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)

A 53-year-old man with end-stage renal disease received a cadaver kidney after 15 months of peritoneal dialysis. Within one year of transplantation he developed hypertension and erythrocytosis. Percutaneous transluminal angioplasty was performed but 13 months later magnetic resonance angiography showed an anastomotic stenosis of the renal artery in the graft. In the meantime, he was submitted to venesections while the hypertension proved resistant to a multiple-drug combination. After two years, color Doppler sonography performed at our unit showed a noncritical stenosis, so we decided to start the patient on ACE inhibitors followed by angiotensin receptor blockers. A reduction of hematocrit to < 50% and partial control of blood pressure with stable renal function was obtained. Later we added minoxidil at low dosage, which resulted in excellent blood pressure control. The diagnosis of hemodynamically significant stenosis is not always easy to make; in this case a correct diagnosis was helpful for the treatment of erythrocytosis.
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PMID:[Erythrocytosis, renal artery stenosis and arterial hypertension in a kidney transplant recipient]. 2092 87

Post-transplant erythrocytosis is defined as an increase in hematocrit above 55%. It occurs in 10%-15% of renal transplant recipients, most commonly from 8 to 24 months after transplantation. Twenty-five percent of patients experience spontaneous remission within 2 years, while 75% develop symptoms and signs of hyperviscosity (headache, hypertension, plethora). The etiology is multifactorial and includes erythropoietin, renin-angiotensin system (RAS) and IGF-1 as the main factors. RAS inhibition with either ACE inhibitors or angiotensin receptor blockers is efficient therapy which decreases hematocrit in 90% of patients within 2 to 6 weeks, thus decreasing the incidence of fatal complications (like pulmonary embolism and stroke).
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PMID:[Post-transplant erythrocytosis]. 2235 5

Post-transplant erythrocytosis (PTE) is a condition with elevated haematocrit (hct) in renal allograft recipients. The mainstay of treatment is ACE inhibitors (ACEi) or angiotensin II receptor blockers (ARB), but seldom phlebotomy. PTE must be recognised early to prevent major thromboembolic events. We present a case of PTE that was refractory to blockade of renin-angiotensin system (RAS) by ACEi and ARB and required phlebotomy for control of hct. Our review of medical literature about prevalence and pathophysiology of PTE suggests that approximately 22% of patients with PTE are refractory to ACEi/ARB treatment. There are four plausible pathways that appear to play a role in causing PTE: disruption of erythropoietin regulation, mitogenic effect of the RAS on erythroid lineage, insulin-like growth factor 1 and androgenic stimulation. Presently, there is no unifying hypothesis involving these factors, but refractoriness to ACEi/ARB may represent a distinct subcategory of PTE.
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PMID:Post-transplant erythrocytosis refractory to ACE inhibitors and angiotensin receptor blockers. 2995 63


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