Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

High doses of the angiotensin converting enzyme inhibitor, captopril, is known to cause significant increases in urinary protein excretion in patients with idiopathic membranous nephropathy. To find whether other angiotensin converting enzyme inhibitors yield similar results, we prospectively examined the effect of enalapril in five consecutive patients with idiopathic membranous nephropathy, elevated arterial pressure, and proteinuria and compared them to age-matched controls receiving clonidine. Glomerular filtration rate, 24-hour urinary protein excretion, and arterial pressure were measured. All patients served as their own controls. Those who received enalapril demonstrated an initial increase in proteinuria (-0.3 +/- 0.7 delta gm/day, clonidine vs 3.9 +/- 0.9 delta gm/day, enalapril: P less than .05) despite similar decreases in arterial pressure (-18 +/- 6 delta mm Hg, clonidine vs -22 +/- 6 delta mm Hg, enalapril: NS) and glomerular filtration rate (-1.1 +/- 0.8 delta mL/min, clonidine vs -1.9 +/- 1.2 delta mL/min, enalapril: NS) when compared to the clonidine group. This increase in proteinuria, however, did not occur when these patients were rechallenged with enalapril. To our knowledge, this is the first report to document a significant increase in preexisting nephrotic range proteinuria following administration of nonsulfhydryl ACE inhibitor. This increase, however, appears to be unique to the initial treatment phase of the disease and does not affect long-term management.
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PMID:The effects of enalapril on urinary protein excretion in patients with idiopathic membranous nephropathy. 231 67

Camostat mesilate, a developed derivative of gabexate mesilate for oral use, was administered in a daily dose of 600 mg for 4 weeks to 17 patients with heavy proteinuria due to various nephropathies. Five patients had glomerulonephritis (3 patients with IgA nephropathy, one each with membranoproliferative GN and membranous nephropathy) and 3 had systemic vasculitis. These patients had been treated with glucocorticoid, cyclophosphamide, anticoagulants, and dipyridamole. Five patients had diabetic nephropathy and had been treated with conventional therapy including angiotensin converting enzyme inhibitors. Two cases with benign nephrosclerosis, one with Alport syndrome, and the rest with end-stage renal failure of undetermined cause were also included in this study. Urinary protein decreased promptly within 2 weeks (from 5.2 +/- 0.7 to 3.5 +/- 0.5, mean +/- SE, p less than 0.005), and serum total protein and albumin levels increased significantly. Serum creatinine levels did not change. Decreases in urinary protein excretion of more than 50% were observed in five out of eight patients with glomerulonephritis or systemic vasculitis, two out of five with diabetic nephropathy, and one with chronic renal failure. However, urinary protein excretion values remained at the same level in two patients with benign nephrosclerosis and a patient with Alport syndrome. We suggest that camostat mesilate caused a change in glomerular capillary permeability for macromolecules through its inhibitory effects on the kallikrein-kinin system, complement system, coagulation system, and platelet function, which contributed to the treatment of the various nephropathies.
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PMID:Effect of camostat mesilate on heavy proteinuria in various nephropathies. 279 62

A 49-year-old woman, who had been diagnosed as sarcoidosis based on bilateral hilar lymphadenopathy and lung biopsy, presented increased serum creatinine and calcium concentrations. Renal biopsy showed the presence of interstitial nephritis with non-caseating epithelioid granuloma and focal membranous transformation. Therapy with prednisolone was effective in normalizing serum creatinine, serum calcium, serum angiotensin converting enzyme, and urine beta2 microglobulin, but these abnormalities reappeared after rapid withdrawal of prednisolone. This is a rare case of sarcoidosis manifested by both membranous nephropathy and granulomatous interstitial nephritis, and indicates the necessity of long-term treatment of corticosteroid.
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PMID:Sarcoidosis with membranous nephropathy and granulomatous interstitial nephritis. 1056 50

