Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured plasma sulphur amino acids in twenty-two patients with chronic renal failure and compared the findings with those obtained in twenty-two normal subjects. In fasting blood (08.00 hours) cysteine-homocysteine mixed disulphide was significantly increased in the renal patients, mean values (+/- SD) being 8.2 +/- 3.4 and 3.1 +/- 1.0 mumol/l respectively (P less than 0.001). The increase was positively correlated with reduced renal function, as assessed by serum creatinine (r = 0.62; P less than 0.01). Homocystine was detected in nineteen patients, the mean concentration (+/- SD) being 1.7 +/- 0.6 mumol/l; it was not found in any normal subject. Methionine levels were not different but there were significant increases in cystine (P less than 0.001) and taurine (P less than 0.05) in the patients. Similar values for these amino acids were found in a second blood sample drawn at 16.00 hours. Changes in the other neutral and acidic amino acids measured were in agreement with those reported in chronic azotaemia. We concluded that plasma levels of all the principal sulphur amino acids except methionine are elevated in chronic renal failure emphasizing the importance of the kidney in sulphur excretion. Prolonged accumulation of homocysteine and cysteine-homocysteine mixed disulphide may be relevant to the development of accelerated vascular disease in patients with chronic renal failure by producing endothelial damage.
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PMID:Sulphr containing amino acids in chronic renal failure with particular reference to homocystine and cysteine-homocysteine mixed disulphide. 11 20

To characterize the renin-angiotensin system in the Aoki-Okamoto spontaneously hypertensive rat (SHR) more fully, serial measurements of plasma renin activity (PRA), plasma renin concentration (PRC), renin reactivity (as relative index of circulating modifiers of the renin reaction) and renin substrate concentration were made in 6- to 64-week-old SHR and in age-matched Wistar-Kyoto normotensive rats (WKY). In the evolving phase of SHR hypertension (6 and 13 weeks of age), PRA was comparable to WKY control values, whereas mature SHR with established hypertension developed, between 13 and 35 weeks of age, a high-PRA state persisting through 64 weeks of age. In 64-week-old SHR, increased plasma volume (3.54 +/- 0.91 in SHR vs. 3.18 +/- 0.90 ml/100 g body weight in WKY, p less than 0.025), together with increased PRA (24.9 +/- 3.8 in SHR vs. 13.1 2.2 ng AI/ml plasma/hr in WKY, p less than 0.025), suggest that volume decrease cannot explain increased PRA. In 42-week-old SHR, PRA was incompletely suppressed by deoxycorticosterone acetate plus 1% saline orally for 4 days: 4.9 +/- 1.2 in SHR vs. 0.6 +/- 0.8 ng angiotensin I/ml plasma/hr in WKY, p less than 0.001. Modestly increased renin reactivity of plasma was observed in SHR at all ages studied, supporting the ubiquity of increased circulating accelerators (or decreased inhibitors) of the renin reaction in hypertensive states. However, elevated renin reactivity did not account for the transition from normal to high PRA observed in mature SHR, nor did renin substrate concentration, which was consistently lower in SHR than in age-matched WKY. Temporal patterns of, and strain differences in PRA were closely paralleled by variations in PRC but not by other reaction components. Significant elevation of serum creatinine in old SHR support the presence of renal injury. We conclude that PRA and PRC are normal in evolving SHR hypertension and progress to abnormally elevated levels after hypertension is established. We postulate that "high-renin" hypertension may develop as a consequence of the hypertensive state per se, perhaps due to nephrosclerotic vascular disease.
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PMID:Serial renin-angiotensin studies in spontaneously hypertensive and Wistar-Kyoto normotensive rats. Transition from normal- to high-renin status during the established phase of spontaneous hypertension. 39 38

Among the diabetic patients we have treated with dialysis blood pressure and blood sugar control have been poor and vascular disease progressive. Intermittent peritoneal dialysis did not improve these problems compared with haemodialysis. Continuous ambulatory peritoneal dialysis was undertaken in three patients as a last resort and electively in another two patients. Insulin was given by the intraperitoneal route and none was used systemically. Self-care was taught from the first using the spouse if visual problems were present. Serum creatinine levels fell and haemoglobin levels rose. Blood pressure was controlled without diet or drugs. Blood sugar levels were controlled without symptomatic hypoglycaemia or rebound hyperglycaemia. The procedure had a demoralising effect on helper spouses, and self-care had to be achieved even with severe visual problems. The advantages of continuous ambulatory peritoneal dialysis to the diabetic with renal failure are greatly improved control of blood pressure and blood sugar.
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PMID:Advantages of continuous ambulatory peritoneal dialysis to the diabetic with renal failure. 54 79

Since vasodilators can restore toward normal the decreased peritoneal clearances associated with vascular disease, the influence of aminophylline on peritoneal solute transport was studied in unanesthetized rabbits. Mean control creatinine clearance was 0.56 ml/kg/min and urea clearance 0.80 ml/kg/min. Neither intraperitoneal nor intravenous aminophylline increased peritoneal clearances, nor did the ratio creatinine clearance/urea clearance change from the control value, 0.70. Bidirectional flux of theophylline occurred at clearances of 0.70 ml/kg/min efflux and 0.64 ml/min influx. The removal rate of theophylline was 0.05% min, allowing therapeutic removal of excess aminophylline and warranting supplemental therapy during dialysis if therapeutic theophylline concentrations are required. As the intraperitoneal aminophylline was well tolerated, this route can be considered for therapeutic administration.
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PMID:Peritoneal dialysis in rabbits. A study of transperitoneal theophylline flux and peritoneal permeability. 61 96

