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)

Recent studies utilizing converting enzyme inhibitors (CEI) in diabetic rats document reductions in both renal hypertrophy and albuminuria. Four separate clinical studies in normotensive patients with diabetes demonstrate reduction of microalbuminuria with CEIs independent of blood pressure reduction. The present pilot study examines the results of reducing an elevated glomerular filtration rate on changes in renal size and microalbuminuria in normotensive, hyperfiltering insulin-dependent diabetic (IDDM) patients. Fifteen IDDM patients were randomized to either placebo or the CEI, lisinopril. Dosage of lisinopril was titrated over 3 months to reduce glomerular filtration rate (GFR) to < or = 2.33 mL/sec. Evaluation at 18 months demonstrated the lisinopril group had a marked reduction in renal size (16.9 +/- 1.1, baseline versus 12.8 +/- 0.9 cm, 18 months; p < 0.05) and microalbuminuria (92 +/- 11 micrograms/min, baseline versus 23 +/- 26 micrograms/min, 18 months; p < 0.05). No change in renal size was noted in the placebo group (15.4 +/- 0.8, baseline versus 14.9 +/- 0.7 cm, 18 months; NS) and albuminuria increased (118 +/- 15 micrograms/min, baseline versus 293 +/- 32 micrograms/min, 18 months; p < 0.05). Mean arterial pressure at 18 months was significantly lower in the lisinopril group compared to placebo (102 +/- 4, placebo versus 87 +/- 6 mm Hg, CEI, p < 0.05). This study supports previous animal studies that document reductions in both microalbuminuria and renal size by a CEI. The overall impact of these findings on preservation of renal function cannot be assessed, however, in this short-term study.
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PMID:ACE inhibitor mediated reductions in renal size and microalbuminuria in normotensive, diabetic subjects. 816 83

The EURODIAB IDDM complications study is a multicenter clinical study for evaluation of the prevalence of microvascular, macrovascular and acute metabolic complications in randomly selected samples of insulin-dependent diabetic patients attending 31 European diabetes centers. A total of 3250 patients were studied (mean age: 32.7 +/- 10 years, mean duration of diabetes: 14.7 +/- 9.3 years) by standardized, validated methods. The third medical department of the Vienna-Lainz hospital participated from Austria. 122 patients, age: 34.9 +/- 9.9 years, duration of diabetes: 16 +/- 10 years were recruited from this center. There was a wide variation in the frequency of complications between the different European centres: Prevalence of diabetic retinopathy 25-60%; Vienna showed the lowest prevalence (25%). Metabolic control (HbA1c) ranged from 5.7-9.4%; Vienna shared the second place with two other centers (6.0%). Despite the very low HbA1c in the Viennese population, the frequency of severe hypoglycemic attacks was in the lower range, which is an extraordinary result in this study. Incipient diabetic renal disease, characterized by microalbuminuria varied in frequency between 15 and 33% (Vienna 23%). Important associations of raised blood pressure (frequency in all centers: 8-41%, Vienna: 29%) with renal disease and retinopathy have implications for the initiation of preventive measures. The data on diabetic complications obtained from the EURODIAB study permit a comparison between the different European centers and emphasize the need for implementation of the St. Vincent recommendations.
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PMID:[Insulin-dependent diabetes mellitus:"EURODIAB IDDM Complications Study"--results from the Vienna center]. 817 69

The prevalence of microalbuminuria was studied in a clinic population of patients with insulin-dependent diabetes mellitus [IDDM] with disease duration longer than 5 years. 75 patients were included in the study, 23 patients (30.7%) had microalbuminuria and 2 patients (2.7%) had macroalbuminuria. Comparison of the clinical and laboratory characteristics of patients with microalbuminuria (n = 23) to patients with normoalbuminuria (n = 50) showed no differences with respect to age, duration of diabetes, blood pressure, presence of retinopathy and glycosylated haemoglobin. The mean glomerular filtration rate (GFR) was higher in the microalbuminuric group than in the normoalbuminuric group (125 +/- 45 ml/min compared to 99 +/- 32 ml/min; P < 0.05). In a multiple regression model excluding patients with macroalbuminuria the following predictors of albumin excretion rate (AER) were identified: systolic blood pressure, glycosylated haemoglobin and GFR. Since microalbuminuria is common in Irish patients with IDDM, we suggest that AER should be determined as part of the annual routine screen. Stricter control of blood pressure and glycaemia should be considered.
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PMID:The prevalence of microalbuminuria and associated risk factors in a population with insulin-dependent diabetes mellitus. 824 55

