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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on clinical experiences obtained in 7 uremic patients treated since January 1976 3 times weekly by chronic hemofiltration. The observations which we collected in more than 300 treatments suggest that hemofiltration might be superior to conventional hemodialysis. The main advantages of this treatment are characterized by its better control of hypertension, hyperhydration, and possibly of uremic bone disease. Furthermore, the applied acrylonitrile membrane allows the removal of substances with a molecular weight up to 60,000, similar to the glomerular basement membrane. Additionally, we report on methodological problems, on the compatibility of hemofiltration, and finally on its efficiency for removal of different uremic solutes.
J Dial 1977
PMID:Clinical aspects of hemofiltration. 60 66

Separate ultrafiltration followed by haemodialysis (U.F.-H.D.) using Gambro Major or Cordis-Dow hollow-fiber dialyzers were evaluated in 10 dialysis patients over a mean period of 4 1/2 months and 455 U.F.-H.D. procedures. Fluid control was facilitated in oedematous patients but the number of hypotensive episodes during the combined procedure requiring intravenous 5% saline did not significantly decrease. No significant improvement in hypertension was noted. Ultrafiltration (U.F.) alone for acutely water overloaded, azotaemic patients proved very useful. Two to five liters of oedema fluid could be removed asymptomatically in one to three hours using transmembrane pressures of 250 to 500 mmHg and U.F. rates of 10 to 42 ml/min. Two patients became acutely and symptomatically hypotensive. One was an insulin dependent diabetic in whom 3800 ml were removed in 75 minutes and the other a hypertensive patient undergoing treatment with Minoxidil and propranolol.
J Dial 1978
PMID:Ultrafiltration followed by haemodialysis. A longterm trial and acute studies. 72 89

Thirty-two patients with advanced chronic renal insufficiency due to juvenile onset diabetes mellitus were submitted to dialytic treatment, 16 with intermittent haemodialysis and 16 with peritoneal dialysis. Both groups were similar with respect to onset of diabetes, course of renal insufficiency, as well as start and duration of dialysis treatment (382 and 389 patient months respectively). Patients on haemodialysis showed a more rapid progress of retinopathy and neuropathy, whereas the control of hypertension proved to be more difficult with peritoneal dialysis. A reduced peritoneal dialysance of urea, demonstrated in patients with diabetic nephropathy, could be improved by dipyridamole administration, whereas this drug showed no effect on the dialysances of urea and inulin in patients with chronic renal insufficiency of non-diabetic origin. There were no differences between the survival rates of the two groups which were substantially lower than in non-diabetic dialysis patients.
Proc Eur Dial Transplant Assoc 1978
PMID:Haemo- and peritoneal dialysis treatment of patients with diabetic nephropathy--a comparative study. 74 Jun 64

This study was carried out to assess the influence of saralasin (SAR), an angiotensin II-analogue, on peripheral and central angiotensin II-receptors by measurements of plasma renin activity (PRA) and arginine-vasopressin (AVP) release. Before and during i.v. infusion of 10 microgram/kg/min of SAR over a 30 minute period, blood samples were obtained from 15 recumbent hypertensive patients (7 renovascular, 8 essential) to determine hormone activities by radioimmunoassay. In 10 patients with a decrease of blood pressure following SAR, PRA increased significantly whereas AVP levels increased significantly in only 7 of these patients. In the remaining 5 patients without a fall of blood pressure, PRA and AVP remained virtually unchanged. The results indicate that an enhanced AVP release may be due to a hypotensive stimulus induced by SAR in angiotensinogenic hypertension. A direct influence of SAR on central receptors is unlikely under the conditions studied.
Proc Eur Dial Transplant Assoc 1978
PMID:Effect of saralasin on plasma renin activity and arginine-vasopressin in hypertensive man. 74 Jun 74

