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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the early 1970s, mandatory kidney disease screening was started with urinalysis in the Japanese health examination program for all workers and school-age children. In 1983, nationwide urinalysis screening in adults aged > or = 40 yr was mandated in the community-based health examination program. Because glomerulonephritis was an endemic disease and the leading cause of end-stage renal disease in Japan until 1997, the urinalysis in the annual health examination program aimed for early detection of glomerulonephritis and early referral of patients to physicians. To the programs, measurement of serum creatinine was added for detection of chronic kidney disease in 1992 for adults aged > or = 40 yr. Kidney disease screening and early intervention brought reduction of progressive glomerulonephritis or an increase in remission. Thus, in children and adults aged < or = 45 yr, the number of patients with end-stage renal disease from glomerulonephritis has declined, and the mean age of patients with new end-stage renal disease has increased significantly. In 1998, the leading cause of end-stage renal disease was shifted from glomerulonephritis to diabetic nephropathy as a result of lifestyle changes in the Japanese population; however, the present comprehensive kidney disease screening in the health examination program for detection of glomerulonephritis must be continued, because even in 2005, 27.3% of newly developed end-stage renal disease was from glomerulonephritis. An additional kidney disease screening program should also be established to target patients with high risk for diabetes, hypertension, and metabolic syndrome, because 42% of newly introduced renal replacement cases were from diabetic nephropathy in 2005.
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PMID:Kidney disease screening program in Japan: history, outcome, and perspectives. 1794 80

Our previous studies indicate that prolonged caffeine consumption exacerbates renal failure in nephropathy associated with the metabolic syndrome. Reduced activity of the antioxidant defense system and beneficial effects of antioxidant therapy have been reported in diabetic rats and humans. The purpose of this study was to examine the early renal effects of caffeine consumption and the effects of concomitant antioxidant therapy in young obese, diabetic ZSF1 rats. Eleven-week-old male ZSF1 rats were randomized to drink tap water, caffeine (0.1%), tempol (1 mmol/L), or a solution containing caffeine and tempol for nine weeks. Caffeine significantly reduced body weight and glycosuria (weeks 2-9), improved glucose tolerance (week 9), had no effect on elevated plasma triglycerides, plasma cholesterol (week 9) and blood pressure (week 9), and significantly increased plasma cholesterol level (weeks 5 and 9). Yet, as early as after two weeks, caffeine greatly augmented proteinuria and increased renal vascular resistance (RVR) and heart rate (HR: week 9). Tempol had no effects on metabolic status and development of proteinuria, did not alter caffeine-induced metabolic changes and early proteinuria, and attenuated caffeine-induced increase in HR and RVR. Immunohistochemical analysis revealed significant glomerular and interstitial inflammation, proliferation, and fibrosis in control animals. Caffeine augmented the influx of glomerular and interstitial macrophages (ED1+ cells) influx, glomerular and tubular proliferative response, and glomerular collagen IV content. Tempol abolished the exacerbation of renal inflammation, proliferation, and fibrosis induced by caffeine. In conclusion, in nephropathy associated with the metabolic syndrome, caffeine--most likely through the interaction with adenosine receptors and interference with anti-inflammatory and/or glomerular hemodynamic effects of adenosine--augments proteinuria and stimulates some of the key proliferative mechanisms involved in glomerular remodeling and sclerosis. Tempol does not prevent early renal injury (i.e., proteinuria) induced by caffeine, yet abolishes late renal inflammatory, proliferative, and fibrotic change induced by chronic caffeine consumption in obese ZSF1 rats.
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PMID:Early renal injury induced by caffeine consumption in obese, diabetic ZSF1 rats. 1799 59

Cardiovascular disease is the leading cause of death in women in most developed countries of the world. Even though cardiovascular deaths of men in the United States have been declining, until recently the number of cardiovascular deaths in US women was on the rise, with 1 in 3 women dying from heart disease. Over the last 30 years numerous studies have reported sex differences in the epidemiology, prevention, diagnosis, and clinical manifestations of coronary artery disease. A higher morbidity and mortality were also noted in women versus men undergoing revascularization during this early period. This has mainly been attributed to the fact that women have more comorbid conditions by the time that they are referred for revascularization. These conditions include increased age, hypertension, diabetes (metabolic syndrome), heart failure, renal disease, peripheral vascular disease, and worse lipid profile. With improvements of both surgical techniques and percutaneous coronary intervention, morbidity and mortality rates have decreased in women undergoing revascularization. However, there are now questions surrounding percutaneous coronary intervention strategies, particularly with drug eluting stents. More recent advances in coronary bypass graft surgery techniques, both off- and on-pump, and analysis of prospective and retrospective data have shown a clearly improved survival rate in patients undergoing coronary bypass graft surgery and the persistence of a durable result.
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PMID:Confusion in revascularization: are women different and why? 1809

