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)

Adiponectin is produced exclusively by adipocytes, and its serum concentration is inversely associated with adiposity. This study examines the relationship among diabetes, renal function, and serum adiponectin in Pima Indians. Serum adiponectin was measured in 1069 people in whom glycemia and renal function had been measured. Serum adiponectin, adjusted for age, sex, and body mass index, was lowest in those with impaired glucose regulation or diabetes of less than 10 yr duration and highest in those with normal glucose tolerance or diabetes of duration of at least 10 yr. Both urinary albumin to creatinine ratio (ACR) and serum creatinine were positively correlated with adiponectin (Spearman's r = 0.43; P < 0.0001, and r = 0.37; P < 0.0001, respectively) in diabetic subjects. After stratification by albuminuria (normoalbuminuria ACR < 30 mg/g, microalbuminuria ACR = 30-299 mg/g, and macroalbuminuria ACR >or= 300 mg/g), the highest adiponectin concentration was in the macroalbuminuria group (geometric mean = 9.6 microg/ml) and the lowest was in the normoalbuminuric group (geometric mean = 5.6 microg/ml). After adjustment for age, sex, body mass index, and diabetes duration, the serum adiponectin concentration in the macroalbuminuria group was significantly higher than in both other groups (P < 0.0001). Serum adiponectin is lowest in the presence of impaired glucose regulation and early diabetes. In the presence of diabetes, serum adiponectin is positively associated with abnormal renal function and diabetes duration.
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PMID:Adiponectin concentrations are influenced by renal function and diabetes duration in Pima Indians with type 2 diabetes. 1529 42

A single-nucleotide polymorphism (SNP) G276T in the adiponectin gene has been associated with lower plasma adiponectin levels and insulin resistance, which are related to the prevalence of type 2 diabetes or diabetic complications of macroangiopathy. We performed a case-control study to examine whether the SNP276 of the adiponectin gene was also related to early diabetic nephropathy. SNP276 was examined with genomic DNA obtained from 108 type 2 diabetic patients with microalbuminuria (urinary albumin creatinine ratio [ACR] between 30 mg/g x Cr and 300 mg/g x Cr; case subjects), and 208 patients with normoalbuminuria (ACR < 30 mg/g x Cr; control subjects). The genotype distribution and G allele frequency of SNP276 in the case subjects (0.71) did not significantly differ from the control subjects (0.69). There were no differences among the genotypes of the adiponectin gene regarding age, duration of diabetes, body mass index (BMI), hemoglobin A(1c) (HbA(1c)), serum lipids, serum creatinine, and plasma adiponectin levels. These data suggest that SNP276 of the adiponectin gene is not an independent risk factor for incipient diabetic nephropathy in Japanese type 2 diabetic patients.
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PMID:Adiponectin gene polymorphism (G276T) is not associated with incipient diabetic nephropathy in Japanese type 2 diabetic patients. 1533 88

Insulin resistance is a principal underlying defect in type 2 DM along with beta-cell dysfunction, and this insulin resistance underpins many of the abnormalities associated with the metabolic syndrome. Peroxisome-proliferator-activated receptor gamma agonists (PPARgamma agonists), also known as glitazones or thiazolidinediones (TZDs) are powerful insulin sensitisers with recent evidence suggesting that they also have a potential to improve pancreatic beta-cell function. TZDs cause a major redistribution of body fat with a decrease in visceral and hepatic fat content with a resultant increase in insulin sensitivity. The glucose lowering effects of TZDs are similar to those seen with the well-established sulphonylureas and metformin. TZDs have a small reducing effect on blood pressure and have been shown to reduce microalbuminuria independent of their blood glucose lowering effect. Both TZDs in clinical practice, pioglitazone and rosiglitazone, reduce small dense LDL-cholesterol and increase HDL-cholesterol levels but pioglitazone would appear to have a more pronounced benefit on these two parameters with a greater reduction in plasma triglycerides. TZDs improved the pro-coagulant state and show benefits in improving endothelial dysfunction and reducing 'non-traditional' inflammatory cytokines and increasing adiponectin levels. The greatest benefit for the TZDs is to directly influence atherogenesis itself and the potential that these so-called pleiotrophic effects of TZDs to reduce cardiovascular events in type 2 DM will be tested when the results of outcome trials are published in the next few years. If the results are positive for the reduction in vascular end-points, then TZDs will represent a major advance in improving the prognosis of type 2 DM subjects with the metabolic syndrome.
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PMID:The Clinical Significance of PPAR Gamma Agonism. 1589 54

