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)

Three blood protease inhibitors were immunochemically quantitated in normo- and hypertensive subjects divided according to their plasma renin activity. As inflammatory reactions could be suspected in many subjects, the inflammatory state was estimated on the basis of three acute phase reactants and allowed one to conclude that total inter-alpha-trypsin-inhibitor and inter-alpha-trypsin-inhibitor derivative, as well as alpha-1-antitrypsin levels were increased in inflammation. Involvement of either protease inhibitor tested in the control of plasma renin activity is unlikely as no relationship between plasma renin activity and protease inhibitor levels could be demonstrated in non-inflammatory conditions. Finally, there was no particular distribution of alpha-1-antitrypsin (PI) phenotypes in the overall population.
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PMID:Quantitative study of human blood alpha-1-antitrypsin, alpha-2-macroglobulin and inter-alpha-trypsin-inhibitor with respect to plasma renin activity. 619 11

This study was aimed at the search of urinary biomarkers which might help to predict the clinical response of IgA nephropathy (IgAN) patients to angiotensin converting enzyme inhibitors (ACEi). First, we studied the urinary proteome of 18 IgAN patients (toward 20 healthy controls) who had been chronically treated with ACEi by using 2-D PAGE coupled to nano-HPLC-ESI-MS/MS analysis. We identified 3 proteins, kininogen (p = 0.02), inter-alpha-trypsin-inhibitor heavy chain 4 (35 kDa fragment) (p = 0.02) and transthyretin (p<0.0001), whose urinary excretion was different in IgAN patients' responders when compared to those who had not responded to ACEi. A reduction of daily proteinuria >50% and a stable renal function over time were used to classify patients as responders. Then, we adopted immunoblotting to confirm the predictive power of one of the above proteins, kininogen, in 20 patients with biopsy-proven IgAN, before starting any therapy. Thus, we confirmed that very low levels of kininogen urine excretion were indeed predictive of an inadequate or absent clinical response to ACEi therapy of IgAN patients, after 6-month follow-up. Concluding, the analysis of urine proteome of IgAN patients generated a set of proteins which distinguished subjects responsive to ACEi from those unresponsive to the inhibition of renin-angiotensin system (RAS).
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PMID:Urine protein profile of IgA nephropathy patients may predict the response to ACE-inhibitor therapy. 1809 57