It is recognised that the metabolic syndrome promotes the development of cardiovascular disease. Although several studies have shown a relationship between the metabolic syndrome and kidney disease, few of these have used non-diabetic subjects, especially in the African population. This was a cross-sectional study of subjects of African origin, using the metabolic syndrome (MS) criteria of the National Cholesterol Education Program (NCEP) third Adult Treatment Panel (ATP III). Subjects with impaired fasting glucose, with two-hour glucose >or= 11.1 mmol/L after a glucose tolerance test, were excluded. Spot urine for albumin-to-creatinine ratio (ACR) was measured and the glomerular filtration rate (GFR) was estimated using the Modification of Diet in Renal Disease (MDRD) equation. Microalbuminuria was defined as ACR between 3-30 mg/mmol. There was a significant decline in GFR and a significant increase in ACR with increasing number of MS traits. ACR increased four-fold between subjects with no MS traits and those with four or more traits. In subjects with the metabolic syndrome, there was a significant correlation between ACR and systolic blood pressure (SBP), diastolic blood pressure (DBP) and fasting glucose. Estimated GFR correlated significantly and inversely with body mass index (BMI) and serum leptin. These observations raise major clinical and public health concerns for developing countries, where both the metabolic syndrome and kidney disease are being reported more and more frequently. The potential economic impact is huge.
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PMID:Microalbuminuria and the metabolic syndrome in non-diabetic black Africans. 1815 9

The aim of this study was to evaluate the relationship between the diagnosis of metabolic syndrome (MetS) or its components and the prevalence of microvascular and macrovascular complications in 130 Japanese type 2 diabetic patients. Out of the 130 patients, 58.5% satisfied the criteria of the MetS as defined by the IDF guideline. The results of logistic regression analysis with adjustment for three variables (age, gender and duration of diabetes) revealed that the presence of MetS as defined by the IDF guideline was not independently related to the presence of proliferative retinopathy, proteinuria, neuropathy, or macrovascular disease in the diabetic patients. The waist circumference per se was not associated with diabetic neuropathy, retinopathy, nephropathy, or macrovascular diseases. These results suggest that neither the presence of MetS, as defined by the IDF guideline, nor the waist circumference was associated with the presence of either microvascular or macrovascular complications in Japanese type 2 diabetic patients.
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PMID:Neither the presence of metabolic syndrome as defined by the IDF guideline nor an increased waist circumference increased the risk of microvascular or macrovascular complications in Japanese patients with type 2 diabetes. 1820 78

Metabolic syndrome, also known as the insulin resistance syndrome (IRS), dysmetabolic syndrome or syndrome X, is a burgeoning global epidemic. This constellation of risk factors, namely glucose intolerance, hypertension, dyslipidemia (high triglyceride and low HDL cholesterol), central obesity, pro-inflammatory and prothrombotic state, culminating to the development of premature cardiovascular and renal disease, has significant impact on life expectancy, societal productivity and quality of life. The underlying mechanism of this complex syndrome remains to be elucidated. In recent years, light has been shed on the roles of neuroendocrine system and adipocytokines on the pathogenesis of IRS. In this review, we summarize the possible links between insulin and various hormones (growth hormones (GH), catecholamines, glucocorticoids and sex hormones), partly mediated through visceral adiposity and adipocytokines (notably adiponectin, leptin, resistin, visfatin, tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6)) in the pathogenesis of this syndrome.
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PMID:The role of adipocytokines and neurohormonal dysregulation in metabolic syndrome. 1822 Jun 44

