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)

Although post exercise proteinuria has long been known, its exact pathophysiology is unclear. Our objective was to determine whether long-term angiotensin converting enzyme (ACE) inhibition by different ACE inhibitors had an influence on post exercise proteinuria. We studied 14 patients who also had mild, chronic proteinuria caused by diabetes mellitus or chronic glomerulonephritis. We compared changes both in chronic (baseline) and post exercise proteinuria, during and after treatment with three different ACE inhibitors, with appropriate washout periods for the three drugs to all 14 patients. Proteinuria (mg/24 hours +/- SD), prior to the treatment was 682 +/- 92. Proteinuria after treatment for 30 days with benazepril was 464.4 +/- 82.6 (p < 0.001), with enalapril: 477.1 +/- 105.5 (p < 0.001), and captopril: 504.7 +/- 100.1 (p < 0.001). Proteinuria three days after discontinuing the treatment with benazepril was 532.4 +/- 113.5, (p < 0.01), with enalapril: 561.3 +/- 128.5, (p < 0.01), and with captopril: 620.8 +/- 101.8, p = n.s. Post exercise proteinuria prior to treatment (mg/min. +/- SD) was: 1.38 +/- 0.32, vs. after a 30-day treatment period with benazepril: 0.81 +/- 0.19 (p < 0.001), enalapril: 0.95 +/- 0.24, (p < 0.001), captopril: 1.09 +/- 0.27 (p < 0.02). Post exercise proteinuria three days after discontinuing the treatment was (blood pressure already back to baseline): in case of benazepril: 1.26 +/- 0.36 (p = n.s.), of enalapril: 1.17 +/- 0.46 (p = n.s.), and of captopril: 1.34 +/- 0.41 (p = n.s.). We conclude that the renin-angiotensin system plays a significant role in the pathogenesis of post exercise proteinuria; the antiproteinuric effect of ACE inhibition in exercise-induced proteinuria seems to be associated chiefly with the hemodynamic changes due to these drugs, whereas in chronic proteinuria the antiproteinuric and antihypertensive effects are, at least partially, dissociated.
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PMID:Effect of ACE inhibition by benazepril, enalapril and captopril on chronic and post exercise proteinuria. 932 8

Proadrenomedullin N-terminal 20 peptide (PAMP) is a novel hypotensive peptide present in the precursor of adrenomedullin (AM), a vasodilative and natriuretic peptide. We examined the plasma and urinary levels of these peptides in patients with chronic glomerulonephritis (CGN). The mean plasma AM concentration of the patients with CGN did not differ from that of control subjects (4.17 +/- 0.17 v 3.87 +/- 0.21 fmol/mL, respectively), whereas urinary AM excretion was significantly less in the patients with CGN (5.96 +/- 0.95 v control, 8.93 +/- 1.02 fmol/mg of creatinine; P < 0.05). Plasma concentrations and urinary excretion of PAMP were significantly less for the patients with CGN compared with control subjects (0.91 +/- 0.08 v 1.23 +/- 0.20 fmol/mL; P < 0.05 and 25.0 +/- 3.0 v 35.0 +/- 3.6 fmol/mg of creatinine, respectively; P < 0. 05). The plasma AM concentration was negatively correlated with plasma renin activity (r = -0.58; P < 0.01) and aldosterone concentration (r = -0.40; P < 0.05). Urinary excretions of AM and PAMP showed significant correlations with urine excretion of sodium (r = 0.39; P < 0.05 and r = 0.49; P < 0.01, respectively). These findings suggest that AM and PAMP may have roles in the regulation of sodium in patients with CGN.
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PMID:Plasma and urine levels of adrenomedullin and proadrenomedullin N-terminal 20 peptide in chronic glomerulonephritis. 1040 Oct 24

This 1.5-year prospective study compared the effects of angiotensin II receptor blocker, candesartan(n = 21), and ACE inhibitor(ACEI, n = 23) on proteinuria and renal function in patients with moderate renal impairment due to chronic glomerulonephritis. Blood pressure reductions were comparable between both groups. Proteinuria was significantly reduced from 2.1 +/- 0.4 (mean +/- SE) to 0.6 +/- 0.2 g/day(p < 0.001) with candesartan, and the reduction was significantly larger than with ACEI(p < 0.01). Serum creatinine did not increase with candesartan or ACEI, suggesting the renoprotective effect. Serum potassium increased significantly with both drugs from 6 months. Plasma aldosterone concentrations(PAC) showed a stronger suppression with candesartan(150 pg/ml before treatment and 51 at 1.5 years) than with ACEI(104 pg/ml at 1.5 years). Plasma renin activity with candesartan(1.0 ng/ml/hr before treatment) decreased from 3.9 ng/ml/hr at 6 months to 1.3 at 1.5 years, whereas PRA remained elevated with ACEI. We speculate that the stronger reduction of PAC contributed to suppression of growth of mesangial matrix and the interstitial fibrosis in the candesartan group.
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PMID:[Comparison of ARB and ACEI for renoprotection in chronic glomerulonephritis]. 1239 99