Most aspects of the nutritional therapy of diabetes mellitus apply equally to IDDM and NIDDM patients and are also appropriate for people with high risk of cardiovascular diseases. A restriction of energy, a reduction of saturated fatty acids as well as of alcoholic drinks and simple sugars are the most important measures. This modification of nutritional intake together with increased fibre consumption is not only appropriate to avoid hyperglycaemia in diabetic patients but has also its benefits in patients presenting with the metabolic syndrome (possible reduction of hyperinsulinaemia, hypertension and hyperlipoproteinaemia). Diabetic patients should have regular screening for microalbuminuria. At first signs of an early stage of nephropathy patients should be advised to restrict their protein intake. About 50% of daily energy intake should be derived from carbohydrates and fat intake should be no more than 35% of total energy (saturated fatty acids less than 10% of energy). Carbohydrate exchange units are usually not necessary in NIDDM patients. In addition diabetes specialty foods are not an essential part of the nutritional therapy. The success of the nutritional therapy in diabetic patients is substantially dependent upon qualified counselling and education of the patients by the physician (as far as possible with the assistance of a dietitian).
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PMID:[Nutritional therapy in diabetes mellitus]. 847 34

On the whole, diabetic microangiopathy can be understood as the clinical renal-retinal syndrome. About 10% of all diabetics die of end-stage renal failure, more frequent in IDDM. With an incidence of 14% diabetic retinopathy is one of the major causes of blindness in adulthood. In the non-proliferative state, the pathological changes are limited to the retina, whereas the alterations affect both retina and vitreous in the proliferative state. Photocoagulation is the treatment of choice. If photocoagulatory treatment is not possible because of cataract, vitreous surgery (pars-plana vitrectomy) could improve visual prognosis. The clinical features hypertension, proteinuria and finally renal failure define the term "diabetic nephropathy". The increased intraglomerular pressure is the main pathological alteration of incipient nephropathy. Microalbuminuria essentially determines the prognosis: in IDDM it concerns the incidence of a manifest nephropathy, in NIDDM the excessively increased incidence of cardiovascular mortality. Sonographically, the kidneys are large with bright and wide parenchyma. Along with the development of end-stage renal disease the kidney size diminishes. According to Mogensen, nephropathy is divided into five stages: Stage 1, the early stage, is defined by hypertrophy and hyperfiltration. Stage 2 shows incipient structural changes without any clinical findings. Stage 3 is characterised by persistent microalbuminuria. Stage 4 leads to increasing renal failure and stage 5 to end-stage renal disease and the necessity of dialysis treatment. Incipient nephropathy demands a strict treatment of both hypertension and diabetes. In the meantime, ACE inhibitors are the treatment of choice. In case of dialysis treatment continuous ambulant peritoneal dialysis (CAPD) is usually preferred.
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PMID:[Diabetic microangiopathy]. 847 38

On the basis of the available data (much of which is contradictory), I suggest that the following might summarize the role of Lp(a) in diabetes currently. 1. Lp(a) in IDDM: Concentrations are probably elevated. Concentrations are probably related to metabolic control. Concentrations are increased with microalbuminuria. 2. Lp(a) in NIDDM: Concentrations are not elevated. Concentrations do not change with metabolic control. Too few data exist to make an assessment of relation of Lp(a) to microalbuminuria in NIDDM. 3. Lp(a) and CHD in diabetes: Little current evidence shows that Lp(a) is a risk factor for CHD in diabetes. More studies--especially prospective studies with larger numbers of subjects--need to be done.
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PMID:Lipoprotein(a) and diabetes. An update. 849 27

Epidemiological data implicate puberty as a factor in the initiation of diabetic nephropathy. However, the mechanism remains unclear. We hypothesized that puberty would result in an increase in glomerular hypertrophy and hypertension; these two early concomitant events are seen as pivotal to the pathophysiology of diabetic nephropathy. We studied the effect of pubertal duration on three surrogate markers of glomerular hypertrophy/hypertension: kidney volume (KV), microalbuminuria (MA), and Na-Li countertransport (CT). We recruited 177 subjects (87 female and 90 male; aged 6.2-22.1 years) with IDDM of 5 to 10 years' duration (6.8 +/- 1.6 years) into three groups with different pubertal duration: prepubertal since IDDM diagnosis; prepubertal at diagnosis, now pubertal; or early puberty at diagnosis, now postpubertal. KV was measured by ultrasound and corrected for body surface area; MA was defined as urinary albumin excretion of 15-200 micrograms/min in two of three 24-h samples, and Na-Li CT was measured in erythrocytes. As pubertal duration increased, there was a disproportionate increase in mean KV (prepubertal, 247 +/- 6 [SE] ml/1.73 m2; pubertal, 282 +/- 7/1.73 m2; postpubertal, 295 +/- 7/1.73 m2, P = 0.001), prevalence of nephromegaly (KV > 300 ml/1.73 m2) (14, 31, and 45%, respectively, P = 0.001), and prevalence of MA (0, 9.7, and 20.5%, respectively, P = 0.003). Subjects with KV > 300 ml/1.73 m2 were eight times more likely to have MA than those with KV < 300 (odds ratio 8.1, 95% confidence interval 2.4-27.4, P = 0.0001). There was no effect of pubertal duration on Na-Li CT. Multiple regression with KV as the dependent variable found an association with pubertal duration, MA, Na-Li CT, and current HbA1c (P < 0.0001). Our findings indicate that pubertal duration is an important determinant of both KV and MA and suggest that nephromegaly precedes microalbuminuria. We postulate that these effects are attributable to the influence of the pubertal milieu on glomerular hypertrophy/hypertension.
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PMID:Effect of puberty on markers of glomerular hypertrophy and hypertension in IDDM. 852 59

