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)

Regional lung function has been studied in 16 children with intracardiac shunts and a variety of associated cardiac anomalies using radioactive nitrogen (13N) and a gamma camera-computer system. The distribution and washout of inhaled 13N were usually normal. The distribution of intravenously injected 13N was often abnormal and could be related to local anatomy. The most important finding was delayed clearance by ventilation of intravenously injected 13N in children with an abnormally raised pulmonary/systemic vascular resistance ratio (Rp/Rs) at cardiac catheterisation. The regional localisation of this ventilation-perfusion imbalance could be related in several children to the probable distribution of hypertensive pulmonary vascular disease, predicted either from local anatomy shown at cardiac catheterisation or from the abnormal distribution of pulmonary perfusion. Abnormalities present on breathing air may be partially reversed on breathing 100 per cent oxygen.
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PMID:Hypertensive pulmonary vascular disease in children. Detection by radioactive nitrogen (13N) inhalation and injection. 90 80

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

We analyzed the records of all residents of Jefferson County, Alabama, accepted for renal replacement therapy between 1982 and 1987 and compared them with those accepted between 1974 and 1978 to determine any changes in the distribution and frequency of end-stage renal disease (ESRD) due to hypertension (H-ESRD). H-ESRD increased from 6.4 to 9.6 per 100,000 in blacks and from 0.36 to 0.62 per 100,000 in whites. Smoothed age- and race-specific yearly H-ESRD rates decreased in blacks under age 50. Peak incidence of H-ESRD shifted from age 40 to 49 in 1974 through 1978 to age 50 to 59 in 1982 through 1987 (P less than 0.0001). Blacks were referred for care with significantly higher blood pressure levels and serum creatinine concentrations than whites, and had more severe retinal vascular disease. Factors significantly associated with a shorter time from referral to renal replacement therapy were black race, female gender, blood urea nitrogen and serum creatinine concentrations, carbohydrate intolerance, and the use of alpha-agonist and/or angiotensin-converting enzyme (ACE) inhibitor. We conclude that racial distribution and risk for H-ESRD have not changed. Peak rates of H-ESRD have been delayed nearly a decade, suggesting a possible effect of better awareness and treatment of hypertension.
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PMID:Changing patterns of end-stage renal disease due to hypertension. 188 25

Adverse drug reactions are more common in patients over sixty-five years of age. There is no significant change of absorption with aging but oxidations reactions are, usually, decreased. The most important change is in the renal elimination of drugs. The renal insufficiency related to the use of NSAIDs is prostaglandin dependent. It is characterized by a fall in urine output, body weight gain, rising of blood urea nitrogen, creatinine and, sometimes, potassium. This situation is usually rapidly reversible after discontinuation of the therapy but an acute renal failure may occur. Patients with atherosclerotic cardio-vascular disease and concurrent diuretic therapy have an increased risk of renal insufficiency. Liver damage induced by NSAIDs presents as an acute hepatitis with a greater or lesser degree of cholestasis. This picture is often indistinguishable from viral hepatitis and sometimes it may resemble chronic active hepatitis. Females with a concomitant impairment of renal function are specially at risk for liver damage and should be carefully followed on with a reduction of NSAIDs dosage.
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PMID:Renal and hepatic effects of NSAIDs in the elderly. 262 76

