Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amyloidosis results from protein infiltration of the extracellular space of organs and tissues. Several amyloidosis proteins have been identified. Protein AL, (deriving from immunoglobulin light chain), protein AA and prealbumin are the most involved in this disease. When AL amyloidosis involves the heart, the illness is often terminal. Most clinical symptoms are heart failure and arrhythmia or block conduction. This case was characterised by the unusual combination of hypertension and amyloidosis. The diagnosis suggested by the echocardiographic but was confirmed by the damaged organ's biopsy. The present case concerns a young woman, who has hypertension and a pulmonary oedema. The echocardiographic scan showed a septal hypertrophy with a shining and granite-like aspect which is compatible with heart amyloidosis. Systolic and diastolic disorder with mitral and aortic regurgitation were also revealed. The kidney and rectum biopsies confirmed amyloidosis AL of the Kappa dysglobulinemia type, without extraosseous plasmocytoma. The heart and kidney failure symptoms disappeared after treatment with diuretics and ACE inhibitors.
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PMID:[Heart failure and arterial hypertension disclosing amyloidosis]. 929 35

Angiotensin II receptor blockers (ARBs) are effective in controlling blood pressure and have been shown to reduce proteinuria with fewer adverse effects than angiotensin converting enzyme inhibitors. In the present prospective study, we evaluated the action of irbesartan, an ARB with a long half life, on proteinuria, peritoneal protein losses, and peritoneal transport in patients with chronic renal failure (CRF) undergoing peritoneal dialysis (PD). We enrolled 15 stable patients (11 with diuresis of more than 500 mL/day; 40% women; 40% with diabetes) into the study. Mean age of the patients was 65 +/- 15 years, and mean time on PD was 33 +/- 21 months. The study was performed in two stages. In stage I, patients received no irbesartan. In stage II, patients received 30 days of treatment with irbesartan (145 +/- 72 mg/day). After treatment with irbesartan, and no changes in blood pressure level as compared with baseline, we observed a reduction in proteinuria (r = 0.690, p < 0.05), decreased peritoneal protein losses at 4 hours' and 24 hours' dwell time (r = 0.910 and r = 0.930, p < 0.001), decreased peritoneal Kt/V(r = 0.586, p < 0.05), and increased peritoneal creatinine clearance (r = 0.943, p < 0.001). Levels of serum albumin (r = 0.630, p < 0.05), prealbumin (r = 0.810, p < 0.001), and transferrin (r = 0.551, p < 0.05) increased after treatment with irbesartan. We conclude that treatment with irbesartan in patients with CRF undergoing PD modifies peritoneal transport and reduces peritoneal and urinary protein loss. This effect probably has a positive impact on nutritional parameters. Further studies are required to elucidate the mechanisms involved.
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PMID:Effects of angiotensin II receptor blocker (irbesartan) on peritoneal membrane functions. 1538 90

Acute thrombotic complications remain a constant, proportionally increasing complication before and after renal transplantation. We sought to investigate predictors for a prothrombotic state that increased the risk of vascular access thrombosis, among chronic renal failure patients during the waiting period prior to cadaveric renal transplantation. Chronic renal failure patients awaiting cadaveric renal transplantation and followed between January 2002 and January 2005 were included in this study. The 109 subjects including, 61 females and 48 males of mean age: 47.4 +/- 12.9 years; There were 36 continuous ambulatory peritoneal dialysis and 73 hemodialysis patients. Serum albumin, prealbumin, CRP, d-dimer, fibrinogen, antithrombin III, anticardiolipin antibodies (immunoglobulins G and M), homocystein, vitamin B12, folic acid, total cholesterol, triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and total platelet count were measured in each patient. Factor V Leiden, prothrombin 20210, ACE and MTHFR gene mutations were studied in all patients. Vascular Access thrombosis was detected in 62 patients. During follow-up 31 of 109 patients died. Vascular access thrombosis occurred in 78 patients who survived and 31 who died. The patients who died showed a significantly higher rate of thrombosis than those who survived (P = .003, OR: 4.61, CI: 1.70 to 12.50). Among the above biochemical risk factors, multiple regression analysis and backward logistic analysis revealed that d-dimer was the strongest biochemical predictor of thrombosis (P = .013, RR: 17.8). Upon evaluation of genetic risk factors, only factor V Leiden mutation was related to vascular access thrombosis (P = .001). In conclusion, the presence of vascular access thrombosis is a risk factor for mortality during the waiting period for cadaveric renal transplantation. As patients with factor V Leiden mutation or high serum d-dimer levels are at high risk for vascular access thrombosis, we recommend close monitorizing of these patients and use of anticoagulant therapy during the waiting period prior to renal transplantation.
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PMID:Predictors of vascular access thrombosis among patients on the cadaveric renal transplantation waiting list. 1654 34