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In spite of a progressive fall in the incidence of traditional risk factors of cardiovascular morbidity (cigarette smoking, high blood pressure, and hyperlipidemia), there is an upward trend in the prevalence of obesity and chronic kidney disease (CKD). Furthermore, there is a strong correlation between body mass indices and the relative risk of progression of CKD. The close biophysiological interaction between obesity and CKD is evident by a similar occurrence of comorbidities including insulin resistance, hyperlipidermia, endothelial dysfunction, and sleep disorders. Truncal obesity is a primary component of metabolic syndrome; unlike peripheral fat, the visceral adipocytes are more resistant to insulin. In addition, lipolysis results in a release of free fatty acid and TG, whereas hypertriglycedemia is potentiated by uremic activation of fatty acid synthase. Hypertriglycedemia and low HDL cholesterol increase the relative risk of progression of CKD. Furthermore, endothelial inflammation and premature atherosclerosis are promoted by hyperhomocysteinemia and oxidation of LDL, both of which are commonly observed in CKD and obesity. Predominance of oxidative stress in both obesity and azotemia stimulate synthesis of angiotensin II, which in turn increases TGF-B and plasminogen activator inhibitor-1, thereby propagating glomerular fibrosis. Furthermore, local synthesis of angiotensinogen by adipocytes, leptin activation of sympathetic nervous system, and hyperinsulinemia contribute to the development of hypertension in obesity and CKD. In addition, increased renal tubular expression of Na-K-ATPase and a blunted response to natiuretic hormones in obesity promote salt and water retention. Glomerular hyperfiltration from systemic volume load and hypertension results in mesangial cellular proliferation and progressive renal fibrosis. In addition, maternal nutritional deprivation increases the incidence of obesity, hypertension, and diabetes in adulthood. Reduced fetal protein synthesis contributes to oxidative glomerular injury and impairment of renal morphogenesis. Thus, kidneys are poorly equipped to handle physiologic stress that may result from the rapid body growth and programmed metabolic dysfunction later in life. Finally, in order to minimize morbidity of obesity-related kidney disease, preventive strategy must include optimal maternal health care, promotion of healthy nutrition and routine physical exercise, and early detection of CKD.
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PMID:The role of obesity and its bioclinical correlates in the progression of chronic kidney disease. 1704 21

Cardiovascular disease is the leading cause of death following renal transplantation, accounting for 40% to 55% of all deaths. An analysis in our center showed a 15% mortality in a cohort of renal transplant recipients followed for an average of 10 years. Various contributing risk factors of cardiovascular diseases in transplant recipients such as tobacco use, hypertension, hyperlipidemia, hereditary risk, diabetes, physical inactivity, obesity, dialysis duration, hyperuricemia, proteinuria, hyperhomocysteinemia, hyperparathyroidism, anemia; C-reactive protein level, and immunosuppressive regimen as well as some rare risk factors, such as cytomegalovirus infection, were evaluated in a population of 1200 kidney transplant recipients. Also we introduced methods for early detection, monitoring, and follow-up of proven risk factors of cardiovascular disease.
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PMID:How to decrease cardiovascular mortality in renal transplant recipients. 1711 56

Cerebral venous thrombosis (CVT) is an under diagnosed condition for acute or slowly progressive neurological deficit. CVT is less frequent than arterial thrombosis. CVT has a wide spectrum of signs and symptoms, which may evolve suddenly or over the weeks. It is clinically challenging and mimics many neurological conditions such as, meningitis, encephalopathy, benign intracranial hypertension, and stroke. With increasing awareness, CVT cases are now being diagnosed more frequently. Newer imaging procedures have led to easier recognition of venous sinus thrombosis, offering the opportunity for early therapeutic measures. It may be difficult to diagnose it on clinical grounds alone. Headache is the most frequent symptom in patients with CVT, present in about 80% of cases. Most common pattern of presentation is with a benign intracranial hypertension-like syndrome. The prognosis of CVT is worse in elderly subjects. The shorter the history the more likely is the presence of focal signs. Sixth cranial nerve palsy usually manifests as false localizing sign. Subarachnoid haemorrhage (SAH) has been described, as the presenting event with CVT. Patients may have seizures that can be recurrent. Cranial nerve syndromes are seen with venous sinus thrombosis. Psychiatric disturbances are sometimes the presenting symptoms. CVT, an important cause of stroke in puerperium, is frequently observed in India. We have seen 6 patients of CVT out of 490 stroke registry. Of these 6, four were females and two were males. The mean age among females was 27.75 years and among males was 41.5 years. Of the 4 females two were postpartum; one was on oral contraceptive and in one Antiphospholipid antibodies (APLA) were positive. Amongst two males one had hyperhomocysteinemia and one had hyperlipidemia.
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PMID:Cerebral venous thrombosis--clinical presentations. 1718 79