Over the past two decades there has been an increasing interest in hypertension as a risk factor for diabetic renal disease and in particular for the possibility of early antihypertensive intervention. Therefore, it would seem timely to review the history of hypertension in diabetes, with special reference to renal disease and the need for normotension, in a manner resembling glycaemic control. Elevated blood pressure (BP) associated with diabetes mellitus has been recognized since the beginning of the century and was initially particularly documented in association with the demonstration of the striking histological lesion in glomeruli, starting with the observation of Kimmelstiel and Wilson in 1936. These patients in many cases also showed hypertension, as confirmed in several subsequent reports, very similar to the studies of Kimmelstiel and Wilson. However, the development was hampered by the lack of effective antihypertensive agents and also by some who believed that elevated BP could be of importance to preserve renal function in these individuals. Indeed, it was suggested that reduction of BP could mean permanent deterioration in renal function. BP remained very high in the standard care of diabetic patients up to the middle 1970s. At this time it was documented that elevated BP was very closely related to development of diabetic renal disease in Type 1 (insulin-dependent) diabetic (IDDM) patients, and studies also showed a correlation between blood pressure and rate of progression. This correlation stimulated research in intervention, and indeed in the 1980s and 1990s several long-term studies reported that antihypertensive treatment can reduce the rate of decline in glomerular filtration rate (GFR) from about 12 ml min-1 yr-1 down to about 2 ml min-1 yr-1 in the most optimistic reports; usually a mean level of 2-5 ml min-1 yr-1 is achievable by antihypertensive treatment, in clinical situations where glycaemic control often is far from perfect. Many studies have also documented that BP starts to rise in the early phase of incipient diabetic nephropathy characterized by microalbuminuria. This is a stage with well-preserved GFR and therefore probably an ideal stage for intervention in these at risk patients. Many studies, in particular those employing angiotensin converting enzyme (ACE) inhibitors based on important pathophysiological concepts proposed by Brenner, have shown that microalbuminuria can be reduced or stabilized by early antihypertensive treatment, just as we see with optimized glycaemic control. ACE inhibitors have also been widely used in patients with overt nephropathy and the rate of decline in GFR has been reduced considerably.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diabetic renal disease: the quest for normotension--and beyond. 854 35

Microalbuminuria in both insulin-dependent (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) is a marker for insulin resistance. Microalbuminuria is also associated with hypertension, itself an insulin-resistant state. Therefore, in order to examine the independent relationships of microalbuminuria with blood pressure and insulin resistance, we measured ambulatory blood pressure (Takeda TM-2420), insulin resistance (modified Harano method), and urinary albumin excretion rate (overnight urine collection) in 36 subjects with NIDDM. Albumin excretion correlated with 24-h systolic blood pressure (r = 0.49, p = 0.003), and insulin sensitivity (r = -0.39, p = 0.007). Microalbuminuric subjects had reduced insulin sensitivity compared with normoalbuminuric subjects [Mean (SD) 2.95 (0.33) versus 4.67 (0.56) ml.kg-1.min-1; p = 0.013]. In multivariate analysis including ambulatory blood pressure and insulin resistance, urinary albumin excretion was associated primarily with insulin resistance, with smaller contributions from glycated hemoglobin and male gender. These data suggest that microalbuminuria in NIDDM, although associated with hypertension, is also independently associated with insulin resistance.
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PMID:Insulin resistance in non-insulin-dependent diabetes mellitus is associated with microalbuminuria independently of ambulatory blood pressure. 857 34

Urinary excretion of heparan sulphate proteoglycan (HSPG), the main anionic component of the glomerular basement membrane (GBM), was estimated in 30 adolescents and young adults with insulin dependent diabetes (IDDM), 10 with microalbuminuria and 20 sex matched, diabetic controls of similar age without evidence of microalbuminuria. A further 10 non-diabetic control subjects were also examined. Both groups of patients with diabetes had significantly elevated excretion of HSPG when compared to normal individuals. There was no difference in HSPG excretion between diabetic subjects with and without microalbuminuria.
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PMID:Urinary heparan sulphate proteoglycan excretion is abnormal in insulin dependent diabetes. 857 88


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