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Gastric bypass surgery is a common treatment for morbid obesity. The presence of comorbid conditions and drugs that are used to treat them can adversely influence kidney function. Risk factors and outcomes of acute kidney injury (AKI) after gastric bypass surgery are not well understood, however. A total of 504 patients underwent gastric bypass between January 2003 and 2005. Primary outcome was AKI, defined as a > or =50% increase in serum creatinine relative to baseline or requirement of dialysis. Secondary outcomes were duration of hospitalization, all-cause hospital mortality, and readmissions within 30 d after surgery. Demographic, comorbid, and laboratory variables and preoperative medication use were examined as potential risk factors for AKI. A total of 42 (8.5%) patients developed postoperative AKI. Hyperlipidemia, preoperative use of angiotensin-converting enzyme inhibitors (ACE-I) or angiotensin receptor blockers (ARB), intraoperative hypotension, and higher body mass index were associated with increased frequency of AKI. By multivariable analyses, the independent risk factors for AKI were body mass index (odds ratio [OR] 1.03; 95% confidence interval [CI] 1.00 to 1.06), hyperlipidemia (OR 2.53; 95% CI 1.21 to 5.28), and preoperative use of ACE-I or ARB (OR 2.06; 95% CI 1.05 to 4.04). The postoperative mortality was 0.45% (n = 2), both of whom had AKI. Duration of hospitalization was greater in patients with AKI versus no AKI (4.0 versus 2.7 d; P = 0.0003). Postoperative AKI is not infrequent after gastric bypass surgery. Certain comorbid conditions and their commonly prescribed treatments, ACE-I or ARB, are independently associated with increased risk for postoperative AKI.
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PMID:Acute kidney injury after gastric bypass surgery. 1769 47

New evidence about diabetic microangiopathy has enabled us to identify an integrated pathogenesis of diabetic complications, including classic metabolic pathways induced by hyperglycaemia, insulin-resistance, hyperinsulinaemia, hormonal alterations and growth factors. Oxidative stress is the most important cause of endothelial damage inducing leukocyte adhesion, altered coagulation and inflammation. Adhesion molecules are a marker of endothelial damage and a potential therapeutic target. Changes in the extracellular matrix induced by TGFbeta1 and lower levels of eparan-sulfate, increased thickness of basement membranes and loss of pericytes are early events of diabetic retinopathy and diabetic nephropathy. Capillary rarefaction produced by genetic factors or by fetal undernourishment contributes to the beginning of insulin-resistance and hypertension. Psychophysical tests, electroretinogram and evoked potentials show retinal functional alterations; fundoscopy and retinal fluorescein angiography show retinal anatomic alterations. The diagnosis of diabetic neuropathy is based not only on traditional neurological examination and electroneurograms, but also on neurothesiometry for sensory testing. Medical treatment of diabetic microangiopathy is based on control of glycaemia, lipemia and blood pressure using glytazones, ACE-inhibitors, angiotensin II receptor antagonists and statins. New knowledgeabout microangiopathy pathogenesis suggests potential drugs for its therapy (ruboxistaurin, AGE-inhibitors, angiopoietin-1 and anti-VEGF, etc.), not yet on sale.
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PMID:Diabetic microangiopathy: physiopathological, clinical and therapeutic aspects. 1791 58

Patients with diabetes are often treated with a statin for hyperlipidaemia and an ACE (angiotensin-converting enzyme) inhibitor or angiotensin receptor antagonist for hypertension or albuminuria. These drugs may also exert beneficial metabolic effects, causing improved glucose tolerance in patients. Gender-related differences have also been observed in the clinical responsiveness to these drugs, but the mechanism behind this is unclear. In the present study, we have investigated whether these drugs and the fatty acid palmitate influence the pancreatic microcirculation, thereby having an impact on insulin secretion and glycaemia in vivo, in spontaneously diabetic male and female Goto-Kakizaki rats. In male rats, pancreatic IBF (islet blood flow) and total PBF (pancreatic blood flow) were increased significantly by pravastatin, captopril and irbesartan. Serum insulin levels were increased by pravastatin and captopril. Palmitate suppressed pancreatic IBF and increased blood glucose. In female animals, pancreatic IBF was stimulated by captopril, candesartan and irbesartan. Total PBF was increased by captopril, candesartan and irbesartan, and by pravastatin. Palmitate suppressed pancreatic IBF and serum insulin secretion. In conclusion, the present study lends support to the view that a local pancreatic RAS (renin-angiotensin system) and pravastatin may be selectively influencing the pancreatic microcirculation and therefore affecting insulin secretion and glycaemia. NEFAs (non-esterified fatty acids) impaired pancreatic IBF, suppressed insulin secretion and increased blood glucose. Substantial gender-related differences in the vascular and metabolic responses to these drugs prevail in this animal model of diabetes.
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PMID:Gender-specific regulation of pancreatic islet blood flow, insulin levels and glycaemia in spontaneously diabetic Goto-Kakizaki rats. 1820 25