Renal transplantation is the gold standard therapy for patients with end-stage renal disease. However, renal transplantation is associated with various metabolic and nutritional complications. This review focuses primarily on factors that have a significant impact on cardiovascular disease, namely, hyperlipidemia, posttransplant diabetes mellitus, and hyperhomocysteinemia. The prevalence of hyperlipidemia in renal transplant patients is estimated at 80% to 90%. Corticosteroids, cyclosporine, and sirolimus are commonly associated with hyperlipidemia. The incidence of posttransplant diabetes mellitus is estimated to be 24% at 36 months post transplant. Glucocorticoids induce metabolic changes that result in hyperglycemia. Calcineurin inhibitors have direct islet cell toxicity and induced alterations in the transcriptional regulation of insulin. Hyperhomocysteinemia is common in renal transplant recipients and is an independent risk factor for cardiovascular disease.
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PMID:Metabolic and nutritional complications of renal transplantation. 1719 43

Peripheral arterial occlusive disease (PAOD) of the lower extremities is becoming more prevalent worldwide. Nonsurgical treatment options provide the foundation for management. Lifestyle and risk factor modification should be emphasized in this patient population because of the associated adverse cardiovascular events. This includes implementation of a regular walking and smoking-cessation programs, aggressive control of hyperlipidemia, hypertension and diabetes mellitus, and treatment of hyperhomocysteinemia. Antiplatelet agents such as aspirin (acetylsalicylic acid) or clopidogrel are not specifically indicated for claudication but these drugs should be used in all patients with PAOD to prevent secondary ischemic events. Currently, cilostazol is the only US FDA approved agent that appears effective for the treatment of claudication symptoms. Several agents have been used with success outside of the US and others are still undergoing testing. Definitive recommendations cannot be made on the use of these drugs until further evaluation is completed. Ongoing research with new strategies for angiogenesis and the use of progenitor cells has yielded encouraging results, particularly for patients with critical limb ischemia and limited options. Advances in endovascular technology over the last several years have greatly enhanced the ability to diagnose and treat specific anatomic lesions that previously would have required open surgical correction. The use of percutaneous transluminal angioplasty and stents in the lower extremities has had considerable success when following specific guidelines such as those set forth by the TransAtlantic Inter-Society Consensus Working Group.
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PMID:Current management of peripheral arterial occlusive disease: a review of pharmacologic agents and other interventions. 1735 66

Aim of the study was to estimate the incidence of coronary heart disease (CAD) in patients (pts) with end stage renal disease (ESRD) maintained on chronic hemodialysis (HD) and its association with the presence of predisposing factors. The study included 171 dialysis pts (107 male (M) and 64 female (F)). Mean age of pts was 67+/-13 years, mean time on dialysis 52.7+/-44 months and Body Mass Index (BMI) 25.9+/-3.7 kg/m2. Fifty pts (29.2%) were clinically diagnosed with CAD. The diagnosis was established by coronary angiography in 24 (48%) and in 26 by combined dipyridamole-exercise thallium imaging (52%). Pts' data in association with the development of CAD that were recorded included age, sex, smoking habits, hypertension, obesity, the presence of diabetes mellitus (DM), hyperlipidemia, anemia, low albumin levels, secondary hyperparathyroidism (SHP), the presence of chronic inflammation, as evidenced by the presence of elevated levels of CRP and hyperhomocysteinemia. There was a statistically significant association of increasing age and CAD (p<0.0001). Relative risk (RR) was significantly increased i) in male pts compared to female pts (RR: 8.56, p<0.001), ii) in anemic pts compared to pts with hemoglobin levels< or =11 g/dL (RR: 8.26, p<0.0001), iii) in obese pts compared to pts with BMI < or =30 (RR: 5.09, p<0.005) and iv) in pts with increased levels of homocysteine compared to pts with levels of homocysteine <15 |IM (RR: 4.14, p<0.0001). Using linear regression analysis, CAD was associated with the inadequacy of HD (r = - 0.05, p<0.0001), time on HD (r =0.04, p =0.012) and increasing age (r =0.24, p<0.001). There was no statistically significant association between CAD and the presence of the other traditional risk factors. The incidence of CAD in dialysis pts is significantly increased with age, male sex, obesity, time on dialysis, the presence of anemia, hyperhomocysteinemia and inadequacy of HD.
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PMID:Incidence and risk factors of coronary artery disease in patients on chronic hemodialysis. 1741 65

We conducted a review of cohort studies and interventional studies on nutritional and life-style risk factors and primary prevention of Alzheimer's Disease. Studies were assessed by the Oxford classification. Interventional studies exist for mental training and vitamin supplementation. For alcohol, fat and fish intake, mediterranean diet, homocysteine, overweight/caloric intake, physical and social activity, hypercholesterolemia, diabetes and smoking, currently there is only evidence from cohort studies. Cognitive stimulation by mental training increases mental functions and can be recommended on the basis of positive interventional studies. Vitamin supplementation cannot prevent AD on the basis of interventional studies. Hyperlipidemia, hyperhomocysteinemia, diabetes and typical life-style factors (alcohol, smoking, obesity etc.) modestly increased AD risk, fish, mediterranean diet and unsaturated fat or n-3 fatty acids and social activity are protective in observational cohorts, but interventional studies are lacking.
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PMID:Non-pharmacologic prevention of Alzheimer's disease: nutritional and life-style risk factors. 1755 31

