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)

Erythrocytosis is infrequently seen in renal transplant recipients. Both theophylline and angiotensin converting enzyme (ACE) inhibitors have been reported to decrease the elevated hematocrit (Hct) and hemoglobin (Hgb) levels. We studied the efficacy of the ACE inhibitors ramipril (n = 6) and enalapril (n = 1) in seven stable renal transplant recipients. Although the ACE inhibitors significantly reduced the elevated Hct and Hgb levels during the short and long term (Hct 53 +/- 1 vs 48.8 +/- 0.7%; Hgb 17.8 +/- 0.4 vs 16.7 +/- 0.3 vs 16.7 +/- 0.3 gm/dl, at 1 year), the clinical significance of these reductions remains unknown. During therapy there were no significant changes in the blood pressure, serum creatinine and potassium levels and the medications were well tolerated.
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PMID:Long term effects of ACE inhibitors on the erythrocytosis in renal transplant recipients. 760 51

Enalapril effectively decreases hematocrits in patients with postrenal transplant erythrocytosis (PTE). We studied the effect of enalapril withdrawal on erythropoiesis in 18 patients with PTE who had been treated for 13 +/- 8 months. Hematocrit, reticulocyte count, plasma erythropoietin, and plasma insulin-like growth factor I were measured biweekly for six weeks. Red cell mass, plasma volume, transferrin saturation, and plasma angiotensin II were measured at withdrawal and six weeks later. Hematocrit increased by at least 0.04 in 13 patients ('responders') but changed by -0.08 to 0.01 in five patients ('nonresponders'). In the responder subgroup, hematocrit increased from 0.43 +/- 0.05 to 0.51 +/- 0.05 (P < 0.001), red cell mass increased from 25.4 +/- 5.9 to 28.9 +/- 5.9 ml/kg body weight (P < 0.001), and transferrin saturation decreased from 41 +/- 16 to 27 +/- 9 percent (P < 0.01). Reticulocyte count increased two weeks after withdrawal of enalapril. Plasma volume did not change significantly. No measurement changed in the nonresponder subgroup. Plasma levels of erythropoietin, total erythroid stimulating activity, insulin-like growth factor I, and angiotensin II did not change significantly in either subgroup. Enalaprilat did not inhibit erythropoiesis in cell culture. Thus, erythropoiesis increased in 13 of 18 patients after stopping enalapril and was independent of changes in circulating concentrations of several erythropoietic factors, including erythropoietin. The pathogenesis of PTE and mechanism underlying the beneficial effect of angiotensin converting enzyme inhibition remain undetermined.
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PMID:Erythropoiesis after withdrawal of enalapril in post-transplant erythrocytosis. 785

This report reviews the features of erythropoietin (Epo) production after renal transplantation. Successful kidney transplantation leads to the correction of renal anaemia over an 8-10 week period. An early ineffective peak of serum Epo may occur when there is delayed graft function. A late peak follows the decrease in serum creatinine and this is associated with a rise in haemoglobin. Serum Epo returns to normal when the haematocrit reaches 32%. Acute early rejection causes a striking reduction in serum Epo and reticulocytosis. In some patients the haematocrit continues to increase after complete correction of anaemia, resulting in post-transplant erythrocytosis (PTE). PTE generally appears to be an idiopathic erythrocytosis independent of Epo secretion. A greater Epo sensitivity of erythroid progenitors has been suggested. Theophylline and angiotensin converting enzyme inhibitors, which attenuate Epo production, can be used to treat PTE. The second part of this report describes the possible impact of human recombinant Epo (rHuEpo) on renal transplantation. The avoidance of blood transfusion with rHuEpo should eliminate the initiation of anti-HLA sensitization in uraemic patients without previous pregnancy and prior allograft. In some but not all presensitized patients transfusion withdrawal may reduce the sensitization level. There is currently no evidence that the reversing of anaemia by rHuEpo in kidney recipients impairs early graft function. Our results suggest that treatment with rHuEpo prior to transplantation may prevent the appearance of PTE. rHuEPO will reverse anaemia in patients with a failing graft and severe anaemia with little risk of accelerating graft failure and adverse events.
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PMID:Erythropoietin and erythropoiesis in renal transplantation. 852 79

