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)

Serum concentration of erythropoietin (EP) was measured with a hemagglutination inhibition technique and plasma renin activity (PRA) with a radioimmunoassay for angiotensin I in 26 renal transplant recipients 2-54 months after renal transplantation. In all patients, the EP values were significantly correlated with the levels of PRA (r = 0.76 p less than 0.001) and hematocrit values (r = 0.72, p less than 0.001). In one patient, erythrocytosis and high blood pressure associated with high EP and PRA levels disappeared after bilateral nephrectomy of his own kidneys. The results indicate an as yet unidentified relationship between the production of EP and renin.
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PMID:Erythropoietin and renin after renal transplantation. 78 10

A 23-year-old-man had true erythrocytosis and the nephrotic syndrome. A renal biopsy specimen showed focal sclerosing glomerulonephritis and nephrosclerosis. Both serum and urinary erythropoietin levels were increased, and plasma renin activity was in the high normal range. The association of erythrocytosis and glomerulonephritis with the nephrotic syndrome is reviewed, and the uniqueness of this association is proposed. Finally, a dissociation between these hormones was demonstrated using water immersion to the peck as a suppressive maneuver.
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PMID:Erythrocytosis associated with the nephrotic syndrome. 87 45

Juxtaglomerular cell tumor of the kidney is an uncommon neoplastic cause of surgically curable hypertension. We report a case of erythrocytosis due to elevated serum erythropoietin with a renin secreting juxtaglomerular cell tumor.
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PMID:Juxtaglomerular cell tumor with elevation of serum erythropoietin. 268 72

Twenty-five patients underwent bilateral native nephrectomy one to 68 months (mean, 15.6 months) following renal transplantation. The indications were erythrocytosis in two patients, recurrent urinary tract infection in three, medically uncontrolled hypertension in 18, and hypertension and urinary tract infection in two. One patient died two months after the nephrectomy, and one allograft was lost because of acute tubular necrosis. Both patients with erythrocytosis had prompt return of the hematocrit level and RBC mass to normal. Native nephrectomy eradicated the infection in each of the five patients with recurrent urinary tract infections. Results of nephrectomy for hypertension were classified as excellent in six patients, good in nine, and poor in four. Native renal-vein renin ratios of patients with excellent or good responses were not statistically different when compared with those of poor responders.
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PMID:Selective posttransplantation bilateral native nephrectomy. Indications and results. 635 7

In seven splenectomised dogs a left renal vein-splenic vein anastomosis was performed and the right kidney removed. Eighteen to twenty-four months after portalisation of renal venous blood no significant alterations of liver function tests were found. Long-term diversion of renal venous blood into the liver was followed by a slight increase of creatinine and 25(OH)D3, a decrease of alpha-amino acid nitrogen in blood plasma and of plasma renin activity in peripheral blood, by symptoms of slight carbohydrate intolerance despite hyperinsulinaemia and a slight decrease of erythrocytosis. No influence of this procedure on plasma proteins, lipids, electrolytes, aldosterone and cortisol was observed. No morphological abnormalities in liver and kidney tissues were found.
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PMID:Metabolic effects of long-term diversion of renal venous blood into the portal system. 701 1

Recent observations indicate that angiotensin-converting enzyme (ACE) inhibition corrects renal transplant erythrocytosis (RTE). The mechanism for this association is not known. We examined the effect of ACE inhibition on hematocrit, erythropoietin (EPO), and renin substrate. ACE inhibition has been reported to suppress renin substrate, which is known to stimulate EPO and erythropoiesis. In 15 patients with RTE, hematocrit dropped from 52.8 +/- 0.6 (SEM) to 45.8 +/- 1.4% after 8 weeks of treatment with Enalapril, 2.5-20 mg/day. Serum EPO (normal range: 9-30 mU/ml) was high in one, normal in seven, and low in seven patients. ACE inhibition reduced EPO in patients with initial high or normal levels but induced no change in patients with initial low levels. ACE inhibition had no significant effect on renin substrate. In one patient who rejected his first graft, erythrocytosis recurred following a second, successful transplant. Treatment was discontinued because of cough in two patients and symptomatic drop in blood pressure in one patient. We conclude RTE is not caused by hypererythropoietinemia. In patients with normal circulating EPO, erythrocytosis may result from an increase sensitivity to EPO, and ACE inhibition lowered hematocrit by further reduction of this hormone. However, the finding of erythrocytosis in half our patients with suppressed EPO, suggests the participation of non-EPO-mediated mechanism(s). The recurrence of RTE in a patient after a second transplant raises the additional possibility of patient-specific factors in the pathogenesis of this disorder. In contrast to other reports, we documented side-effects (cough, hypotension) in three (20%) of our patients. Our clinical experience, coupled with prior reports of spontaneous resolution of RTE in some patients, suggests that intermittent courses of ACE-inhibition may be the optimal strategy in the use of this form of therapy for RTE.
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PMID:Angiotensin-converting enzyme inhibition in the treatment of renal transplant erythrocytosis. Clinical experience and observation of mechanism. 762 54

