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)

Clinical course, complications and outcome were analyzed in 75 patients (14 women, 61 men) who started CAPD at age 55 years or older (55-81). These patients were separated in three groups. Group A patients had high risk for vascular disease (diabetes, hypertension, N = 45), group B patients had a presumed lower risk for vascular disease (primary renal disease, N = 22), and group C patients had miscellaneous conditions (N = 8). Group A was compared to group B. Patient and technique survival was statistically higher for group B than for group A. The rates of peritoneal dialysis related complications (peritonitis, tissue infections, catheter loss, hernias) were comparable between groups A and B. Hernias were seen frequently in all groups and had severe sequellae, including discontinuation of CAPD. Catastrophic vascular events were also seen in all groups, but the frequency of such events, particularly of catastrophic vascular events of the limbs, was statistically higher in group A than in group B. Vascular disease accounted for the majority of deaths in all groups. Four patients died from cardiovascular instability soon after changing from CAPD to hemodialysis. In conclusion, vascular disease is the major factor limiting survival in older CAPD patients. CAPD is superior to hemodialysis for a relatively small fraction of older patients with severe cardiovascular instability.
Adv Perit Dial 1990
PMID:Vascular disease: the critical risk factor for mortality in older patients on CAPD. 198 41

At post-mortem we examined heart tissue of (i) 31 patients with uraemia not on dialysis, (ii) 42 patients on haemodialysis for less than 6 months, (iii) 60 patients on haemodialysis for more than 6 months, (iv) 16 patients after renal transplantation, and (v) 11 patients on CAPD. Patients with stenosing coronary lesions were excluded. Diffuse non-coronary intermyocardiocytic fibrosis, assessed by a score system in trichrome-stained sections, was found in 91% of chronically uraemic patients, but not in non-hypertensive, non-diabetic controls. The lesion was present even in non-dialysed uraemic patients; in dialysed patients its severity was related to the duration of dialysis; it was demonstrable even years after renal transplantation. On electron-microscopy, collagen fibres were seen, while beta 2-M amyloid was consistently absent. Logistic regression analysis showed that uraemia was a determinant of intermyocardiocytic fibrosis independent of hypertension, diabetes mellitus, anaemia, heart weight, and presence or absence of dialysis procedure.
Nephrol Dial Transplant 1990
PMID:Diffuse intermyocardiocytic fibrosis in uraemic patients. 210 83

Anuria complicated the malignant phase of hypertension in twelve patients (ten males and two females). Five were black; five had primary hypertension; one had HBs virus angiitis; the six remaining cases suffered from previously documented renal disease, including two with Berger's disease. Renal angiography showed interruption of renal blood flow as far as the main branches of the renal artery and/or a false impression of 'cortical necrosis' and of 'renal infarcts'. In contrast, renal biopsy did not show irreversible vascular damage. Thus, anuria was mainly functional and due to active renal vasoconstriction. This was confirmed by the subsequent course; diuresis resumed after 1 week to 24 months of dialysis. Repeat angiography in six cases showed recovery of renal circulation and disappearance of 'cortical infarcts', even when plasma renin activity remained elevated and hypertension was not controlled. In one case captopril induced a new reversible episode of anuria. These observations suggest that active vasoconstriction with prolonged anuria might be due to some vasoconstrictive substance other than angiotensin II.
Nephrol Dial Transplant 1990
PMID:Protracted anuria due to active vasoconstriction in primary or secondary malignant hypertension. 211 43