Erythrocytosis represents a common complication in renal allograft recipients. Traditional therapies including phlebotomy and bilateral native nephrectomies are cumbersome for both the clinical personnel and the patient. Recently, pharmacological agents such as angiotensin converting enzyme inhibitor and theophylline have been proposed as effective therapies for post-transplant erythrocytosis (PTE). We have treated a PTE patient successfully with enalapril without any side effects and renal dysfunction after theophylline treatment showed no improvement in PTE. A decline in Ht levels was independent of the changes in Epo levels during enalapril treatment. Although the mechanism underlying the beneficial effect of enalapril remains undetermined, enalapril is recommended for the initial treatment of PTE.
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PMID:Efficacy of enalapril after ineffective theophylline treatment on erythrocytosis after renal transplantation. 928 12

GUIDELINE: In the case of erythrocytosis, the first-line treatment should be administration of ACE inhibitors or angiotensin II receptor antagonists.
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PMID:European best practice guidelines for renal transplantation. Section IV: Long-term management of the transplant recipient. IV.9.3. Haematological complications. Erythrocytosis. 1467 Oct 73

The use of angiotensin-converting enzyme inhibitors can be accompanied by a number of adverse events, including cough, angioedema, and hyperkalemia, as well as a peculiar form of functional renal insufficiency. Other, less obvious side effects accompany ACE inhibitor use, such as a reduction in red blood cell production. This feature of ACE inhibitor use may be employed to good effect, as in the management of post-transplant erythrocytosis. Alternatively, the suppressive effect of ACE inhibitors on red blood cell production may intensify the anemia of chronic renal failure and/or congestive heart failure. The untreated congestive heart failure patient typically has an increased red blood cell mass as a consequence of increased erythropoietin levels, with the latter governed by congestive heart failure-related renal hypoxia. This is not expressed as an increase in hemoglobin concentration because of the increase in plasma volume that marks advanced congestive heart failure. ACE inhibitor therapy can be expected to both reduce plasma volume and decrease red blood cell production. As a result, the hemoglobin concentration changes very little in the ACE inhibitor-treated congestive heart failure patient and usually falls in the low normal range. Recently, erythropoietin has been employed to good effect in congestive heart failure patients with borderline anemia. (c)2000 by CHF, Inc.
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PMID:Pharmacotherapy in congestive heart failure: ACE inhibitors and anemia in congestive heart failure. 1218 39

Posttransplantation erythrocytosis (PE) is a frequent problem in renal transplant patients. The pathogenesis and mechanisms of both the problem and therapy strategy are unknown. Since ACE and angiotensin 2 receptor inhibitors have been used to successfully manage PE, we speculated a relation between gene polymorphisms and this complication. Ninety-six ( 30 women, 66 men, age 34.4 +/- 11.0 years) renal transplant patients evaluated retrospectively, for gene polymorphisms of ACE, angiotensinogen, angiotensin 1 and 2 receptors (ATR1 and ATR2), as well as endothelial nitric oxide synthase (ecNOS). They were divided into two groups; patients with versus without PE, which was defined as >15 g/dL hemoglobin levels during the first year after renal transplantation. PE was found to be significantly more prevalent among D/D than I/I gene polymorphism of ACE genes (P <.04). The distribution of D/D, I/D, and I/I polymorphisms were 39.1%, 45.9%, and 7.6%, respectively. There was no difference between D/D and I/D polymorphisms. Comparing the I/D and I/I polymorphisms showed PE to be statistically more prevalent in the I/D polymorphism (P <.01). Logistic regression analysis revealed that D/D and I/D polymorphisms were significant risk factors for PE (P <.05, RR = 7.714 and P <.03, RR = 10.199, respectively). While previous studies revealed a relation between angiotensin II and PE, our study discovered the contribution of ACE gene polymorphism.
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PMID:Angiotensin-converting enzyme gene polymorphism significantly affects renal posttransplantation erythrocytosis. 1501 33

