Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 19 patients with unilateral renal artery stenosis and subsequent renovascular hypertension plasma renin activity (PRA), plasma concentrations of atrial natriuretic peptide (ANP), erythropoietin (Epo), H+ and HCO3-, as well as pO2 and pCO2 were assessed in renal venous blood of the 'ischaemic' and normally perfused kidney, both in arterial blood and in the inferior vena cava distally from the orifices of the renal veins. PRA and ANP were significantly elevated in venous blood of the ischaemic kidney as compared with the normally perfused kidney. In contrast to PRA and ANP, plasma concentrations of Epo were similar in blood withdrawn at all vascular sites. pO2 and pCO2, as well as blood H+ and HCO3- concentrations in venous blood of the ischaemic kidney were of the same magnitude as of the normally perfused kidney. From the results presented in this paper it follows that (i) in contrast to plasma renin activity and ANP, unilateral renal 'ischaemia' does not influence plasma concentrations of Epo in renal venous blood, and (ii) chronic haemodynamic alterations do not seem to influence Epo secretion by the kidneys.
Nephrol Dial Transplant 1992
PMID:Plasma erythropoietin concentrations in renal venous blood of patients with unilateral renovascular hypertension. 131 93

Plasma, urine, erythrocyte and leukocyte magnesium were measured in normotensive and hypertensive renal transplant patients who were being treated with either azathioprine or cyclosporin. These were compared with essential hypertensive patients and normal subjects. Erythrocyte and leukocyte magnesium were reduced in renal transplant patients in independent association (ANOVA) with both cyclosporin treatment (P = 0.03, P = 0.016 respectively) and hypertension (P less than 0.001 for both). Therefore, hypertensive transplant patients on cyclosporin had the lowest magnesium content of both erythrocytes (1.22 +/- 0.09 mmol/l cells) and leukocytes (2.68 +/- 0.2 nmol/10(6) cells) compared to normal subjects (1.96 +/- 0.17 and 4.11 +/- 0.58 respectively) whereas normotensive transplant patients on azathioprine had normal values (2.12 +/- 0.16 and 5.13 +/- 1.0 respectively). Plasma magnesium was also reduced with cyclosporin treatment. Urine magnesium was not significantly different between any of the groups. Therefore, magnesium depletion may have a role in hypertension in renal transplant patients. Since cyclosporin treatment is also associated with magnesium depletion, this could explain the increased occurrence of hypertension in these patients.
Nephrol Dial Transplant 1992
PMID:Reduced erythrocyte and leukocyte magnesium is associated with cyclosporin treatment and hypertension in renal transplant patients. 133 72

Twenty-five patients with transplant artery stenosis were identified among 1141 renal graft recipients. Impaired graft function (9 patients), hypertension (4 patients) or both (12 patients) were the indications for arteriography. All were treated by percutaneous angioplasty (PTA). The immediate technical success rate was 88% and actuarial graft survival was 88% and 80% at 2 and 5 years respectively. The long-term success rate on graft function was 67% (median observation time 24 months) and on hypertension 63% (median observation time 23 months). Six patients needed rePTA (8 procedures) and in only one patient was surgical repair performed. No case of graft loss due to PTA was recorded and in only one case did occlusion of a segmental artery lead to impairment of graft function. Minor complications were recorded in four other cases and in no case was surgical intervention necessary. Based on these results we favour PTA as a first-line interventional procedure in transplant renal artery stenosis, and the need for surgical repair has been low.
Nephrol Dial Transplant 1992
PMID:Long-term clinical results of percutaneous transluminal angioplasty in transplant renal artery stenosis. 131