Coronary heart disease and osteoporosis are common diseases in aging populations. Traditionally, these diseases have been considered as distinct and unrelated. However, nowadays there has been increasing evidence indicating a pathological link between these two disorders. Both diseases share etiological factors as hyperlipidemia, hypertension, diabetes, oxidative stress, inflammation, hyperhomocysteinemia. Statins, hypolipidemic drugs, not only reduce atherogenesis but also stimulate bone formation. Bisphosphonates, drugs used in osteoporosis treatment, have been shown to influence serum cholesterol levels and inhibit atherosclerotic plaque formation.
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PMID:[Coronary heart disease and osteoporosis: factors related to development of both diseases]. 1794 67

A causal relationship between diet-induced hyperhomocysteinemia (HHcy) and accelerated atherosclerosis has been established in apolipoprotein E-deficient (apoE(-/-)) mice. However, it is not known whether the proatherogenic effect of HHcy in apoE(-/-) mice is independent of hyperlipidemia and/or deficiency of apoE. In this study, a comprehensive dietary approach using C57BL/6J mice was used to investigate whether HHcy is an independent risk factor for accelerated atherosclerosis or dependent on additional dietary factors that increase plasma lipids and/or inflammation. C57BL/6J mice at 4 wk of age were divided into 6 dietary groups: chow diet (C), chow diet + methionine (C+M), western-type diet (W), western-type diet + methionine (W+M), atherogenic diet (A), or atherogenic diet + methionine (A+M). After 2, 10, 20, or 40 wk on the diets, mice were sacrificed, and the levels of total plasma homocysteine, cysteine, and glutathione, as well as total plasma cholesterol and triglycerides were analyzed. Aortic root sections were examined for atherosclerotic lesions. HHcy was induced in all groups supplemented with methionine, compared to diet-matched control groups. Plasma total cholesterol was significantly increased in mice fed the W or A diet. However, the W diet increased LDL/IDL and HDL levels, while the A diet significantly elevated plasma VLDL and LDL/IDL levels without increasing HDL. No differences in plasma total cholesterol levels or lipid profiles were observed between methionine-supplemented groups and the diet-matched control groups. Early atherosclerotic lesions containing macrophage foam cells were only observed in mice fed the A or A + M diet. Furthermore, lesion size was significantly larger in the A + M group compared to the A group at 10 and 20 wk; however, mature lesions were never observed even after 40 wk on these diets. The presence of lymphocytes, increased hyaluronan staining, and the expression of endoplasmic reticulum (ER) stress markers were also increased in atherosclerotic lesions from the A + M group. Taken together, these results suggest that HHcy does not independently cause atherosclerosis in C57BL/6J mice even in the presence of increased total plasma lipids induced by the W diet. However, HHcy can accelerate atherosclerotic lesion development under dietary conditions that increase plasma VLDL levels and/or inflammation.
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PMID:Hyperhomocysteinemia induced by methionine supplementation does not independently cause atherosclerosis in C57BL/6J mice. 1836 97

The present study was designed to investigate the antioxidant effect of curcumin on methionine-induced hyperlipidemia and hyperhomocysteinemia in Wistar rats (200-250 g) of either sex. The vehicle control rats were treated with 1% Tween 80 in normal saline (2 ml/kg, po) for 30 days. Hyperlipidemia and hyperhomocysteinemia was induced by methionine administration (1 g/kg, po) for 30 days. A significant increase in total cholesterol, triglycerides, low density lipoprotein cholesterol (LDL-C) and homocysteine levels in serum and thiobarbituric acid reactive substances (TBARS) levels in heart homogenates were observed with a concomitant decrease in serum high density lipoprotein (HDL-C) levels in pathogenic control (i.e. group II) rats, as compared to vehicle control (i.e. group I) rats. Further, curcumin (200 mg/kg, p.o.) treatment in methionine treated rats for 30 days significantly decreased the total cholesterol, triglycerides, LDL-C and homocysteine levels in serum and TBARS levels in heart homogenates and increased serum HDL-C levels, as compared to pathogenic control (i.e. group II) rats. The results of biochemical observations were supplemented by histopathological examination of rat's aortic section. The results of test drug were comparable to that obtained with folic acid (100 mg/kg, p.o.). The results suggest that curcumin has significant antihyperlipidemic and antihyperhomocysteinemic effect against methionine-induced hyperlipidemia and hyperhomocysteinemia in rats.
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PMID:Modulatory effect of curcumin on methionine-induced hyperlipidemia and hyperhomocysteinemia in albino rats. 1880 58


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