Endothelin is a 21-residue peptide vasoconstrictor produced by endothelium. Using a radioimmunoassay, endothelin values were measured in four groups of individuals: normal controls (0.54 +/- 0.12 pmol/l, n = 20); undialysed patients with chronic renal failure (CRF) (0.82 +/- 0.13 pmol/l, n = 38); chronic renal failure patients on continuous ambulatory peritoneal dialysis (CAPD) (2.81 +/- 0.63 pmol/l, n = 20); and patients with CRF on haemodialysis (HD) (4.52 +/- 1.21 pmol/l, n = 14). The endothelin values were significantly greater in undialysed patients with CRF when compared with controls (P less than 0.001) and significantly greater in both dialysis groups when compared with controls and the undialysed CRF group (P much less than 0.001). The difference between the two dialysis groups was not significant (P = 0.07). There was no correlation between endothelin and serum creatinine, mean arterial pressure, presence of chronic hypertension and/or diabetes, use of calcium-channel blockers and/or ACE inhibitors, or primary renal diagnostic category. A single haemodialysis session had no significant effect on endothelin values in the ten patients in whom this was assessed. Fast protein liquid chromatography (FPLC) appeared to confirm that the molecular species found in chronic renal failure were the same as those found in diabetic patients.
Nephrol Dial Transplant 1990
PMID:Endothelin in renal failure. 212 16

The absence of a reduction in peripheral vascular resistance secondary to hypervolaemia leads to so-called volume hypertension. In order to study whether a deficient formation of the vasodilator autacoid prostaglandin E2 (PGE2) contributes to the preservation of inadequate vascular tone during extracellular volume expansion, arterial plasma PGE2 and the stable PGE2 metabolite 13,14-dihydro-15-keto-PGE2 (PGE2-M) were determined in 13 oligoanuric women on chronic haemodialysis. Prior to treatment eight of them had hypervolaemia and hypertension (mean arterial pressure (MAP) 128 +/- 3 mmHg (mean +/- SE] and five patients had hypervolaemia of a similar degree but were not hypertensive (MAP: 99 +/- 4 mmHg P less than 0.005). Before haemodialysis the arterial PGE2 and PGE2-M concentrations were less (P less than 0.05) in hypertensive (11 observations in eight patients) than in normotensive patients (ten observations in five patients). As blood pressure decreased during the course of haemodialysis of volume hypertensive patients, the concentration of PGE2 and PGE2-M increased (P less than 0.02) by 104 +/- 43% and 89 +/- 32%, respectively. In normotensive patients neither blood pressure nor the concentration of PGE2 and PGE2-M were found to change during treatment. Since volume hypertension was associated with reduced values and dialysis induced normalisation of blood pressure with increased arterial values of PGE2 and PGE2-M, we hypothesise that the development of hypertension associated with fluid overload of haemodialysed patients may be related to a decreased release of prostaglandin E2.
Nephrol Dial Transplant 1990
PMID:Changes of arterial prostaglandin E2 during haemodialysis. 212 29

Erythrocytosis after renal transplantation confers risks of thromboembolic complications and therefore necessitates repeated phlebotomies and/or anticoagulation therapy. Erythropoietin production from the retained native kidneys is one aetiological possibility for this condition. During 1982-1987, 22 patients with renal transplants underwent bilateral nephrectomy because of erythrocytosis with a median duration of 13 months. The median follow-up time was 36 months. After nephrectomy, blood counts returned to normal in all patients; these remained normal in all but two patients, who relapsed with erythrocytosis after 6 and 18 months respectively. Concomitant hypertension was cured or improved in most cases. One patient had a myocardial infarction postoperatively. No other per- or postoperative complications occurred. The mean duration of hospital stay was 7.5 days. We consider bilateral nephrectomy of the native kidneys a safe and effective alternative in the management of post-transplant erythrocytosis.
Nephrol Dial Transplant 1990
PMID:Erythrocytosis after renal transplantation; treatment by removal of the native kidneys. 212 35