A 50-year-old man with WPW syndrome and chronic atrial fibrillation controlled by digoxin exhibited nephrotic syndrome due to membranous nephropathy in 1994. For massive edema resistant to loop diuretics, administration of 2 mg/day of Temocapril, an ACE inhibitor with biliary excretion, was started. It provided marked natriuresis and rapid improvement of massive anasarca. Moreover, 6 months later at the time of writing this report, nephrotic proteinuria has decreased and abnormally depressed Ccr level has elevated. For massive edema resistant to loop diuretics in nephrotic syndrome, Temocapril might bring about a beneficial effect possibly through the induction of natriuresis, which has been suppressed by the over-expression of angiotensin II in tubulointerstitium.
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PMID:[A case of significant natriuresis and improvement of proteinuria by Temocapril, an ACE inhibitor with biliary excretion, in loop diuretics resistant edema in membranous nephropathy]. 1065 30

Previous reports have clarified that focal and segmental glomerulosclerosis(FSGS) appearing in membranous nephropathy(MN) is associated with a poorer prognosis than that of MN without FSGS. However, the etiology and pathogenesis of such FSGS lesions may show substantial individual differences. In some patients, hemodynamic alterations secondary to hypertension and vascular disorders seem to play a crucial role in the development of such FSGS lesions. In such instances, steady regulation of blood pressure might slow down further progression of FSGS lesions. Here we describe two cases of biopsy-proven MN with FSGS. Case I was a 44-year-old man who had shown massive proteinuria with hematuria at the age of 39 years. Renal biopsy specimens obtained at the age of 40 and 41 years showed MN without FSGS and MN with FSGS, respectively. His blood pressure control was fairly good throughout the course. Although he was on a steroid, an immunosuppressant, a low protein diet, and an ACE inhibitor, his renal function declined in 5 years. Case 2 was a 61-year-old woman who showed nephrotic syndrome at the age of 39 years. A renal biopsy specimen obtained at the age of 58 years showed MN with FSGS and remarkable atherosclerotic changes of the interlobular arteries. Her blood pressure control was rather poor throughout the course. Her renal function gradually declined over 22 years. Since parts of the FSGS lesions of the second case may have been caused by hypertension, it is tempting to speculate that day-to-day control of blood pressure could improve the long-term prognosis. We believe that, at least in some patients of MN with FSGS, careful management may lead to a more favorable course of decline in renal function.
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PMID:[Two cases of idiopathic membranous nephropathy with focal and segmental glomerulosclerotic lesions in which renal function progressively deteriorated]. 1099 19

We experienced a 24-year-old Japanese man, who was a hepatitis B virus carrier with nephrotic syndrome. Liver biopsy showed that he was suffering from chronic hepatitis (activity 2, fibrosis 2). Renal biopsy revealed membranous nephropathy(MN) with focal segmental glomerulosclerosis(FGS). Immunofluorescentic findings revealed the presence of HBe antigen along the glomerular capillaries as well as HBe antigenemia in circulation. Therefore, we diagnosed this case as HB virus-related membranous nephropathy associated with FGS lesions. He was treated with interferon(IFN) alpha-2b for over a month and angiotensin converting enzyme inhibitor. These therapies reduced urinary protein excretion from 4-6 g/day to 1-2 g/day, in accordance with a decrease in the titer of HBV DNA polymerase. The second renal biopsy revealed that the histological change from MN to membranoproliferative glomerulonephritis Type III after IFN therapy. These results suggest that IFN therapy might be effective for HB virus-related MN associated with FGS.
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PMID:[Effect of interferon therapy on hepatitis B virus related membranous nephropathy associated with focal segmental glomerulosclerosis]. 1128 Feb 14

While blood pressure is a recognized major determinant of renal function deterioration, the role of self blood pressure measurement (BPM) in predicting the loss of renal function in hypertensive patients with chronic renal insufficiency (CRI) has not been adequately addressed. One hundred and thirteen patients (F/M: 46/67; 56 +/- 1 years) with CRI (mean serum creatinine: 1.87 +/- 0.08; range: 1.4 to 3.5 mg/dl; average urinary protein excretion: 1.2 +/- 0.2 g/24 hrs.) were followed for 3 years. The record of renal biopsy revealed that 74 patients had IgA nephropathy, 16 had chronic glomerulonephritis, and 6 had membranous nephropathy, while 17, unbiopsied patients had underlying renal disease of unknown origin. Self BPM were made at regular intervals throughout the course of the study. All recorded blood pressures were included in a stepwise multiple regression analysis in which the decline in GFR per year was the dependent variable. Patients were primarily treated with a combination of amlodipine (5 to 20 mg daily), a calcium antagonist, and benazepril (2.5 to 5 mg daily), an ACE inhibitor in an effort to reduce their blood pressure at the office to < 130/85 mmHg. The simple correlation between blood pressures (i.e., office, home morning and home evening) and the decline in GFR were all statistically significant. The correlation coefficients of determination for this model were as follows: r = 0.64 for home morning SBP; 0.43 for office SBP; 0.39 for office DBP; and 0.38 for home morning DBP. The level of urinary protein excretion did not correlate with the decline in GFR. These data suggest that self BPM improves prognostic ability in hypertensive patients with CRI.
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PMID:Self-measured systolic blood pressure in the morning is a strong indicator of decline of renal function in hypertensive patients with non-diabetic chronic renal insufficiency. 1206 56