Angiotensin receptor blockers (ARB) have been emerging as drugs to treat atherosclerosis. The effectiveness of the ARB losartan at reducing atherosclerosis was compared with that of ACE inhibitors in hypertensive patients. A total of 50 patients with hypertension were divided into 3 groups: a control group receiving neither an ARB nor an ACE inhibitor (n = 14), a losartan group (n = 22) receiving 50 mg/day of losartan, and an ACE inhibitor group (n = 14) receiving either 5 mg/day of enalapril or 5 mg/day of imidapril. Atherosclerosis was evaluated based on the intima-media thickness (IMT) of the common carotid artery measured by B-mode ultrasound at baseline and after approximately 12 months of treatment. After the treatment, IMT significantly decreased with losartan (from 0.87 +/- 0.14 to 0.79 +/- 0.16 mm, P < 0.05) and with ACE inhibitor (from 0.81 +/- 0.14 to 0.74 +/- 0.11 mm, P < 0.05). The reduction was comparable between the two groups, -0.078 +/- 0.136 with losartan and -0.073 +/- 0.109 mm with ACE inhibitor, and the rate of the reduction was similar between the two drugs; -0.098 +/- 0.142 mm/year with losartan and (-0.076 +/- 0.118 mm/year) with ACE inhibitor. On the contrary, IMT did not change in the control group (from 0.90 +/- 0.20 to 0.95 +/- 0.26 mm) during the treatment period. Concomitant medication and coronary risk factors such as hyperlipidemia, diabetes mellitus, and smoking did not differ significantly among the groups. The antiatherosclerotic effect of losartan on the carotid artery was comparable to that of ACE-inhibitors, and less adverse effects, such as coughing that occurs with ACE inhibitors, were observed. Losartan appears to be a better alternative to ACE inhibitors for treating atherosclerosis in Japanese hypertensive patients.
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PMID:A one-year study of the antiatherosclerotic effect of the angiotensin-II receptor blocker losartan in hypertensive patients. A comparison with angiotension-converting enzyme inhibitors. 1836 68

Risk factors are associated with disease and are not necessarily causative; as they are additive they should not be judged in isolation. Thus, 'mild blood pressure' does not imply a 'mild' risk in a cigarette-smoking, hypertensive diabetic. Cardiologists are usually fortunate, in that they see patients when there is already evidence of disease (ie, when secondary prevention is the issue, which is much less contentious than primary prevention). In the 'whizz-bang' specialty of cardiology, a balloon can remove in a matter of seconds what a lipidologist has toiled over for years. Attention to detail may not come easily in a stressful world: it is the detail of prevention that is likely to slow the progression of disease and induce regression rather than angioplasty or bypass surgery. In the presence of coronary artery disease, the essence of management is the team approach, the patient being the most important member of the team. Furthermore, the factors that need the most concentrated effort include cigarette smoking, hypertension, and hyperlipidaemia. As risk factors are additive, treatment of one should not make another one worse. Some drugs for hypertension can exacerbate hyperlipidaemia or impair glucose tolerance (eg thiazides), while ACE inhibitors can beneficially decrease insulin resistance in diabetes. Therapy must be tailored to the individual, but the overall prognostic benefits of drugs that might have slightly adverse metabolic profiles (such as beta-blockers) must not be ignored. Science is often a loser when faced with the power of marketing. When one risk factor (eg hypertension) is present, it is important to be vigorous in treating other factors (eg hyperlipidaemia) with general advice and support, as well as with specific drug therapy if indicated. There are two individuals that tend to lack education in risk factors--the patient and the cardiologist. The patient is a victim of poor investment in prevention, while the cardiologist is put off by a perceived lack of balance from the medical protagonists.
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PMID:Risk factor management: the cardiologist's perspective. 872 89

Nephrotic syndrome is characterised by proteinuria >3.5 g/24h, oedema, hypoalbuminaemia and hyperlipidaemia. Several glomerular diseases, either primary or secondary, may lead to nephrotic syndrome. Investigations for nephrotic syndrome include immunological and infectious evaluations. Renal biopsy is often mandatory, except in diabetes. Depending on aetiology specific treatment, often with immunosuppressive agents, may be implemented. In any cases nonspecific treatment should be started with ACE inhibitors or ARBs. Urinary protein loss leads to several complications: water and sodium retention, hyperlipidaemia, increased risk of thromboembolism and infection, anaemia and alteration of mineral metabolism. Each of these complications must be identified.
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PMID:Management of patients with nephrotic syndrome. 1968 Aug 31