We compared some of our latest experiments on blood pressure control and erythrocytosis in spontaneously hypertensive rats with Gaar's computer-simulated studies, which suggest that erythrocytosis is a key to understanding the hemodynamic changes in hypertension. We tested two of Gaar's several predictions: (i) peripheral vascular resistance decreases when the feedback control of erythrocytosis is blocked and (ii) in primary hypertension, blood volume is increased slightly. We also studied the interrelation of systolic blood pressure and plasma renin substrate in spontaneously hypertensive rats, and the effect of diet on renin, blood pressure, and erythrocytosis. Our data showed that (i) on a percentage basis the renin system supports blood pressure essentially in the same manner in normal and hypertensive rats, (ii) peripheral vascular resistance decreased when erythrocytosis was partially blocked by feeding a low-iron diet, (iii) blood volume was similar in normal and hypertensive rats, and (iv) dextrin stimulates plasma renin, packed cell volume, and blood pressure in hypertensive rats. We conclude that blood pressure and erythrocytosis are interrelated, that the combined data of stimulated and experimental studies support the notion that primary hypertension is a blood-vessel adaptation in response to a renal energy need that may require additional oxygen.
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PMID:Blood pressure control and erythrocytosis in rats: theory and observations. 795

True erythrocytosis is a relatively common complication of successful renal transplantation. From a group of 17 patients with post-transplant erythrocytosis (PTE), four underwent selective venous catheterization of the native and transplanted kidneys because of arterial hypertension. In three who presented with active PTE at the time the procedure was performed the peripheral blood (PB) concentration of EPO was elevated, and the level of erythropoietin (EPO) in native kidney veins was significantly higher than the PB and allograft EPO levels. Additionally, only one of the three cases had high levels of plasma renin activity (PRA). The fourth patient showed normal levels of EPO and PRA in PB and in venous blood from the native and transplanted kidneys. However, the PTE had subsided 4 months before the performance of the catheterization after he redeveloped terminal renal failure; the loss of a functioning allograft might have blunted the overproduction of EPO by the native kidneys. In conclusion, in patients with PTE, inappropriate EPO production seems to originate from the diseased native kidneys, and there seems to be no correlation between the production of EPO and the PRA.
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PMID:Postrenal transplant erythrocytosis: further evidence implicating erythropoietin production by the native kidneys. 800 62

Post-transplant erythrocytosis (PTE) has been increasingly recognized as a complication of kidney transplantation, and several risk factors have been defined. Recent evidence suggests renal function may also play a role in hematological recovery after transplantation and risk of PTE. In this study of kidney transplant recipients (n = 123), simultaneous Tc99m DTPA GFR (n = 710) and hemoglobin levels were compared with possible clinical determinants. The frequency histogram of post-transplant hemoglobin was bell-shaped and continuously distributed above and below the arbitrary definition of PTE, suggesting that PTE is not a separate disease entity. Hemoglobin reached a plateau at 12 months after transplantation and was correlated with isotopic GFR (r = 0.46, p < 0.001). This consistent and statistically independent relationship became prominent 3 months after transplantation. Hemoglobin was independently predicted by multivariate analysis by time after transplantation, presence of polycystic renal disease, greater serum albumin and reduced serum urea (which in turn were reflected by number of infective and rejection episodes), shorter kidney anastomosis time and a higher GFR, but not by immunosuppressive therapy. Rejection or infection episodes impaired hematological recovery. The independent determinants of GFR included hematological recovery. The independent determinants of GFR included hemoglobin level, kidneys from young, male donors, fewer HLA-DR mismatches and rejection episodes, shorter time on dialysis and greater azathioprine dose. Renal function was not altered by therapeutic phlebotomy. Determination of hemoglobin level by both donor and recipient variables supports the relevance of tubular and glomerular function in control of erythrocystosis after renal transplantation. A role for renin-angiotensin mediation in the alteration of intraglomerular hemodynamics and erythropoietin secretion is postulated.
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PMID:Erythrocytosis after renal transplantation: risk factors and relationship with GFR. 854 30

Erythrocytosis is a relatively common complication of renal transplantation. Recent observations indicate that angiotensin-converting enzyme inhibitors correct renal transplant erythrocytosis. Other drugs to inhibit the renin-angiotensin system have been developed recently. The newest of these is losartan, a specific antagonist of the angiotensin II type I receptor. We report three patients in which the use of losartan controlled posttransplant erythrocytosis. Our findings suggest that losartan can be effective and safe in the treatment of posttransplant erythrocytosis.
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PMID:Effects of losartan on the treatment of posttransplant erythrocytosis. 969 33


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