia can increase the risk of cardiovascular disease potentially by low triglyceride metabolic capacity. The role of insulin must also be considered. Some lipoprotein abnormalities could be attributed to peripheral hyperinsulinaemia, insulin resistance or type of insulin infusion for insulin-dependent diabetes mellitus patients. In diabetes lipids and lipoproteins are potentially atherogenic although their concentrations may be strictly normal. The achievement of optimum lipid and lipoprotein levels as a goal of treatment for diabetic patients would reduce the current rates of morbidity and mortality from vascular disease.
 ...
PMID:[Hyperlipidemia during diabetes mellitus. Recent developments]. 814 78

Reflux nephropathy is an important cause of chronic renal failure in children. After the parenchymal scar, the progression is thought to be mediated by glomerular hypertension in remnant nephrons resulting in modifications in permselectivity to macromolecules. Proteinuria correlates with a progressive course. The glomerular permselectivity to macromolecules in basal conditions and after acute hemodynamic stress was investigated in 28 children whose bilateral vesico-ureteric reflux (VUR) had been previously surgically corrected (meanly 5.6 years before) and with normal creatinine clearance (CrCl). Bilateral renal scarring (0 to 8 scale for both kidneys) was 4.3 +/- 1.6. Albuminuria (UAE) was evaluated in basal conditions and under acute hyperfiltration induced by amino acid (Aa) infusion. After isotonic saline at 310 ml/hour/1.73 m2, 6 mg/kg/min of Aa were infused for 2 hrs. UAE was significantly higher than controls in basal conditions (p < 0.01), and further increased after Aa infusion (p < 0.02). Microalbuminuria was detectable in 53.5% of the children in basal conditions and in 64.3% after Aa. Also urinary beta 2 microglobulin significantly increased at the end of the test (p < 0.001). CrCl significantly increased at the first hour (p < 0.05). Children with severe renal parenchymal scarring had greater UAE (p < 0.01) and beta 2M (p < 0.02) values after provocative test than those with mild renal damage. In 8 children GFR and ERPF were measured by means of inulin and p-hippurate clearance respectively. The variations in UAE during Aa infusion were significantly correlated with GFR dynamics (p < 0.05) while they were not influenced by ERPF modifications.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Glomerular permselectivity to macromolecules in reflux nephropathy: microalbuminuria during acute hyperfiltration due to aminoacid infusion. 829 36

Extensive ablation of renal mass in experimental animals leads to progressive glomerulosclerosis and chronic renal failure (CRF). Clinical studies are far from answering the question whether patients with reduced renal mass are at risk of developing progressive CRF. The aim of our study was to examine the morphological and functional aspects of the remnant kidney in a group of patients who underwent unilateral nephrectomy for renal tuberculosis: 313 patients (161 M, 152 F) mean age 57.2 +/- 10.7, were examined after a period ranging from 13.56 to 591.2 months. All patients were on ad libitum diet. Hypertension was found in 34.19% of the patients; SBP was 155.29 +/- 19.9 mmHg and DBP was 92.74 +/- 13.07 mmHg. Estimation of renal size performed by ultrasound scanner gave the following results: length 116.78 +/- 8.99 mm; width 58.24 +/- 7.21 mm; thickness 17.88 +/- 1.96 mm. Kidney function assessed by serum creatinine levels showed a mean level of 1.28 +/- 0.53 mg%. Forty-two patients (13.41%) had serum levels > 1.5 mg% but 18 of them had nonconcomitant systemic or renal involvement. Microalbuminuria determined by RIA assay was found in 50.5% of the patients. In our group of patients renal functional impairment was low and hyperfiltration expressed as microalbuminuria does not appear to be a primary factor in the progression of renal failure.
 ...
PMID:Unilateral nephrectomy and progression of renal failure. 851


1 2 3 4 5 Next >>