Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary sclerosing cholangitis (PSC) is a progressive liver disease without adequate treatment. Because the pathogenesis of PSC is not well understood, specific therapies designed to alter the pathogenesis are not available. Animal models suggest a link between bacterial overgrowth, lipopolysaccharides from the bacterial cell walls and stimulation of endogenous TNF formation which can be inhibited by pentoxifylline. Unfortunately, in humans treated with pentoxifylline, little effect was seen. Antibiotics such as metronidazole, vancomycin, tetracycline and azithromycin in small studies show biochemical improvement. Docosahexanoic acid has been used for treating patients in a small pilot study and led to some improvement in liver biochemistries. Immunologic abnormalities have been considered to be potentially important. Attempts to treat PSC with mycophenolate mofetil and tacrolimus have been largely unsuccessful. Budesonide has shown a limited benefit, but perhaps more so in patients with elevated IgG4 levels. PSC is characterized by marked fibrosis. Modulation of the renin-angiotensin system as well as use of rapamycin may reduce fibrosis, but data from this approach has been scant. Bile acids have been tested, but initial doses used in primary biliary cirrhosis led only to biochemical improvement. Higher doses of ursodeoxycholic acid (28-30 mg/kg/day) seemed to be associated with a worsening outcome. Intermediate doses have been tested in a study where biochemical improvement was seen and trends towards enhanced survival were found, but only about two thirds of the anticipated enrollment occurred. Currently, there are multiple potential therapeutic avenues to explore for patients with PSC, and it is hoped that one of these will lead to identification of a proven therapy for this disease.
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PMID:New treatment strategies for primary sclerosing cholangitis. 2169 Nov 16

IgA nephropathy is an immune-mediated chronic glomerulonephritis with a great variability in clinical presentation and outcome. The disease can progress to end-stage renal failure in 25% of patients. For this reason we should identify patients with potential to progress. Most important risk factors for progression are persistent proteinuria, hypertension, decreased renal function and some histological lesions. The actually suggested treatment is summarized in KDIGO Clinical Practice Guideline from 2012. They suggest to give firstly non-specific supportive treatment (especially renin-angiotensin system blocking agents). Recommendation about steroid/immunosuppression treatment is based on low level of evidence. Recently three studies were organised concerning benefits and risk of steroid/immunosuppressive treatment added together with specific supportive treatment. In the STOP-IgAN study, systemic steroid/immunosuppressive treatment significantly decreased proteinuria but did not stop progression. In the TESTING study, systemic steroid treatment significantly decreased proteinuria and progression. However, the study was recently discontinued due to several severe side effects of steroid treatment. Involvement of intestinal mucosal immunity in the pathogenesis of IgA nephropathy suggested the NEFIGAN study with budesonide treatment. Budesonide releases corticosteroid in distal small intestine and colon. Proteinuria was significantly decreased and renal function remained stabile. High number of withdrawals owing to adverse effects is a major concern implying a substantial systemic effect of budesonide. We need further information on the characteristics of patients who most likely benefit from steroid/immunosuppressive treatment given after or together with specific supportive treatment. Orv Hetil. 2017; 158(49): 1946-1952.
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PMID:[Considerations on the treatment of IgA nephropathy on the basis of the results of the latest studies (STOP-IgAN, TESTING, NEFIGAN)]. 2919 36