Chronic glomerulonephritis (GN) is one of the leading causes of end-stage renal disease (ESRD). The possibilities for successful treatment in the earliest stages are still limited. Immunosuppressive treatment leads to complete or partial remission only in some patients. Even then, a non-immunological evolution to chronic renal insufficiency often enters a progressive course. By applying a consistent strategy for their individual evaluation and management, it is possible to improve the outcome of patients with GN. The early referral to a nephrologist and an early histomorphological diagnosis; the precise assessment of the type of injury, i.e. proliferative or non-proliferative; the indices of activity and chronicity; and the prognostic indicators are helpful for the therapeutic approach. The goal of the management of GN has to be to suppress the disease with minimum side effects of the treatment. Many unanswered questions and controversies remain concerning the immunosuppressive therapy. A precise distinction is needed between the problematic assertions and evidence-based protocols. A common task for the treatment of all types of chronic GN should be the protection of renal structure and function: control of blood pressure, action on renal haemodynamics and proteinuria via pharmacological inhibition of the renin-angiotensin system, control of hyperlipidaemia and limitation of fibrosis. Some novel and promising pharmacological approaches to extracellular matrix accumulation and chronic interstitial fibrosis are in progress.
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PMID:The treatment of glomerular disease--a compromise between the standard and the individual approach. 1281 65

Remarkable regional differences in the annual incidence of endstage renal disease (ESRD) was found within Japan, which has a relatively homogeneous ethnic composition. In addition, there existed no regional difference in the incidence of ESRD due to polycystic kidney disease, the major genetic disorder of the kidneys. These findings suggest that the presence of factors other than genetic disposition contribute to the differences. On the other hand, there were similar regional variations in the incidences of ESRD between two causes of ESRD: chronic glomerulonephritis and diabetic nephropathy. Because it is unlikely that the regional distribution of underlying disease incidence and the disease-specific progression rate would be similar for two different causes, this observation suggests that factors governing the progression rate, which operate commonly for all causes of ESRD but differ among regions, may play an important role in generating the regional differences. Finally, we examined regional differences in the amounts of inhibitors of the renin-angiotensin system used, especially angiotensin-converting enzyme (ACE) inhibitors, in our search for an explanation of the regional differences in ESRD dynamics. Among antihypertensive agents examined, only ACE inhibitors were negatively correlated with the annual incidence of ESRD. The renal protective effects of ACE inhibitors have been established by results with animal models of progressive nephropathy and by large-scale clinical trials. Our epidemiological results for Japan as a whole show the same protective effects still more convincingly from a different approach. It is not completely clear yet at present, however, how regional variations in the incidence of ESRD are generated. If we could identify in future the factors that contribute to the regional differences, strategies for the treatment of renal disease will become available from different angles. Thus, much effort will be encouraged for the further analysis of regional differences in ESRD dynamics.
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PMID:Proposal for mapping renal failure in Japan and its application for strategy to arrest endstage renal disease. 1654 72

IgA nephropathy (IgAN) is an important cause of progressive kidney disease with 25-30% of patients developing end-stage renal disease within 20 years of diagnosis. There is still no treatment to modify mesangial IgA deposition and available treatments are those extrapolated from the management of other patterns of chronic glomerulonephritis. There remains no consensus on the use of immunosuppressive agents for treatment of progressive IgAN and this is compounded by the relative lack in IgAN of randomized controlled trials relevant to current clinical practice. Patients with recurrent macroscopic hematuria or isolated microscopic hematuria and proteinuria <1 g/24 h require no specific treatment. Those with nephrotic syndrome and minimal change on renal biopsy should be managed as for minimal change nephropathy. There is no evidence to support the use of corticosteroids for nephrotic IgAN outside this group of patients. Patients presenting with acute renal failure require evaluation to distinguish acute tubular necrosis, which requires supportive therapy only, from crescentic IgAN, for which treatment with cyclophosphamide and corticosteroids in a regimen similar to that for renal small vessel vasculitis is indicated in the absence of significant chronic histologic injury. Patients at greatest risk of progressive renal impairment are those with hypertension, proteinuria >1 g/24 h, and reduced glomerular filtration rate at diagnosis. All such patients should be treated to a blood pressure of 125/75 mm Hg with dual blockade of the renin-angiotensin system with angiotensin-converting enzyme inhibition and angiotensin receptor blockade. At present, there is insufficient evidence for the additional use of immunosuppressive agents, antiplatelet agents, or anticoagulants.
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PMID:Treatment of IgA nephropathy. 1705 Dec 61