Membranous nephropathy remains the most common cause of nephrotic syndrome in adults. The common variant is idiopathic membranous nephropathy with no evidence of any known precipitating factors. Membranous nephropathy also occurs as a secondary form in association with inflammatory or neoplastic diseases. Prognosis is mostly favorable as shown by the frequency of spontaneous remissions which averages 30%, although about one-third of patients progress to end-stage renal failure. Risk factors for a poor prognosis include severe proteinuria, hypertension, older age, male gender and impaired renal function. Therapy should include an ACE-Inhibitor and/or angiotensin-II receptor blocker to lower proteinuria (blood pressure < or =130/80 mmHg). The majority of patients should be observed for six months whilst receiving conservative treatment before deciding about an immunosuppressive approach. The debate over its management continues today. Steroids alone are ineffective. Evidence-based medicine supports the use of cyclosporine or the Ponticelli regimen (monthly cycling routine of chlorambucil or cyclophosphamide alternating with prednisone).
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PMID:[Membranous glomerulonephritis]. 1456 65

Membranous nephropathy is the most common histologic phenotype associated with the primary nephrotic syndrome in adults and the second most common etiological diagnosis in over sixteen hundred renal biopsies on native kidneys processed at our institution over a 30 year period. Renal survival at 10 years is about 70%, but the course of the disease is related to a series of factors which have constituted the basis for mathematical models developed to predict the natural history in a given individual. These factors are gender, age, renal function at the time of diagnosis, presence of the nephrotic syndrome, high blood pressure and the degree of structural damage. Although in low risk patients a period of observation and the use of ACE inhibitors is a reasonable option, most nephrologists would elect to use pharmacological treatment to induce remissions of proteinuria and preserve renal function. The use of steroids and cytotoxic agents in alternating monthly cycles over six months is firmly supported by controlled, randomized clinical trials. If patients are resistant to this regimen or clinical considerations indicate it may be inappropriately toxic, the use of cyclosporin over 6 to 12 months is also a good choice, and it has been shown to be useful even in the context of deteriorating renal function. Mycophenolate mofetil and possibly rituximab may be options of last resort before considering the patient resistant to therapy. At all times, treatment of hypertension, non-specific antiproteinuric measures, and preventing complications of the nephrotic state should be top priorities in the overall therapeutic strategy.
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PMID:[Membranous kidney diseases in adults]. 1503 60

Idiopathic membranous nephropathy (IMN) remains the most common histologic entity associated with adult-onset nephrotic syndrome. The therapy for IMN is challenging. Steroids and various other immunosuppressive agents have been tried in IMN; however, current agents have not altered the course of IMN, are nonspecific and can be very toxic. In native kidneys affected by IMN, rituximab, a monoclonal antibody against the B-cell surface antigen CD20, has been shown to reduce proteinuria and prevent disease progression. In this report, we describe a 39-year-old white male with end-stage renal disease secondary to IMN that, 4 months post living unrelated kidney transplant, developed recurrent IMN with 18 g/day of proteinuria. In addition to angiotensin converting enzyme inhibitor and statins, the patient was treated with 4 weekly doses of 375 mg/m2 of rituximab with significant reduction in proteinuria, a corresponding increase in serum albumin and improvement in hypercholesterolemia. At 3 years post-transplant, his kidney function remains stable with 0.5 g/day of proteinuria.
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PMID:Anti-CD20 monoclonal antibody (rituximab) for the treatment of recurrent idiopathic membranous nephropathy in a renal transplant patient. 1729 27


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