Cardiovascular impairment is considered a major cause of reduced tolerance to haemodialysis in elderly patients and is thought to require a soft dialysis strategy in these patients. To verify these observations we compared dialysis strategy and tolerance of patients over 65 years old to those of patients under 45 years, since atherosclerotic/involutional changes of vasculature should be quite different in these groups. Seventy-seven elderly and 57 young patients (age 72 +/- 5 and 35 +/- 6 years respectively, mean and SD) were selected from a population of 292 patients undergoing regular dialysis treatment exclusively on the basis of the age criterion. Cardiovascular impairment was found to be greater (as expected) in older than in younger patients, as documented by a larger proportion of diabetic patients (19% vs 3%), a greater incidence of cardiovascular manifestations both before the beginning of dialysis (27% vs 10% of patients affected) and after the beginning of dialysis (35% vs 16%), a greater incidence of ECG abnormalities (78% vs 56%), a longer exposure to hypertension (9.2 vs 3.5 years), and a greater utilisation of digitalis (36% vs 5%) and nitrates (19% vs 2%). Dialysis strategy in elderly patients differed from that in young patients only for a moderately lower blood flow rate (243 vs 279, 244 vs 279, ml/min, males and females respectively). Dialysis sessions were shorter in older than in younger males (11.8 vs 12.4 h/week). The incidence of intradialytic hypotension did not differ significantly between the two groups (44% vs 32%), although the elderly showed a greater pre-to-post-dialysis systolic arterial pressure reduction (21 vs 15 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1990
PMID:Cardiovascular impairment, dialysis strategy and tolerance in elderly and young patients on maintenance haemodialysis. 212 51

The renal selectivity properties towards albumin were evaluated in ten diabetic patients with arterial hypertension before and after the pharmacological normalisation of blood pressure, and were compared to 12 subjects with essential hypertension. While all patients of the control group were normoalbuminuric during hypertension, six of the diabetic group were microalbuminuric when hypertensive and became almost normoalbuminuric after blood pressure pharmacological control. All microalbuminuric diabetic patients presented altered properties of renal selectivity as epitomised by a non-preferential urinary excretion of glycosyl albumin (GA) (urinary GA/serum GA less than or equal to 1). At variance the selectivity properties were normal in normoalbuminuric diabetic patients and in essential hypertension. It was concluded that in diabetes mellitus arterial hypertension is associated with microalbuminuria when the renal properties of selectivity are altered, but does not implicate any proteinuric effect in those cases where the GBM function is preserved.
Nephrol Dial Transplant 1990
PMID:Hypertension and renal selectivity properties in diabetic microalbuminuria. 212 64

The clinicopathological picture of 'isolated C3 mesangial nephritis' was studied in our case records. Focal and segmental or generalised deposits of C3 in the mesangium were found in 12 of 157 (7.6%) patients with primary glomerulonephritis. The clinical picture, similar to Berger's disease, was characterised by episodes of gross haematuria and/or persistent or recurrent microhaematuria and/or proteinuria. Arterial hypertension and mild renal failure were observed in one case. Light-microscopy showed minor glomerular changes such as focal and segmental increase of mesangial matrix and mesangial hyperplasia. During the short-term follow-up (median 25.5 months) no deterioration of renal function was observed. The clinical course and short-term prognosis suggest that this form of glomerulonephritis is benign.
Nephrol Dial Transplant 1990
PMID:Clinicopathological features in patients with isolated C3 mesangial proliferative glomerulonephritis. 212 68

In the past, cardiac changes in renal failure have commonly been ascribed to hypertension and poorly specified toxic effects ('uraemic cardiomyopathy'). Our recent experimental and clinical studies suggest (a) that cardiac hypertrophy can be dissociated from hypertension and that blood pressures may have only a permissive role, (b) that experimental uraemia is associated with specific activation of pericytes and intermyocardiocytic fibrosis. Cardiac hypertrophy not correlated with elevated blood pressure, and intermyocardiocytic fibrosis not observed in similarly hypertensive non-uraemic patients, have recently been documented in dialysis patients. The implications of these findings may be (a) electrical instability and predisposition to a sudden cardiac death and (b) diastolic cardiac malfunction with impaired LV filling and predisposition to dialysis hypotension. Some evidence for the latter possibility is provided.
Nephrol Dial Transplant 1990
PMID:Cardiac changes in uraemia and their possible relationship to cardiovascular instability on dialysis. 215 43


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