Acute renal failure (ARF) following infusion intravenous pyelography (IVP) has been reported in patients with chronic renal insufficiency, particularly diabetics. Renal function was evaluated before and after infusion IVP in 40 patients with chronic renal insufficiency. In 11 of 12 (92%) diabetics and 17 of 28 (61%) nondiabetics, a 25% or greater increase in serum creatinine values and/or decrease in creatinine clearance was noted after IVP despite adequate hydration in all patients. The maximum decrease in kidney function occurred within three days and usually returned to or near pre-IVP levels in seven to ten days. At least 70% of the patients had hypertension and/or evidence of vascular disease. The data suggest that preexisting vascular disease in the kidney, possibly associated with the known vasoconstricting effects of contrast media, may be an important factor in the ARF following infusion IVP.
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PMID:Infusion intravenous pyelography and renal function. Effects in patients with chronic renal insufficiency. 67 77

Amniotic fluid (AF) creatinine concentrations, determined in 353 samples from 167 pregnancies complicated by maternal diabetes, are similar to those found at comparable gestation in uncomplicated pregnancy. Added maternal vascular disease significantly raises AF creatinine to such a degree that overestimation of fetal (renal) maturity is a clinical hazard if based solely on this parameter. Relative concentrations of creatinine in AF and maternal plasma (AF/MP ratio) are related to gestational age. Failure of AF creatinine to rise consistently on successive serial samples accompanies an increased risk of perinatal death in the pregnancy complicated by diabetes, four of five deaths in the present series following declines in this measurement.
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PMID:Amniotic fluid creatinine in pregnancies complicated by diabetes. 113 Apr 43

Crescents, defined as any proliferative or fibrous space occupying reaction of the parietal layer of Bowman's capsule, occur as a regular and integral feature of the glomerular changes of diabetes mellitus. The frequency of crescents and adhesions to the capsule increases with increasing total severity of diabetic glomerular and vascular disease in glomeruli with mild-moderate diffuse glomerulosclerosis (GS), severe diffuse GS, and nodular GA. The high frequency (greater than 90 per cent) of crescents and adhesions in glomeruli with exudative lesions is unrelated to over-all severity of diabetic renal disease. The 8.73 per cent of glomeruli with exudative lesions had 45 per cent of the total crescents observed. The mechanism of crescent formation in diabetes is probably similar to the proposed pathogenesis of crescents in other renal diseases. The underlying injury in the glomerular capillaries in diabetes is mainly the "exudative lesion." The percentage of diabetic glomeruli with crescents correlated better with blood urea nitrogen and creatinine that did the percentage of end stage glomeruli (a measure of severity of vascular disease), the percentage of diabetic glomeruli with severe diffuse GS, the percentage of diabetic glomeruli with nodular GS, or the percentage of diabetic glomeruli with exudative lesions. The percentage of diabetic glomeruli with crescents correlated better with severity of vascular disease than did any of the other diabetic glomerular changes. No correlation existed between incidence of crescents and "capsular drops."
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PMID:Crescents in diabetic glomerulopathy. Incidence and clinical significance. 120 85

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.
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PMID:Increased morbidity and mortality in patients with diabetes mellitus after kidney transplantation as compared with non-diabetic patients. 132 80

Fifteen patients presented between January 1986 and January 1991 with deterioration in renal function coincident with the introduction of angiotensin converting enzyme inhibitors. There was evidence of extrarenal vascular disease in 12 patients and preexisting renal impairment in 13. Four patients remained dialysis-dependent and died within 4 weeks of presentation. Five patients required short-term dialysis. Serum creatinine remained above pre-treatment values in seven patients. Conventional explanations of the decline in renal function with ACE inhibition do not account for irreversible decrements in renal function. Possible mechanisms for this observation and clinical guidelines to identify patients at risk are suggested. We conclude that these agents should be used with great care in patients in whom atherosclerotic vascular disease is likely.
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PMID:Deterioration in renal function associated with angiotensin converting enzyme inhibitor therapy is not always reversible. 147 49

A prospective study was performed to determine urinary albumin excretion in a group of 28 patients with systemic sclerosis. At the initial screen one patient had proteinuria and three had microalbuminuria. One year later these abnormalities persisted and in two of of the patients serum creatinine had significantly increased. In addition, a further three patients had developed microalbuminuria. In a control group of 10 patients with primary Raynaud's disease none had microalbuminuria. In a second control group of 16 patients with unrelated skin diseases one patient had microalbuminuria and one proteinuria, but both these patients had a history of hypertension. It is concluded that microalbuminuria is more common in patients with systemic sclerosis than in patients of equivalent age with other dermatological conditions but no vascular disease.
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PMID:Microalbuminuria in systemic sclerosis. 157 87


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