Cardiovascular diseases (CVD) are the leading cause of mortality in Croatia and in Europe. Primary prevention of CVD involves intervention before the onset of disease, and prevention of modifiable risk factors, i.e. cigarette smoking, hyperlipidemia, arterial hypertension, diabetes mellitus, inactivity, obesity. These risk factors are strongly associated and lead to impaired vascular endothelial function, chronic injury of endothelium, platelet activation and aggregation, atherosclerotic plaque formation, and in the end manifestation of CVD. The risk of any coronary event increases exponentially when two or more risk factors are present. Aside from conventional factors, it has been demonstrated that raised levels of C-reactive protein (CRP), cytokines, homocysteine and fibrinogen are also important promotors of the disease, pointing to partially inflammatory nature of coronary atherosclerosis. The effects of risk factors such as smoking, arterial hypertension and hyperlipidemia on vascular endothelium are proven to be reversible. According to Guidelines on Cardiovascular Disease Prevention in Clinical Practice of the European Society of Cardiology (2007), population is advised to follow the formula 0 3 5 140 5 3 0. It suggests that crucial measures in preserving cardiovascular health are as follows: no smoking (0), walking 3 km daily or 30 minutes of any moderate activity (3), blood pressure less than 140 mm Hg systolic (140), total blood cholesterol less than 5 mmol/L (5), LDL cholesterol less than 3 mmol/L (3), avoidance of overweight and diabetes (0). There are many studies proving the beneficial effects of statins and ACE inhibitors in improving endothelial function and endorsing primary prevention.
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PMID:[Primary prevention of cardiovascular disease]. 1968 67

Multifactorial risk-factor modification-especially intensive ways to manage hyperlipidemia-may slow, halt, or even reverse the progression of coronary artery disease. The American Heart Association recently published comprehensive risk-reduction strategies in patients with coronary heart and vascular disease. These recommendations, endorsed by the American College of Cardiology, have been expanded and can be easily remembered as the ABCDESs of tertiary prevention: 'A': aspirin, alpha-tocopherol, and ACE inhibitors; 'B': beta-blockers, B-vitamins, and blood pressure control; 'C': cholesterol management; 'D': diabetes management and diet; 'E': exercise and estrogen therapy; and 'S': social support, smoking cessation, and stress management.
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PMID:Avoiding Repeat Cardiac Events: The ABCDESs of Tertiary Prevention. 2008 58

Membranous nephropathy is the most common cause of nephrotic syndrome in adults. Binding of circulating autoantibodies to the glomerular filtration barrier leads to the development of this autoimmune disease. The clinical symptoms range from small proteinuria to severe nephrotic syndrome with enormous oedema, not controllable hyperlipidaemia and increased disposition for infection. One third of patients reach complete or partial remission of proteinuria under symptomatic treatment, which includes ACE-inhibitors and AT-I-blockers, loop diuretics and statins. Untreated the disease leads to loss of renal function over 5-10 years in 20-30% of patients. A risk score based on proteinuria and renal function is used to guide the decision when to start with an immunosuppressive therapy. A better adapted diagnostic and therapy of membranous nephropathy may be possible through measurement of circulating autoantibodies directed against a podocytic phospholipase-A(2) receptor.
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PMID:[Membranous glomerulonephritis: better therapy with autoantibody monitoring?]. 2187 6

Aortic valve stenosis (AS) is the most common form of valvular heart disease in the Western world, affecting ~40% of the population over the age of 80; to date the only established treatment is valve replacement. However, AS progression occurs over many years, and is associated from its earliest stages with increased risk of coronary events. Recent insight into the pathophysiology of AS has included central roles for angiotensin II, for diminished nitric oxide effect at the level of valve endothelium and matrix, and for inflammatory activation/redox stress culminating in activation of pro-calcific stimuli. Despite the presence of atheroma within the stenotic valve, hyperlipidemia per se does not play a critic role in the development of obstructive disease. We review emerging options for pharmacotherapy of AS, including in particular retardation of disease progression. The various clinical evaluations of lipid-reducing therapy have been uniformly unsuccessful in slowing AS progression. However, recent studies in animal models and retrospective evaluations in humans suggest that ACE inhibitors and/or angiotensin receptor blockers may be effective in this regard. Furthermore, agents normally utilized to treat osteoporosis also offer promise in retarding AS. Given the considerable morbidity, mortality and health care costs associated with AS, such therapeutic developments should be expedited.
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PMID:Prevention of aortic valve stenosis: a realistic therapeutic target? 2251 38


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