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We reported a case of a 38-year-old woman with both massive proteinuria and severe obesity. We diagnosed her as metabolic syndrome from her waist size of over 90 cm around her umbilicus, hyperlipidemia (high TG level) and hypertension. The urinary protein was more than 3.5 g/day and body mass index was 38.7 at admission. The renal biopsy specimen revealed IgA nephropathy. According to Clinical guidelines of IgA nephropathy 2nd version, Committee of IgA Nephropathy-the Special Study Group on Progressive Glomerular Disease, the Ministry of Health, Labor and Welfare of Japan-, her prognosis belonged to a rather poor group. We planed to administer steroid treatment first, however considering the adverse effects of steroid therapy, such as hyperlipidemia and diabetes mellitus, we tried to decrease her body weight as much as possible, and then treated her with both angiotensin converting enzyme inhibitor and anti-platelet drug. After her body mass index (body weight) was approximately 30.1 % (30 kg) less than that on admission, a parallel reduction of urinary protein was observed, and the final level was approximately 0.18 g/day. Decline in the body weight, diet and exercise were the chief measures that reduced the urinary protein without corticosteroid therapy.
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PMID:[An IgA nephropathy case with highly reduced urinary protein concomitant with reduced obesity]. 1712 85

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

Substantial evidence suggests that the intrarenal renin-angiotensin system (RAS) plays a role in the pathogenesis of diabetic nephropathy. Although the glomerular RAS is activated in the streptozotocin (STZ)-diabetic rat, the status of the glomerular RAS in the Zucker diabetic fatty (ZDF) rat, which is a commonly used genetic model of diabetes, is not known. Angiotensinogen (AGT), angiotensin II (Ang II), angiotensin converting enzyme (ACE), and angiotensin converting enzyme 2 (ACE2) were measured in glomeruli isolated from 4-week-old STZ-diabetic rats and 32-week-old ZDF rats. Glomerular injury was evaluated by histopathologic methods. Both STZ-diabetic and ZDF rats exhibited marked hyperglycemia and renal hypertrophy, but only ZDF rats demonstrated proteinuria and glomerulosclerosis. Glomerular AGT and Ang II levels were increased significantly in STZ-diabetic compared with nondiabetic control rats, accompanied by a reduction in ACE2 activity. In contrast, glomerular AGT, Ang II, and ACE2 were similar in ZDF rats and lean controls. ACE levels were not affected by diabetes in either diabetic model. In conclusion, the glomerular RAS is activated in the STZ diabetic rat but not in the ZDF rat despite a similar degree of hyperglycemia. The mechanism of nephropathy in the ZDF rat may involve factors other than hyperglycemia and RAS activation, such as hypertension and hyperlipidemia.
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PMID:Glomerular renin angiotensin system in streptozotocin diabetic and Zucker diabetic fatty rats. 1835 68

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

Long-term allograft survival poses a major problem in pediatric renal transplantation, with allograft nephropathy being the principal cause of graft failure after the first post-transplant year. The mechanisms of nephron loss resulting in graft dysfunction are multiple, comprising both immunologic factors such as acute and chronic antibody- or T-cell-mediated rejection and non-immunologic components. The latter include peri-transplant injuries and renovascular lesions (renal artery stenosis, thrombosis) as well as cardiovascular risk factors such as arterial hypertension and hyperlipidemia. Another relevant issue leading to progressive nephron loss and declining kidney transplant function is acute and chronic nephrotoxicity induced by the calcineurin inhibitors (CNIs) ciclosporin (cyclosporine microemulsion) and tacrolimus. Furthermore, the presence of an abnormal lower urinary tract as well as bacterial (recurrent pyelonephritis) and viral (cytomegalovirus [CMV], polyomavirus [BK virus; BKV]) infections are crucial factors involved in the incidence of chronic allograft dysfunction and graft failure. Renovascular lesions and lower urinary tract obstruction are typical indicators for surgical intervention. The aim of treatment in pediatric patients with renal failure secondary to a dysfunctional lower urinary tract is to create a sterile, continent, and nonrefluxive reservoir. Surgical techniques such as bladder augmentation and the introduction of intermittent catheterization and anticholinergic therapy have significantly improved graft outcome. Arterial hypertension, another factor responsible for graft function deterioration in pediatric renal transplant recipients, is controlled preferably by the use of angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor antagonists, which are known to possess nephroprotective properties in addition to their potent antihypertensive effects. Although treatment of subclinical rejection with augmented immunosuppression has been associated with better graft survival, an increase of the immunosuppressive level to avoid subclinical rejection should be weighed against the risk of infection. The majority of viral infections affecting kidney allografts are caused by CMV and BKV. Antiviral CMV prophylaxis or pre-emptive therapy with ganciclovir has been shown to have beneficial effects in the pediatric renal transplant population. Treatment of BKV-induced nephropathy is based on reduction of the immunosuppressant therapy, although specific antiviral agents such as cidofovir and leflunomide are known to inhibit BKV. However, cidofovir itself is nephrotoxic and should therefore be administered cautiously to pediatric renal transplant patients. Since CNIs are likewise known for their nephrotoxic effects, especially with long-term use, alteration of the immunosuppressant regimen is necessary in case of deteriorating graft function due to CNI-induced histopathologic changes. Complete CNI avoidance seems inappropriate because, in this situation in pediatric renal transplant recipients, other relatively potent immunosuppressant agents such as lymphocyte-depleting antibodies, which are frequently accompanied by a higher incidence of infections, are needed for rejection prophylaxis. CNI withdrawal and switching of the immunosuppressant regimen from CNI therapy to sirolimus may be an option for some pediatric renal transplant patients with less advanced graft function deterioration. Nevertheless, potential adverse events such as aggravation of proteinuria, hyperlipidemia, myelosuppression, and hypergonadotropic hypogonadism have to be considered, and controlled studies are lacking. At present, an immunosuppressant maintenance therapy composed of low-dose tacrolimus or ciclosporin (CNI minimization) and mycophenolate mofetil with low-dose corticosteroids appears to be the most promising strategy to adopt in pediatric renal transplant recipients at low or normal immunologic risk.
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PMID:Treatment strategies to minimize or prevent chronic allograft dysfunction in pediatric renal transplant recipients: an overview. 1987 24


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