Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with chronic glomerulonephritis and mild hypertension show a consistent behaviour in their renin-aldosterone-system. There is a close correlation between the elevation of mean blood pressure and destruction of glomeruli. No correlation has been found between renin values and the degree of hypertension. Thus the cuase of mild hypertension occurring in the early stages of chronic GN remains to be elucidated. Normal PRA values in spite of hypertension and expansion of ECFV accompaning progression of chronic glomerulonephritis could be a sign of "relative hyperreninemia". Apparently various mechanisms are involved in the pathogenesis of renal hypertension. These include sodium retention, increased cardiac output. anemia, renin, aldosterone, prostaglandins, expanded plasma volume and peripheral vasoconstriction. These factors are more or less active in the different stages of hypertension and renal failure.
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PMID:Plasma renin activity (PRA) and aldosterone (PA) in patients with chronic glomerulonephritis (GN) and hypertension. 94 54

Preliminary results of this retrospective-prospective analysis of renal hypertension in 110 children indicate that hypertension may be secondary to a wide variety of acute progresive, and chronic renal diseases which may be either congenital or acquired. Affected children may be detected at any time from infancy through adolescence. Symptoms usually associated with acute glomerulonephritis (i.e., headache, swelling, nausea, vomiting, anorexia, fatigue, dizziness, and fever) occur in both acute and chronic renal diseases associated with hypertension. Headache and swelling are the most common symptoms in this series. Peripheral edema, rales, and increased heart size were found in between 10 and 25% of these children. Differential diagnosis may be approached by a consideration of causes of acute and chronic hypertension. The child with chronic renal disease usually presents with a long history of fatigability, poor growth, and pallor, and laboratory tests reveal elevation of the creatinine and BUN along with anemia, hypocalcemia, and hyperphosphatemia. In contrast, the child with acute renal disease and hypertension presents with a history of prior good health followed by the abrupt onset of signs and symptoms of renal disease; laboratory tests usually reveal modest elevations of creatinine and BUN, anemia is unusual, an abnormal urinalysis is common, and serum calcium and phosphorous levels are usually normal. Renovascular and asymmetric renal parenchymal disease represent uncommon but important conditions because surgery may be curative. Treatment may be surgical, medical, or combined. Surgical conditions include renal trauma, hydronephrosis, asymmetric renal disease, and renal arterial disease. Adequate blood pressure control without medication can be expected following surgery in instances of unilateral involvement with a normal contralateral kidney. Meticulous assessment of the contralateral kidney is needed to determine that it is normal. If surgery is unsuccessful or is not indicated, pharmacologic therapy is initiated with a stepwise regimen starting with the mildest agent (e.g., thiazides) and then adding additional antihypertensive drugs when adequate blood pressure control has not yet been achieved. The goal of therapy is the lowest, safest, tolerated blood pressure levels. Long-term, carefully designed studies of antihypertensive agents for children with renal hypertension are not available. The need for collection and critical analysis of data concerning the clinical course of children with renal hypertension is evident from a review of the literature and from the preliminary data presented in this series. The presentation of such information and a critique of outcome variables will provide a basis for program planning for affected children and improvement in patient care where indicated.
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PMID:Renal hypertension in children. 99 44

Cardiac output, total peripheral vascular resistance, renal, extrarenal, forearm muscle and skin hemodynamics and an indicator of the splanchic vascular resistance were estimated in 20 subjects with chronic renal disease without signs of chronic renal failure and without anemia. The data were compared with a group of subjects with essential hypertension. The high blood pressure of chronic renal disease of mild or moderate severity was maintained in the first place by a high cardiac output, this being due to a rise of the stroke volume, while the heart rate was only slightly increased. The total peripheral vascular resistance was within the normal range in most of the subjects. The vascular resistance in the skin was slightly raised, that in the splanchnic area and muscle unchanged in renal hypertension. The possible pathogenic mechanisms are considered.
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PMID:General and regional hemodynamics in hypertension in chronic renal disease. 119 19

A 4-year-old dog of the Appenzeller strain with experimentally induced renal hypertension presented with apparently longstanding retinal changes, including hemorrhage, detachment, tears/holes, and anemia, in one eye and intravitreal hemorrhage in the other. The retinal tears/holes probably occurred following constant vitreous traction due to retinal hemorrhage and subsequent exsanguination of most of the retinal vasculature. This animal was reexamined six months later and most of these changes had persisted. Photodocumentation is presented.
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PMID:Rhegmatogenous retinal detachment in a hypertensive dog. 227 25

In order to characterize left ventricular diastolic filling abnormalities in uremic cardiomyopathy in 50 patients on hemodialysis, the ratio VE/VA of peak early (VE) and late (VA) filling velocity was calculated using CW-Doppler echocardiography. Compared with normal subjects of identical age, VE/VA was found to be significantly lower in patients younger than 40 years, but without, however, significant differences in patients aged 40-60 years and older than 60. Thus, the incidence of diminished VE/VA-ratios fell from 64% in patients younger than 40 years to 5% in patients older than 60. Whereas duration of dialysis, extent of renal anemia and interdialytic volumeload showed no influence, diastolic malfunction was correlated to renal hypertension. Therefore, an actualized characterization of uremic cardiomyopathy can be achieved by CW-Doppler echocardiography, describing diastolic malfunction in most patients with terminal renal failure. In elderly patients, however, a distinction from physiologic alteration of diastolic filling is not possible. Clinical significance of diastolic malfunction is characterized by reduced tolerance of interdialytic volume-expansion, as well as intradialytic volume-depletion.
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PMID:[Doppler echocardiography description of diastolic function disorder in terminal renal failure--new characterization of uremic cardiomyopathy]. 239 61