In the arteries of 17 rejected renal grafts 'activated' smooth muscle cells (ASMC) were discerned from a 'resting' type. Proliferation and fibre production by ASMC resulted in a marked thickening of intima. Each of four normal Wistar rats received 20 mg prednisolone i.v./day for one week and the development of hypertension was therapeutically prevented. Changes similar to those in the graft arteries were found in the rat aortas. We assume that SMC were stimulated by several mechanisms in rejection but also by extremely high dosed corticoids.
Proc Eur Dial Transplant Assoc 1976
PMID:Corticosteroids and proliferation of smooth muscle cells in arteries of renal transplants. 77 34

The incidence of hypertension defined as a mean diastolic pressure above 90 mmHg has been evaluated in 85 transplanted patients with a follow-up ranging from 3 to 78 months. The proportion of hypertensive patients rises during the first three months and stabilises subsequently around 60 percent. Over the years hypertension fluctuates so that one-third of the initially hypertensive patients become normotensive, whereas one-third of the initially normotensive patients become hypertensive. The main single aetiological factor is renal failure. No clear relationship was found between prednisolone dosage and hypertension. Renal artery stenosis was found in 2.4 percent of the cases. Finally no single aetiological factor was found in one third of the hypertensive patients. It is speculated that in some of them, minute intrarenal vascular lesions are responsible for the hypertension and lead ultimately to decreased renal function.
Proc Eur Dial Transplant Assoc 1976
PMID:Hypertension after renal transplantation. 77 38

Basal and stimulated plasma renin activity (PRA) and plasma aldosterone (PA) were measured in 13 hypertensive and 16 normotensive patients with kidney allografts one to nine years after transplantation. In both groups no significant differences were observed between mean basal and stimulated PRA and PA values. Therefore, we conclude that abnormal renin secretion might not be the main factor causing hypertension in renal allograft recipients. Other mechanisms seem to be involved in the pathogenesis of hypertension in these patients.
Proc Eur Dial Transplant Assoc 1976
PMID:Plasma renin activity (PRA) and plasma aldosterone (PA) in hypertensive kidney allograft recipients. 77 39

Of 13 patients with severe post-transplant hypertension, in 11 (85%) the hypertension was secondary to TRAS. Surgical correction of arterial stenosis reversed renal failure in 2 patients and cured or improved hypertension in 9 patients. Renin levels from TRV was normal in patients studied and was not useful in predicting surgical success. The patient's own kidneys are not the cause of post-transplant hypertension. Demonstration of an increased renin activity in the patient's own renal veins is not always associated with relief of hypertension by bilateral nephrectomy.
Proc Clin Dial Transplant Forum
PMID:Renal artery stenosis in renal transplant recipients. 80 Oct 61

Late onset (3-7 yrs) post-transplant renal hypertension is usually an indication of chronic, irreversible renal damage, and is a poor prognostic sign. In a small percent of patients (10%) however, hypertension can persist for years in conjunction with excellent renal function, and the absence of any known causes of early or late hypertension. This primary hypertension does not seem related to the recipient's pre-transplant blood pressure nor to the original renal disease. Rather, the high incidence of essential hypertension in the respective living related donor suggests that either a hypertensive diathesis exists, common to donor and recipient, or a transplantable factor inherent to the graft, or both causes, predispose to late onset primary hypertension.
Proc Clin Dial Transplant Forum
PMID:Late hypertension in renal transplant recipients: possible role of the donor in late primary hypertension. 80 Oct 58

Hypertension is prevalent in 49% of renal transplant recipients. Chronic rejection and impaired renal function may account for mild to moderate hypertension in most patients. The development of severe hypertension following renal transplantation, however, suggests TRAS, which is amenable to surgical correction with a high probability of success. Post-transplant hypertension did not correlate with renal diagnoses, sex, donor source and/or prednisone dose.
Proc Clin Dial Transplant Forum
PMID:Relationship of renal transplantation to hypertension in chronic renal failure. 80 Oct 57


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