This Practice Point commentary discusses a recent meta-analysis by Catapano et al. of 13 randomized controlled trials (n = 425) that investigated the antiproteinuric response to dual blockade of the renin-angiotensin system in patients with proteinuric primary glomerulonephritis. Combination therapy was associated with a significantly greater decrease in proteinuria than either angiotensin-converting-enzyme inhibitor or angiotensin II type I receptor antagonist monotherapy. Dual blockade did not affect glomerular filtration rate, but was associated with a moderate increase in potassium levels. The renin angiotensin system plays a major role in proteinuria, and, therefore, one might expect that more-complete inhibition of the system would offer therapeutic advantages. There are still uncertainties regarding the safety of combination therapy, however, particularly in elderly patients and those with advanced kidney disease. More studies are needed before dual blockade can be widely recommended for all patients with chronic glomerulonephritis, and close monitoring is necessary for those currently receiving this therapy.
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PMID:Antiproteinuric response to dual blockade of the renin-angiotensin system in primary glomerulonephritis. 1846 48

The state of the renin-aldosterone system in 100 patients with hypertonic form of chronic glomerulonephritis (CGN) with the preserved renal function was assessed by RIA. The control group comprised 35 patients with CGH without arterial hypertension (AH). The study showed that plasma active renin (PAR) and aldosterone (PAL) levels remained unaltered in normotensive CGN patients with the preserved renal function but tended to increase in patients with AH. PAR levels correlated with the severity of AH. The PAL level was significantly elevated in CGN patients with grade II and III AH. Results of the study suggest an important role of elevated PAR levels in the development of AH in patients with CGN and preserved renal function. Moreover, such patients show a tendency toward a rise in their PAL level.
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PMID:[Renin-aldosterone system in patients with hypertensive form of chronic glomerulonephritis and preserved renal function]. 1982 34

The three main causes of Chronic Kidney Diseases [CKD] are diabetes mellitus, chronic glomerulonephritis and hypertension. CKD is an increasing burden in the community as more patients fall prey to kidney failure. Both dialysis and renal transplantation are expensive modalities of treatment for end stage renal failure [ESRF]. Through the years many clinical trials have been performed to retard the progression of CKD to ESRF. Most of the trials focus on three main strategies which aim at renal retardation, namely, control of hypertension, treatment of proteinuria and control of hypercholesterolaemia. More recently, investigators have been exploring the role of high dose ARBs as well as the use of Aliskiren, a renin inhibitor. Early therapeutic intervention is necessary as it will contribute to better chances of minimising glomerular damage and in the case of some, even lead to the improvement of renal function with regression of glomerulosclerosis.
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PMID:Clinical trials of the past decade in the management of chronic kidney disease. 2002 26

Angiotensin-converting enzyme inhibitors (ACE-i) and angiotensin II receptor blockers (ARBs) are of paramount importance in everyday clinical practice. Developed as antihypertensive drugs, they soon acquired another important indication as a result of their antiproteinuric activity and capacity to delay the progression of chronic kidney disease. ACE-i and ARBs started out being used as single drugs and were subsequently combined to obtain more complete blocking of the renin-angiotensin-aldosterone system (RAAS). The most evident advantages derived from the administration of these drugs - alone or in combination - have been obtained in proteinuric nephropathies, such as chronic glomerulonephritis and diabetic nephropathy, where they have become the treatment choice. Dual RAAS blockade has been recently evaluated in a large trial of high-risk cardiovascular patients, in whom no related benefits were shown. To the contrary, a higher risk of worsening renal function emerged. It is now quite clear that patients with high proteinuria levels are the ones that benefit most from RAAS inhibition, also with combined ACE-i and ARB. It is very important to pay the utmost attention when these drugs are used in patients in whom no benefit is obtained by RAAS inhibition, such as patients with chronic kidney disease and atherosclerosis, elderly patients, and those without any significant proteinuria.
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PMID:[Lights and shadows on single and dual RAAS blockade]. 2092 79


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