Microalbuminuria, and recently, hypoadiponectinemia, have been associated with progression of atherosclerotic disease and increased cardiovascular risk. We examined the possible associations of urinary albumin excretion, expressed as the ratio of albumin to creatinine (ACR), with plasma adiponectin and high-sensitivity C-reactive protein (hs-CRP) levels in men who had essential hypertension. The study population consisted of 108 men who did not have diabetes and were newly diagnosed with stage I to II essential hypertension (age 44.6 years, office blood pressure 148/95 mm Hg) and 110 men matched according to age and body mass index as controls. According to ACR values, which were determined as the average of 2 nonconsecutive overnight spot urine samples, subjects who had hypertension were categorized into 2 groups: those who had microalbuminuria (n = 28; mean ACR 30 to 300 mg/g) and those who had normal albuminuria (n = 80; mean ACR <30 mg/g). Subjects who had hypertension compared with controls exhibited higher ACR and log hs-CRP levels and a trend toward lower log adiponectin values (p = 0.062), whereas those who had normal albuminuria compared with controls had similar log adiponectin levels but significantly higher levels of ACR and log hs-CRP. Moreover, subjects who had hypertension and microalbuminuria compared with those who had hypertension and normal albuminuria had higher log hs-CRP and lower log adiponectin concentrations independently of confounding factors. Among those who had hypertension, ACR exhibited an independent positive correlation with log hs-CRP and a negative correlation with log adiponectin. Multiple linear regression analysis showed that age, body mass index, systolic blood pressure, log hs-CRP, and log adiponectin were significant independent predictors of the ACR. In conclusion, microalbuminuria is accompanied by decreased adiponectin and increased hs-CRP levels in the setting of essential hypertension, reflecting a rather diffuse atherosclerotic process.
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PMID:Relation of microalbuminuria to adiponectin and augmented C-reactive protein levels in men with essential hypertension. 1618 22

Obesity is a major risk factor for the development of the metabolic syndrome, a cluster of diseases including insulin resistance, type 2 diabetes, dyslipidemia, hypertension, microalbuminuria, atherosclerosis, and non-alcoholic steatohepatitis. On the other hand, it is now generally accepted that adipose tissue acts as an endocrine organ producing a number of substances with an important role in the regulation of food intake, energy expenditure and a series of metabolic processes. Adiponectin is a recently discovered hormone produced exclusively by adipocytes. In fact, adiponectin is considered currently as a major factor in obesity-related insulin resistance and atherosclerosis. This new hormone differs from other adipocytokines in that its production and concentrations are actually decreased in insulin resistant subjects. The aim of this review is to summarize the current knowledge about the chemistry and physiology of adiponectin and to discuss its implications in the pathophysiology and potential treatment of insulin resistance and non-alcoholic fatty liver disease.
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PMID:Adiponectin, structure, function and pathophysiological implications in non-alcoholic fatty liver disease. 1678 75