A significant relationship between hematocrit values and serum parameters such as the insulin like growth factor (IGF-1) and calcium was observed in patients with posttransplant erythrocytosis (PTE). Since angiotensin-converting enzyme inhibitors (ACEI) decrease hematocrit (Ht) levels in these patients, ACE genotype should play an important role. We designed this study to investigate whether ACE genotype or baseline concentrations of IGF-1, IGF-blood binding protein 3 (BP3), growth hormone (GH), or Ca influenced the response of Ht to ACEI treatment. Twenty-one kidney graft recipients with PTE were treated with enalapril (2.5 to 5 mg/d) for 1 year. IGF-1, BP3, GH, Ca, and Ht were determined before as well as 15, 30, 90, 180, and 365 days after enalapril treatment. ACE polymorphism was also determined. Enalapril treatment significantly decreased Ht levels. Only IGF-1 baseline levels showed a positive correlation to the decreased Ht (P < .025). ACE genotype as determined in 18 patients, showed no correlation with the response to enalapril. Patients with ACE genotype II showed a tendency to an earlier display of PTE. We conclude that low doses of enalapril decrease Ht levels in PTE patients; that PTE begins earlier in patients with II ACE genotype; and that only IGF-1 baseline levels influence the Ht decrease after treatment. These observations suggest that ACEI decrease the Ht via an inhibitory effect on IGF-1, which has a stimulary effect on erythropoiesis.
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PMID:Influence of angiotensin-converting enzyme polymorphism gene, IGF-1, and other factors in the response rate of hematocrit to enalapril treatment in patients with posttransplant erythrocytosis. 1584 8

Post-transplant erythrocytosis (PTE) is a well known phenomenon occurring in 5-17% of renal transplant recipients (RTR). In this retrospective study, we studied 47 RTR which included 39 males and eight females. They were divided into two groups according to the presence or absence of PTE, which was defined as a hematocrit of more than 51%. Nine of the 47 patients (19%) developed PTE all of whom were males. The mean age of patients with PTE was 44 +/- 9 years versus 40 +/-11 years for patients without PTE. The mean follow-up period was 113 +/- 26 months and 93 +/- 58 months for the PTE and non-PTE groups respectively. The mean period after transplant when PTE developed was 9.8 +/- 9 months and it lasted for 37 +/- 3 months. Thromboembolic complications in the form of lower limb deep vein thrombosis occurred in one patient. Most patients were treated with phlebotomies, and one received an angiotensin converting enzyme inhibitor. There were no apparent predisposing factors in any but one patient, who had autosomal dominant polycystic kidney disease and developed hydronephrosis of the transplanted kidney. This might have caused excessive production of erythropoietin resulting in PTE. The serum creatinine values were higher, although statistically insignificant in patients with PTE. Chronic rejection was more commonly seen in patients with PTE (44%) than those without PTE (11%). Our findings suggest that PTE is a benign condition affecting males more than females. It may have an association with chronic rejection. Most cases can be controlled using phlebotomy.
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PMID:Post-transplant erythrocytosis: a review of 47 renal transplant recipients. 1764 78

Chronic mountain sickness (CMS) and high altitude pulmonary hypertension (HAPH) have been well described in different mountainous regions of the world as chronic high altitude (HA) diseases. This review briefly summarizes the available data from some genes known to be regulated by hypoxia-inducible factor 1 (HIF-1) and/or by hypoxia that have been studied in populations from these regions suffering from CMS and/or HAPH. Excessive erythrocytosis, caused by a lower oxygen saturation and hypoxic ventilatory response and/or ventilatory inefficiency, is the outstanding sign of CMS, and right ventricular enlargement, pulmonary hypertension, and remodeling of pulmonary arterioles are hallmarks of HAPH. Familial character and heritability studies have suggested that genetic factors could make a contribution to the pathogenesis of CMS and HAPH. Even though some alleles are more prevalent (G allele of eNOS polymorphism Glu298Asp in Sherpas and ACE I allele in HAPH Kyrgyz) or less prevalent (ACE D allele in HA Andeans) in the different high altitude populations, published data to date are insufficient for a rigorous test of any hypothesis regarding the implications of these gene polymorphims in CMS or HAPH.
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PMID:Gene expression in chronic high altitude diseases. 1857 44


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