The role of circulating humoral agents in the pathogenesis of abnormal vascular wall cation composition in benign and malignant renal hypertension was investigated. Male F344 rats with chronic benign (n = 38) and malignant (n = 44) one-kidney, one clip (1K1C) hypertension and normotensive control rats (n = 63) were studied. Malignant hypertension developed spontaneously and was characterized by failure to thrive, weight loss, oedema, renal insufficiency, anaemia or haemoconcentration and hyperkalaemia. For bio-assay, monolayers of quiescent vascular smooth muscle cells from F344 rats were incubated in plasma or plasma extracts of normotensive and hypertensive rats for measurement of labelled rubidium (86Rb) uptake in the presence and absence of 2 mmol/l ouabain and/or 1 mmol/l furosemide. Compared with controls, ouabain-sensitive Rb uptake of cells was reduced in plasma extracts but not in whole plasma of rats with benign hypertension. Ouabain-sensitive Rb uptake was unchanged and ouabain-insensitive Rb uptake was reduced in both plasma and plasma extracts of rats with malignant hypertension. The latter was due to a reduction in furosemide-sensitive Rb uptake. In malignant hypertension, the increased sodium (Na) content of the aorta which characterizes benign hypertension was reversed and bladder wall Na content was reduced. The findings suggest that in malignant hypertension a circulating, furosemide-like inhibitor of ouabain-insensitive cation transport is the cause of vascular wall Na depletion and of diuresis and natriuresis that trigger the syndrome.
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PMID:Different cation transport inhibitor in benign and malignant experimental renal hypertension. 379 32

The chest X-ray films of 251 patients with cardiovascular lesions, collected in the major hospitals of Papua New Guinea, were reviewed. Cor pulmonale (18%) and rheumatic heart disease (16%) were the predominant cardiac disorders, and cor pulmonale was the most common cause of cardiac failure (58%). Cardiomegaly or cardiac failure of unknown cause, possibly due to cardiomyopathy or myocarditis, made up 9% of the group and may be more important than has been thought previously. Aortic-arch calcification typical of atheroma was present in 21% of the patients, and is thus quite common, even though ischaemic heart disease remains very rare (1%). More than half of the patients with aortic atheroma had chronic lung disease, and though this could be explained by the coincidental frequency of both conditions, the possibility of an association or link in pathogenesis between them deserves further consideration. Anaemia was a common cause of cardiac enlargement (14%), and sometimes led to cardiac failure. Only 16 patients had hypertension (essential in 10 patients and renal in six), and this may indicate a change from the previously reported predominance of renal hypertension in Papua New Guinea towards a more equal incidence of the two conditions. Aneurysms of unknown cause were encountered in three fairly young patients. They had some resemblance to the aneurysms in arteritis of obscure origin described in Africa. There were also two dissecting aneurysms and one syphilitic aneurysm of the aorta. Congenital lesions (8%), pericarditis due to various causes (including tuberculosis), bacterial endocarditis (in four patients with rheumatic heart disease), and miscellaneous conditions made up the remainder of the series.
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PMID:Cardiovascular disease in Papua New Guinea. 644 34

Therapy of chronic renal failure requires individual management in diet and vigorous treatment of disorders of fluid and electrolyte metabolism and renal acidosis. Concomitant diseases such as renal hypertension, arrhythmia, cardiac insufficiency, pulmonary complications, gastrointestinal disorders, renal anaemia, affection of central nervous system, disturbance in glucose, uric acid and lipid metabolism and infections, demand careful medication Selection of drugs and doses related to impaired renal functions, is indicated.
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PMID:[Therapy in chronic renal insufficiency (author's transl)]. 724 18

M-mode echocardiography was performed 18 to 22 hours after a haemodialysis session in 16 patients under chronic dialysis. The patients (12 men and 4 women, mean age 21 years, haematocrit 24 +/- 5%) were normotensive and had no clinical or radiological sign of heart failure. Patients with renal hypertension, diabetes or amyloidosis had been excluded from the study. Eight healthy subjects of similar age, heart rate and blood pressure were used as controls. In all 24 individuals the following parameters were calculated: end diastolic time diameter index (DTDI), end systolic time diameter index (STDI), ejection time (ET), mean velocity of circumferential fiber shortening (VCF) and ejection fraction (EF). DTDI was greater in haemodialyzed patients (31 +/- 2 mm/m2) than in controls, but STDI and ET were the same in both groups. This would explain the increase of VCF (1.68 +/- 0.1 c/sec) and EF (0.78 +/- 0.05) observed in dialyzed patients. After compression of the fistula for 3 min the differences disappeared. These results suggest that the echocardiographic measurements listed above give a better idea of the true contractile state of the left ventricle in haemodialyzed patients, disregarding load changes due to the fistula, to anaemia and to intermittent volume expansion.
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PMID:[Echocardiographic measurement of true left ventricular inotropism in patients under haemodialysis (author's transl)]. 731 3

CHF is highly prevalent in ESRD and is a leading cause of death in such patients. Hypertension, renal anemia, and comorbid conditions such as coronary artery disease are particularly important risk factors for CHF in ESRD. Dialysis hypotension may be a marker of poor prognosis in such persons. Recent studies suggest that lipid peroxidation and L-carnitine deficiency may contribute to CHF in some patients with ESRD. All forms of renal replacement therapy are capable of ameliorating symptoms of CHF, but their effect on cardiovascular mortality has not been firmly established. Drug therapy, particularly angiotensin-converting enzyme inhibitors and beta-adrenergic receptor blockers, is under-used in patients with ESRD and CHF. Heart/kidney transplantation may be a viable option for some patients with advanced CHF and ESRD.
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PMID:Congestive heart failure in patients with chronic kidney disease and on dialysis. 1269 23


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