Excess body weight may be associated with various functional/structural lesions of the kidney. The spectrum ranges from glomerulomegaly with or without focal or segmental glomerulosclerosis, to diabetic nephropathy, to carcinoma of the kidney and nephrolithiasis. The first sign of renal injury is microalbuminuria or frank proteinuria, in particular in the presence of hypertension. The occurrence of microalbuminuria and/or chronic kidney insufficiency (glomerular filtration rate < 60 mL/min/1.73 m2) is related to the increasing number of components of the metabolic syndrome, ie, central obesity, elevated fasting blood glucose level, hypertriglycerides, low high-density lipoprotein cholesterol, and hypertension. In the long run, end-stage renal failure may develop. An increased body mass index is particularly harmful in patients with reduced renal functional mass (unilateral renal agenesis or nephrectomy) and other renal diseases (immunoglobulin A nephritis and chronic graft dysfunction after kidney transplantation). In the pathogenesis of obesity-associated glomerulopathy, hyperfiltration is of fundamental importance. The factors involved are energy intake (high protein and salt), hyperinsulinemia, and enhanced tubuloglomerular feedback because of increased sodium reabsorption. The adrenergic and renin-angiotensin-aldosterone systems as well as glucocorticoids are stimulated. In addition, several active proteins generated in the central adipose tissue, such as leptin, proinflammatory cytokines, plasminogen activator inhibitor-1, angiotensinogen, and growth factors (transforming growth factor-beta1), as well as low levels of the protective adiponectin, may contribute to renal injury. Of greatest importance is the development of hypertension and of diabetes, which are directly related to the severity of central obesity. Obesity-associated renal disease should be prevented or retarded by weight reduction following lifestyle modification (salt restriction, hypocaloric diet, aerobic exercise), or eventually by antiobesity medication or bariatric surgery. In the presence of glomerulopathy and/or hypertension, angiotensin converting enzyme inhibitors or angiotensin II type I receptor blockers are the drugs of choice to improve glomerular hyperfiltration.
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PMID:Renal disease in obesity: the need for greater attention. 1682 23

Adiponectin is an adipose-derived protein which has anti-inflammatory and anti-atherogenic properties in addition to insulin-sensitizing effects. To date, the role of adiponectin in the pathogenesis of diabetic nephropathy remains unclear. The aim of the present study was to explore the relationship between adiponectin and renal tubular injury in diabetic nephropathy. We determined serum and urinary adiponectin levels in type 2 diabetic patients with normoalbuminuria (n = 19), microalbuminuria (n = 18), and overt diabetic nephropathy (n = 16), and then analyzed the correlations between serum and urinary adiponectin, urinary N-acetylglucosaminidase (NAG) as a clinical marker of renal tubular injury, urinary monocyte chemoattractant protein-1 (MCP-1) as an inflammatory marker in renal tubulointerstitium, and clinical markers of renal disease. Notably, serum and urinary adiponectin levels were significantly increased in patients with overt diabetic nephropathy compared to those with normoalbuminuria and microalbuminuria. In univariate linear regression analysis, serum adiponectin levels were positively correlated with serum creatinine (r = 0.648, P<0.0001), urinary albumin (r = 0.583, P<0.0001), urinary NAG (r = 0.406, P<0.01), urinary MCP-1 (r = 0.514, P<0.0001), and urinary adiponectin (r = 0.691, P<0.0001) levels in all diabetic patients. Urinary adiponectin levels were also positively correlated with serum creatinine (r = 0.729, P<0.0001), urinary albumin (r = 0.799, P<0.0001), urinary NAG (r = 0.701, P<0.0001), and urinary MCP-1 (r = 0.801, P<0.0001) levels in all diabetic patients. Multiple linear regression analysis showed that serum creatinine and urinary adiponectin levels were independently associated with serum adiponectin levels (r(2) = 0.522), and that serum creatinine, urinary NAG, urinary MCP-1, and serum adiponectin levels were independent determinants of urinary adiponectin levels (r(2) = 0.851). These results collectively indicate that renal insufficiency and tubular injury possibly play a contributory role in increases in serum and urinary adiponectin levels in overt diabetic nephropathy. We presume that an increase in circulating adiponectin in overt diabetic nephropathy might be a physiological response to mitigate renal tubular injury and to prevent the further progression of diabetic nephropathy through its anti-inflammatory and anti-atherogenic effects.
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PMID:Possible relationship between adiponectin and renal tubular injury in diabetic nephropathy. 1696 29

