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)

Collapsing glomerulopathy is a morphologic variant of focal segmental glomerulosclerosis (FSGS) characterized by segmental and global collapse of the glomerular capillaries, marked hypertrophy and hyperplasia of podocytes, and severe tubulointerstitial disease. The cause of this disorder is unknown, but nearly identical pathologic findings are present in idiopathic collapsing glomerulopathy and human immunodeficiency virus (HIV)-associated nephropathy, and collapsing glomerulopathy has been associated with parvovirus B19 infection and treatment with pamidronate. The pathogenesis of collapsing glomerulopathy involves visceral epithelial cell injury leading to cell cycle dysregulation and a proliferative phenotype. Clinically, collapsing glomerulopathy is characterized by black racial predominance, a high incidence of nephrotic syndrome, and rapidly progressive renal failure. Collapsing glomerulopathy also may recur after renal transplantation or present de novo, often leading to loss of the allograft. The optimal treatment for collapsing glomerulopathy is unknown. Treatments may include steroids or cyclosporine in addition to aggressive blood pressure control, angiotensin converting enzyme inhibitors and/or angiotensin II receptor blockers, and lipid lowering agents. The role of other immunosuppressive agents such as mycophenolate mofetil in the treatment of collapsing FSGS remains to be defined. Prospective clinical trials are needed to define optimal therapy of this aggressive form of FSGS.
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PMID:Collapsing glomerulopathy. 1270 81

Anemia in children after renal transplantation is more common than previously appreciated. Multiple factors appear to play roles in the development of post-transplant anemia, the most common of which is absolute and/or functional iron deficiency anemia. Most experts recommend that iron limited anemias in transplant patients should be diagnosed using the same criteria as for chronic renal failure patients. Serum erythropoietin (EPO) levels are expected to normalize after a successful renal transplantation with a normal kidney function, yet both EPO deficiency and resistance have been reported. While no large controlled trials comparing the effect of different immunosuppressive agents on erythropoiesis after transplantation have been performed, generalized bone marrow suppression attributable to azathioprine (AZA), mycophenolate mofetil (MMF), tacrolimus, antithymocyte preparations has been reported. Pure red cell aplasia (PRCA) occurs rarely after transplantation and is characterized by the selective suppression of erythroid cells in the bone marrow. PRCA has been reported with the use of AZA, MMF, tacrolimus, angiotensin converting enzyme inhibitors (ACEI), but not with cyclosporine (CSA) use. Post-transplant hemolytic uremic syndrome has been reported with orthoclone anti T-cell antibody (OKT3), CSA and tacrolimus therapy. Viral infections including cytomegalovirus, Epstein-Barr virus and human parvovirus B19 have been reported to cause generalized marrow suppression. Management of severe anemia associated with immunosuppressive drugs generally requires lowering the dose, drug substitution or, when possible, discontinuation of the drug. Because this topic has been incompletely studied, our recommendation as to the best immunosuppressive protocol after renal transplantation remains largely dependent on the clinical response of the individual patient.
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PMID:Anemia in children after transplantation: etiology and the effect of immunosuppressive therapy on erythropoiesis. 1289 2

We report three childhood cases of myocarditis associated with human parvovirus (B19 virus). All three children presented with significant cardiac decompensation, with one requiring extracorporeal membrane oxygenation support. Left ventricular function was severely impaired in all three. Myocardial biopsy confirmed histological myocarditis and was positive for B19 virus by nested polymerase chain reaction. Serum was positive for IgG B19 virus but negative for IgM in all three cases. All three children were treated with diuretics, ACE inhibitors, and immunosuppression. Prednisone and cyclosporin were continued until there was echocardiographic and histological improvement. All made a full clinical and echocardiographic recovery.
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PMID:Three cases of myocarditis in childhood associated with human parvovirus (B19 virus). 1462 16

We describe two children with previous anthracycline exposure for cancer who presented with acute decompensated left ventricular dysfunction. Both patients had evidence of dilated cardiomyopathy and required mechanical ventilation and inotropic support. Parvovirus B19 was detected by polymerase chain reaction of the blood. After several weeks of ventilation and inotropic support, both patients were weaned from ventilation and managed with oral carvedilol, ACE inhibition, and diuretics. Acute left ventricular decompensation in patients following anthracycline exposure may not be solely attributed to drug exposure, and viral etiologies should be considered.
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PMID:Parvovirus B19 infection associated with dilated cardiomyopathy in patients with previous anthracycline exposure. 1763 83