Systemic hypertension as assessed by causal blood pressure measurements is a frequently reported side-effect of recombinant human erythropoietin (rHuEpo) treatment. We investigated the effect of rHuEpo treatment on the 24-h ambulatory blood pressure and heart rate profiles of 13 chronic haemodialysis patients. After 3-4 months of rHuEpo therapy it was found that the mean haematocrit had increased from 24.5 +/- 1.0% to 32.0 +/- 1.1% (P less than 0.005), while body-weight and control of uraemia as assessed by routine laboratory data remained unchanged. Despite gradual and incomplete correction of anaemia by use of low doses of rHuEpo, increases in the ambulatory systolic and diastolic blood pressure were found. The greatest increases affected day-time systolic blood pressure and night-time diastolic blood pressure, and these increases were significant (P less than 0.05). As a result, pulse pressure increased during day-time (P less than 0.05) while the night-time decline in diastolic blood pressure disappeared. An increase in peripheral resistance after partial correction of renal anaemia might explain these observations. rHuEpo therapy increased the percentage of abnormal ambulatory blood pressure measurements (defined as systolic blood pressure greater than 140 mmHg and/or diastolic blood pressure greater than 90 mmHg) from 33% to 52% (P less than 0.05) while in contrast, mean casual prehaemodialytic and posthaemodialytic blood pressure values remained unchanged. We conclude that changes in 24-h blood pressure profiles should be carefully assessed by ambulatory blood pressure monitoring in haemodialysis patients treated with rHuEpo, since these changes are likely to be missed when only causal blood pressures are measured.
Nephrol Dial Transplant 1992
PMID:Effect of recombinant human erythropoietin therapy on ambulatory blood pressure and heart rate in chronic haemodialysis patients. 131 80

Diagnostic criteria of analgesic nephropathy with well-defined sensitivity and specificity are not available. During a 2-year period all new patients (n = 273) starting renal replacement therapy in 13 Belgian dialysis units were investigated aiming to select diagnostic criteria of analgesic nephropathy with acceptable performance. Using several interview techniques, a history of analgesic abuse was found in 31% of the patients. Analgesic abusers presenting a clear non-analgesic-related renal diagnosis were excluded from analysis (n = 25). Comparing the remaining abusers (n = 60) and patients without a history of analgesic abuse (n = 188) it was found that renal imaging investigations (sonography plus tomography), showing a decrease in length combined with bumpy contours of both kidneys, presented a sensitivity of 90% and a specificity of 95%. The additional finding of signs of renal papillary necrosis resulted in an overall sensitivity of 72% and a specificity of 97%, giving a positive predictive value of 92%. Other signs frequently mentioned in the literature (hypertension, anaemia, sterile pyuria, bacteriuria, proteinuria) showed insufficient sensitivity and/or specificity to be of help for diagnosing analgesic nephropathy in end-stage renal failure (ESRF) patients starting renal replacement therapy.
Nephrol Dial Transplant 1992
PMID:Diagnostic criteria of analgesic nephropathy in patients with end-stage renal failure: results of the Belgian study. 132 Feb 26

Urinary excretion of tissue kallikrein is reduced in essential hypertension. Although a similar finding has been reported in spontaneously hypertensive rats (SHR), only a few studies have been concerned with the amount of enzyme within the kidney both at the time of onset and during progression of the hypertension. We have performed an ontogenic study on the renal parenchymal values and immunoreactivity of tissue kallikrein in Okamoto SHR aged 4-78 weeks. Additionally, these two parameters were analysed in human biopsies taken from patients with hypertensive nephropathy. The enzymatic activity of renal tissue kallikrein (active and total; specifically antagonized by anti-tissue kallikrein antibodies), increased from 4 to 52 weeks in SHR when compared to normotensive Wistar Kyoto (WKY) rats; this increase was associated with a significant increase in blood pressure. In contrast, 78 weeks SHR and human biopsy tissue showed a substantial reduction in tissue kallikrein values. Also, both renal tissues showed a reduction in immunoreactivity in the cells of the connecting tubules that specifically store the enzyme. In advanced hypertension the observed reduction in tissue kallikrein was probably secondary to a loss of distal tubular mass, as a result of tubular atrophy and fibrosis. The greater values for renal tissue kallikrein in the kidney and reported reduced urinary excretion during the early phases of spontaneous hypertension may be explained by a primary defect in the mechanisms that regulate release of tissue kallikrein from the connecting tubule cells.
Nephrol Dial Transplant 1992
PMID:An ontogenic study of renal tissue kallikrein in Okamoto spontaneously hypertensive rats: comparisons with human hypertensive nephropathy. 132 Feb 31