We examined whether moxonidine influences lipid profile, insulin resistance, adiponectin levels, renal function and microalbuminuria in women with essential hypertension in a study of 55 non-diabetic hypertensive patients and 53 normotensive women. Hypertensive patients received moxonidine for 12 weeks. At baseline the hypertensive group had significantly higher mean blood pressure, low-density lipoprotein cholesterol, triglycerides, total cholesterol, fasting glucose, urinary albumin excretion and homeostasis model assessment of insulin resistance (HOMA-IR), together with significantly lower mean high-density lipoprotein cholesterol, creatinine clearance and serum adiponectin than the normotensive group. Moxonidine significantly decreased blood pressure, fasting glucose, triglycerides, total cholesterol, HOMA-IR and albumin excretion, but significantly increased serum adiponectin. The change in adiponectin level was negatively correlated with the change in HOMA-IR. Moxonidine treatment may improve unfavourable metabolic status related to insulin resistance by increasing adiponectin levels in patients with essential hypertension. Since it can improve adiponectin levels, it may be used in the antihypertensive treatment of patients at high risk of diabetes and cardiovascular disease.
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PMID:Effects of sympatholytic therapy with moxonidine on serum adiponectin levels in hypertensive women. 1823 Feb 71

Approaching epidemic levels, diabetic kidney disease (DKD) is now the leading cause of end-stage renal disease (ESRD). Microalbuminuria is an early clinical marker of DKD that results from damage to the glomerular filtration barrier at the level of the highly differentiated glomerular podocyte cells. Injury to these epithelial cells, podocytopathies, includes cellular hypertrophy, foot process effacement, detachment from the glomerular basement membrane, and apoptosis. Here we review the role of a number of recently identified factors that contribute to podocytopathies in DKD. These factors include members of the renin-angiotensin system (RAS), including angiotensin-converting enzyme (ACE) types 1 and 2, prorenin and its receptor, reactive oxygen species (ROS), prostanoids, peroxisome proliferator-activated receptors (PPAR), advanced glycation end-products (AGEs) and their receptors (RAGE), adiponectin, and microRNAs. As the number of therapeutic options that slow, but do not halt, the progression of DKD to ESRD remains limited, a more comprehensive understanding of the signaling events that contribute to this increasingly prevalent disease may identify novel avenues for treatment and prevention.
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PMID:The podocyte in diabetic kidney disease. 1983 99

Several studies found that adiponectin, an adipokine withstands atherosclerosis in vivo, is significantly increased in subjects with diabetic nephropathy (DN), but its clinical meaning remains unclear. For its structural similarity to complement C1q and collagen, we performed this study to explore the relationship between adiponectin and the vascular endothelial function alterations in DN patients. 50 type 2 diabetic patients without clinical cardiovascular complications were assigned to control group, microalbuminuria group (Micro-MA), and macroalbuminuria group (Macro-MA) according to the Mogensen's criteria. Plasma adiponectin and soluble vascular cell adhesion molecule-1 (sVCAM-1) were detected. Flow-mediated dilatation (FMD), nitroglycerin-induced dilatation (NID) and cardiologic parameters were measured by ultrasound cardiogram. Plasma adiponectin level was significantly and gradually increased in agreement with the amount of urine albumin excretion. sVCAM-1 was higher in Micro-MA and Macro-MA patients than in the controls, but it was comparable between the former 2 groups. FMD and NID were both remarkably decreased in Macro-MA group compared with Micro-MA and control group. For the whole subjects, plasma adiponectin was negatively related to FMD (r=-0.397, P<0.01) and NID (r=-0.413, P<0.01). These results suggest that increased plasma adiponectin may predict co-existing vascular endothelial dysfunction in DN patients.
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PMID:Increased plasma adiponectin closely associates with vascular endothelial dysfunction in type 2 diabetic patients with diabetic nephropathy. 2013 82


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