The metabolic syndrome (MetS) is defined by a set of metabolic risk factors, including insulin resistance, central obesity, dyslipidemia, hyperglycemia, and hypertension for type 2 diabetes and cardiovascular disease. Although both retrospective and prospective clinical studies have revealed that MetS is associated with chronic renal disease, even with a nondiabetic cause, the cellular and molecular mechanisms in this association remain largely uncharacterized. Recently, increasing evidence suggests that peroxisome proliferator-activated receptors (PPARs), a subgroup of the nuclear hormone receptor superfamily of ligand-activated transcription factors, may play an important role in the pathogenesis of MetS. All three members of the PPAR nuclear receptor subfamily, PPARalpha, -beta/delta, and -gamma, are critical in regulating insulin sensitivity, adipogenesis, lipid metabolism, inflammation, and blood pressure. PPARs have also been implicated in many renal pathophysiological conditions, including diabetic nephropathy and glomerulosclerosis. Ligands for PPARs such as hypolipidemic PPARalpha activators, and antidiabetic thiazolidinedione PPARgamma agonists affect not only diverse aspects of MetS but also renal disease progression. Emerging data suggest that PPARs may be potential therapeutic targets for MetS and its related renal complications. This review focuses on current knowledge of the role of PPARs in MetS and discusses the potential therapeutic utility of PPAR modulators in the treatment of kidney diseases associated with MetS.
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PMID:PPARs and the kidney in metabolic syndrome. 1823 57

The article presents results on the study on the state of carbohydrate and lipid metabolism in patients with arterial hypertension (AH) and a metabolic syndrome (MC), verified according to criteria NCEP ATP III (2001) in the presence of insulin resistance confirmed by HOMA-IR index Metabolic disorders were revealed both in patients with AH, and in patients with MC. These disorders have the unidirectional character and differ not qualitatively but quantitatively and according to the correlation and dispersive analysess, in many respects are defined by concomitant diseases of the digestive tract, hepatobiliary system, pancreas and nephropathy which is typical for patients with II stage AH.
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PMID:[Carbohydrate and lipid metabolism in patients with metabolic syndrome]. 1827 Nov 78

Aldosterone is traditionally viewed as a hormone regulating electrolyte and blood pressure homeostasis by acting on the distal nephron. Accumulating evidence suggests that aldosterone also plays pathogenetic roles in cardiovascular and renal injury. For example, aldosterone is a potent inducer of proteinuria. We demonstrated that podocyte injury underlies the pathogenesis of proteinuria in aldosterone-infused rats on a high salt diet. Mineralocorticoid receptor was detected in the podocytes in vivo and in vitro, and aldosterone caused induction of its effector kinase Sgk1, activation of NADPH oxidase and generation of reactive oxygen species. Selective aldosterone blocker eplerenone, as well as antioxidant tempol, ameliorated aldosterone-induced podocyte injury and proteinuria. Aldosterone was also involved in the podocyte damage and proteinuria of metabolic syndrome model SHR/NDmcr-cp. Adipocyte-derived aldosterone releasing factors were suggested to contribute to the aldosterone excess of this model. Furthermore, high salt diet markedly worsened the renal injury of SHR/NDmcr-cp. Although salt lowered serum aldosterone levels, it caused MR activation in the kidney. Accordingly, eplerenone dramatically improved the salt-evoked nephropathy. Taken together, aldosterone blockers can be an excellent therapeutic strategy for the treatment of podocyte injury, proteinuria, and cardiovascular and renal complications, not only in high aldosterone states but also in patients with activated MR signaling in the target tissue, whose circulating aldosterone level is not necessarily high. Addition of aldosterone blockers in patients treated with ACEIs or ARBs are also promising, because of "aldosterone breakthrough" phenomenon. Careful monitoring of hyperkalemia is necessary, especially in patients with impaired renal function.
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PMID:Aldosterone and glomerular podocyte injury. 1831 76

The level of serum uric acid in human has been increasing over the last decades, and correlates with an increase prevalence of renal disease and metabolic syndrome. Understanding the role of uric acid in these conditions may provide clues for preventing the current epidemic of renal disease. Controversy still remains if hyperuricemia is simply a consequence or a cause of renal disease although epidemiological studies have attempted to resolve this issue. In this review, we discuss the clinical and experimental evidence for a causal role of hyperuricemia in renal diseases and potential relationships of hyperuricemia with metabolic syndrome.
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PMID:The conundrum of hyperuricemia, metabolic syndrome, and renal disease. 1951 86


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