The development and evolution of hypertensive vascular lesions affecting the arterial supply of (a) the kidney and (b) organs other than the kidney were studied in rats developing either malignant (MHY) or benign (BHY) hypertension 3, 6, 9 and 12 days after aortic ligation between the renal arteries. Vascular disease evolved into two distinct patterns which suggested acute renal damage to be the determinant for the development of either the malignant or benign form of hypertension. Three days after aortic ligation MHY and BHY animals showed widespread fibrinoid deposition in vascular territories above the aortic ligature. However, in MHYs these lesions were much more severe and, in the kidney, they were accompanied by the development of focal parenchymal atrophy, microinfarcts and hyalin droplet degeneration of cells of the Bowman capsule. The degree of renal damage correlated with elevations in blood urea nitrogen (BUN) and plasma creatinine; however, there was no correlation with rises in blood pressure, plasma renin activity (PRA), aldosterone or corticosterone which were similarly elevated in 3-day MHY and 3-day BHY animals. Between 6 and 12 days a marked clearance of fibrinoid took place in all organ beds of BHYs, but in the non-renal vasculature of MHY animals fibrinoid remained prominent and served as the central core for necrotising arterial lesions. In the kidney of MHYs some reduction in the fibrinoid content was observed, but the parenchymal damage perpetuating from the earlier stages had exacerbated leading to collagen deposition and a marked increase in the collagen concentration of the renal cortex. These features were accompanied by further elevations in PRA and corticosteroids and a progressive deterioration of renal function. By contrast, in 12-day BHY animals, despite sustained hypertension, PRA and corticosteroids were falling from their previously higher levels and normal renal function was maintained. These studies warrant inference that extensive parenchymal damage of the kidney due in part to severe arterial fibrinoid deposition is one of the initial events in the development of malignant hypertension.
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PMID:Acute arterial fibrinoid deposition and ischaemic parenchymal damage of the kidney. Pathogenic factors in the development of malignant hypertension. 636 44

Chronic psychosocial stress in male mice produces chronic interstitial nephropathy not explained by renal vascular disease or urinary infection. Four groups of male CBA mice were studied. Group 1 and group 2 were placed in Henry-Stephens complex population cages for 5 months. Group 2 had caffeine, 800 micrograms/ml, added to their drinking water. Control groups 3 and 4 were unstressed, but group 4 had 800 micrograms/ml of caffeine added to their water. Stressed animals developed chronic interstitial nephropathy which was more severe in animals drinking caffeinated water. In addition, the percent of cortex involved in interstitial fibrosis was higher in group 2, 18.0 +/- 1.4, than in group 1, 15.2 +/- 2.3 (p less than 0.05). Both groups had more fibrosis than unstressed animals (p less than 0.01). Blood urea nitrogen was more elevated in group 2, 47 +/- 13 mg/dl, than in group 1, 29 +/- 17 mg/dl (p less than 0.05). Again both values exceeded those in unstressed animals (p less than 0.01). It is concluded that prolonged environmental stress can lead to the renal morphologic changes of chronic interstitial nephritis. Both renal pathology and function are worse when there is concurrent high caffeine intake. The relevance of this model to human disease related to analgesic use or with affective illness requires further study.
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PMID:Chronic interstitial nephropathy in mice induced by psychosocial stress: potentiation by caffeine. 668 61

Risk for renal insufficiency (RI) resulting from nonsteroidal anti-inflammatory drugs (NSAID) exists in cirrhosis with ascites, nephrotic syndrome, decompensated congestive heart failure, and chronic renal disease. We saw seven cases of NSAID RI that demonstrate important additional clinical risk factors. These include advanced age (mean, 76 years), use of diuretic drugs (6/7 patients), and evidence of renal vascular disease as suggested by long-standing hypertension, diabetes, or atherosclerotic cardiovascular disease (7/7 patients). Analysis of past case reports of NSAID RI also showed these features. Treatment of acute gouty arthritis was the most common precipitating event. Evolving NSAID RI was suggested by rising serum urea nitrogen, serum creatinine, and serum potassium levels, and body weight gain associated with low fractional excretion of sodium. We conclude that since NSAID RI is preventable and reversible, it is important to recognize and monitor the conditions of those patients at risk.
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PMID:Identification of risk for renal insufficiency from nonsteroidal anti-inflammatory drugs. 686 44