The relationship between the renin-angiotensin system and erythropoietin was studied in twenty patients with renal artery stenosis and hypertension. Ten of the patients had a unilaterally activated renin-angiotensin system (group 1), while ten patients had not (group 2). Plasma erythropoietin was simultaneously measured in a brachial artery and both renal veins before and 5 and 30 min after an intravenous injection of 1.25 mg enalaprilat. The mean (+/- SD) arterial erythropoietin concentration was 27.3 +/- 16.8 mU/ml in group 1 and 14.1 +/- 11.3 mU/ml in group 2 patients (P less than 0.05). There was no significant change after enalaprilat i.v. in either group. The venous erythropoietin concentration in plasma from the stenotic kidney did not differ from that of the contralateral kidney. The higher erythropoietin concentration in group 1 patients may be explained by a systemic stimulatory effect of the renin-angiotensin system on erythropoietin production. As no side-differences were found, renal vein as well as peripheral erythropoietin measurements cannot be used as a tool in the diagnosis of the functional significance of a renal artery stenosis.
Nephrol Dial Transplant 1992
PMID:Diagnostic use of renal vein erythropoietin measurements in patients with renal artery stenosis. 132 75

The results of renal transplantation in patients with juvenile-onset diabetes mellitus were compared to those of a well-matched control group of non-diabetic patients. All transplantations were performed between 1977 and 1988. In the diabetic group hypertension (72 versus 41%), coronary artery disease (17 versus 0%), and peripheral vascular disease (19 versus 0%) had been significantly more frequent pretransplantation. Fewer diabetic patients had previously been treated with dialysis therapy (69 versus 97%). Graft function measured by creatinine clearance after 1 year follow-up, and incidence of proteinuria were not significantly different. The overall graft survival was significantly worse in the diabetic group compared to the control group: 42 versus 69% after 60 months and 21 versus 62% after 90 months. This was caused by a significantly worse patient survival in the diabetic group after 105 months: 28 versus 78% in the control group. The graft survival following exclusion of the patients who died with a functioning graft did not differ significantly between the groups after 60 and 90 months: 62 and 31% in the diabetic group and 69 and 62% in the control group. The existence of any vascular disease before transplantation, especially pre-existing peripheral vascular disease, had a significant effect on mortality in diabetic patients (P = 0.0003). After transplantation, diabetic patients had significantly more cerebrovascular accidents (23 versus 3%), peripheral vascular disease (31 versus 3%), and number of infections (1.9 versus 1.2). Retransplantation was carried out in each group to the same extent, with the same success rate.
Nephrol Dial Transplant 1992
PMID:Increased morbidity and mortality in patients with diabetes mellitus after kidney transplantation as compared with non-diabetic patients. 132 80

We report three cases of primary aldosteronism associated with autosomal dominant polycystic kidney disease. The diagnosis of primary hyperaldosteronism was based on the presence of hypokalaemia with excessive urinary potassium excretion and/or the characteristic hormonal changes. Renal function impairment due to autosomal dominant polycystic kidney disease could mask hypokalaemia. The interpretation of adrenal imagery may be hindered by adjacent renal cysts. In one case an adrenal adenoma was detected and surgically removed, with only partial correction of the blood pressure. This could be explained by the persisting underlying autosomal dominant polycystic kidney disease. We conclude that in a hypertensive patient with polycystic kidney disease, extrarenal causes of hypertension may be present.
Nephrol Dial Transplant 1992
PMID:Autosomal dominant polycystic kidney disease with primary hyperaldosteronism. 839 25

Chronic hypertension with renal failure is the most common cause of death in a large family (10 children, 40 grandchildren, 109 great-grandchildren) with acute porphyria. A prospective study of 26 porphyric (19 latent) and 26 nonporphyric subjects shows a significant difference between mean systolic (141 versus 123 mmHg, P < 0.05) and diastolic (88 versus 74 mmHg, P < 0.05) blood pressures and plasma creatinines (geometric mean 99 versus 79 mmol/l, P < 0.02). Five of the 19 porphyric grandchildren have died of the complications of chronic hypertension, with renal failure in three. When the results of the retrospective and prospective studies in these 19 subjects are combined, 10 of the 16 tested (62%) had hypertension and seven of the 14 tested (50%) had renal impairment. Neither hypertension nor renal failure are known to affect the 21 grandchildren who were either not porphyric or of unknown status. This family provides a unique opportunity to study these common but little reported sequelae of acute porphyria. These complications affect subjects with latent porphyria as well as those who have experienced clinical attacks.
Nephrol Dial Transplant 1992
PMID:Hypertension and renal impairment as complications of acute porphyria. 133 93


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