This study evaluated the diagnostic utility of the nitroblue tetrazolium test on pleural fluid. Pleural fluids from 62 patients, including nine with congestive heart failure, 27 with malignant neoplasms, nine with tuberculosis, 14 with pneumonia, and three with collagen vascular disease, were studied. Results of nitrobule tetrazolium were tabulated for each patient for three different cellular types (polymorphonuclear leukocytes, small lymphocytes, and mononuclear cells other than small lymphocytes). The three patients with collagen vascular disease had very high scores on the nitrogen tetrazolium test for all three cellular types. Their average scores were higher than were those of 57 of the other 59 patients. The nitroblue tetrazolium test on pleural fluid was not useful in separating patients with congestive heart failure, pneumonia, malignant neoplasms, or tuberculosis. The results on the nitroblue tetrazolium test did not help to identify those patients with pneumonia who eventually required tube thoracostomy. From this study, we conclude that the nitroblue tetrazolium test on pleural fluid is of limited use diagnostically but may help to identify those individuals with collagen vascular disease involving the pleura.
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PMID:Nitrobule tetrazolium test in the diagnosis of pleural effusions. 724 9

The author assessed the physiological aging parameters of 38 apparently healthy subjects who were over 80 years old 1989, who were not on medication, and who had consulted with the Keio Health Counseling Center over 10 years. All subjects had no history of overt vascular disease and/or malignancy in 1989. In 17 of 38 subjects, physical, hematological and blood chemical parameters when they were in their 70s were analyzed. Many parameters were unchanged and remained within normal limits for ordinary adults. Cataract, atherosclerotic change of optic fundi and diagonal ear lobe creases were seen in all subjects during the study period. Concerning standard deviations, those of forced expiratory volume in one second/predicted vital capacity and pure tone average (acoustic ability) decreased with age, unlike those of other parameters. Furthermore, multiple regression analysis, revealed that serum albumin decreased but pure tone average, Scheie's atherosclerotic score, senile cataract, HDL-cholesterol blood urea nitrogen and forced expiratory volume in one second/predicted vital capacity increased with age. This study was not cohort study with selected subjects but shows very slight change of almost any parameter irrespective of age and abnormality can suggest the existence of disease.
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PMID:[The changes in physico-chemical parameters obtained from apparently healthy aged people followed over ten years]. 823 Jul 84

Apolipoprotein E (apoE), a plasma apolipoprotein that plays a central role in lipoprotein metabolism, is localized in the senile plaques, congophilic angiopathy, and neurofibrillary tangles of Alzheimer disease. Late-onset familial and sporadic Alzheimer disease patients have an increased frequency of one of the three common apoE alleles, epsilon 4, suggesting apoE4 is associated with increased susceptibility to disease. To follow up on this suggestion, we compared the binding of synthetic amyloid beta (beta/A4) peptide to purified apoE4 and apoE3, the most common isoform. Both isoforms bound synthetic beta/A4 peptide, the primary constituent of the plaque and angiopathy, forming a complex that resisted dissociation by boiling in SDS. Oxygen-mediated complex formation was implicated because binding was increased in oxygenated buffer, reduced in nitrogen-purged buffer, and prevented by reduction with dithiothreitol or 2-mercaptoethanol. Binding of beta/A4 peptide was saturable at 10(-4) M peptide and required residues 12-28. Examination of apoE fragments revealed that residues 244-272 are critical for complex formation. Both oxidized apoE4 and apoE3 bound beta/A4 peptide; however, binding to apoE4 was observed in minutes, whereas binding to apoE3 required hours. In addition, apoE4 did not bind beta/A4 peptide at pH < 6.6, whereas apoE3 bound beta/A4 peptide from pH 7.6 to 4.6. Together these results indicate differences in the two isoforms in complexing with the beta/A4 peptide. Binding of beta/A4 peptide by oxidized apoE may determine the sequestration or targeting of either apoE or beta/A4 peptide, and isoform-specific differences in apoE binding or oxidation may be involved in the pathogenesis of the intra- and extracellular lesions of Alzheimer disease.
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PMID:Binding of human apolipoprotein E to synthetic amyloid beta peptide: isoform-specific effects and implications for late-onset Alzheimer disease. 836 70


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