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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Medical records of patients having unilateral nephrectomies done between 1953 and 1978 at a university hospital were reviewed after 5 to 30 years of follow-up to determine if this procedure causes insidious renal insufficiency. Forty patients (selected from 571) ranging in age from 20 to 72 years met the following criteria for inclusion in the study: subject over 20 years of age at nephrectomy; initial serum creatinine concentration less than 1.6 mg/dL; normal arterial blood pressure (less than 150/90 mm Hg); absence of risk factors for chronic renal disease, eg, systemic lupus erythematosis, diabetes mellitus, chronic glomerulonephritis; an initial and a follow-up serum creatinine level; at least 5 years of follow-up. After a mean follow-up of 11.8 years, paired analysis of changes in serum creatinine concentrations showed insignificant differences between pre- and post-nephrectomy levels (0.19 +/- 0.11 mg/dL +/- SEM). Only one patient had a post-nephrectomy serum creatinine level above 2.0 mg/dL. Six patients (four women, two men) developed hypertension (15%) after uninephrectomy, an incidence of hypertension not greater than that found in the population at large. We conclude that uninephrectomy at ages older than 20 years does not lead to renal insufficiency or hypertension in adult patients with normal prenephrectomy serum creatinine and blood pressure levels.
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PMID:Long-term effect of uninephrectomy on serum creatinine concentration and arterial blood pressure. 403 59

One hundred and twenty-five patients with different morphoclinical variants of chronic glomerulonephritis (CGN) were examined for the efficacy of cytostatic-anticoagulant-antiaggregation (CAA) therapy. The treatment appeared successful in 47 (37%) of patients. The efficacy largely depended on the degree and intensity of the disease clinical manifestations as well as on a dramatic increase in the permeability of the glomerular filter for medium- and high-molecular serum proteins and on superimposition of sclerotic transformation of renal glomeruli. The use of CAA therapy was most successful in GN whatever superimposition of fibroplastic transformation. The treatment was abortive in prolonged (more than 12 months) persistence of pronounced proteinuria combined with hematuria and/or arterial hypertension, in the nephrotic-hypertonic pattern of GN irrespective of the disease stage, in disease patterns manifesting themselves chiefly by hematuria and negligible proteinuria.
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PMID:[Further study of the indications for combination cytostatic-anticoagulant-antiaggregation-corticosteroid therapy of chronic glomerulonephritis]. 407 18

Morphology of nephrosclerosis at the early stage of its development is characterized by its nosological specificity which is determined by qualitative alterations and by the degree of renal structural components involvement into the sclerotic process. Complex morphometric assessment allows one to reveal and make it objective the morphological differences between nosological variants of nephrosclerosis. All the structural renal components equally undergo sclerosis at the late stages of nephrosclerosis and this leads to the leveling off the nosological specificity in the majority of cases. Arterial hypertension in chronic glomerulonephritis and chronic pyelonephritis favours the progressing of the nephrosclerosis and leveling off its nosological differences.
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PMID:[Morphological characteristics of nephrosclerosis of different etiologies]. 407 43

The present study was performed to investigate whether or not there were enkephalins in plasma and urine in normal subjects and in patients with various diseases. Two kinds of antisera were developed to detect M-enk and L-enk. One has specific affinity with the C-terminus of methionine-enkephalin sulfoxide (M-O-enk), the oxidized form of M-enk, and the other with the N-terminus of L-enk. M-enk-like substance (MELS) was present in blood and urine in normal subjects, but not L-enk-like substance (LELS). Plasma MELS and its urinary output averaged 38 +/- 14 pg/ml (N = 19) and 605 +/- 235 ng/day (N = 15, M. +/- S.D.), respectively. There was a significant increase in plasma MELS and its urinary output in patients with pheochromocytoma. Plasma MELS did not show any significant increase or decrease in Cushing's disease. Addison's disease, panhypopituitarism or chronic glomerulonephritis. The urinary output of MELS was significantly increased in patients with essential hypertension, renovascular hypertension and primary aldosteronism, but was decreased in central diabetes insipidus.
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PMID:The presence of methionine-enkephalin in plasma and urine in normal human subjects and various patients. 408 13

Clinical findings and structural alterations in the kidneys of 6 patients with sarcoidosis and an associated glomerulonephritis are described. Five of the 6 patients manifested the nephrotic syndrome during some phase of their illness. Additional clinical evidence of renal disease included persistent microscopic hematuria (5 patients), hypertension (4 patients) and progressive renal failure (3 patients). Glomerular pathology varied and included proliferative glomerulonephritis (3 patients), membranous glomerulonephritis (1 patient), and chronic glomerulonephritis (2 patients). In 2 patients sequential examination of the kidney was possible, with renal biopsies preceding autopsy examination by 3 and 6 years, respectively. Glomerular pathology had progressed in severity in each case. Immunofluorescent studies in 2 patients revealed patterns of glomerular antibody localization consistent with immune complex disease. Electron microscopic studies of 1 revealed membranous changes characterized by electron-dense subepithelial and intramembranous deposits. Totally unexpected were virus-like intraendothelial structures in the glomeruli identical to those previously reported in systemic lupus erythematosus. Since current evidence suggests that the pathogenesis of both membranous and proliferative types of glomerulonephritis is immunologic, it should not be surprising that sarcoidosis, a disease which quite possibly results from an immune response to a disseminated antigen(s), should occasionally include glomerulonephritis as a part of its histologic expression.
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PMID:Glomerulonephritis associated with sarcoidosis. 455 25

For the past 7 years we have treated 30 patients with malignant hypertension with hemodialysis. The diagnosis of the disease was made according to the criteria recommended by the Ministry of Public Welfare, Japan, as described below. These patients were divided into three groups according to the therapies. Group A (15 patients) were medicated with large doses of beta-blockers for the control of hypertension. Characteristic features of this group were abnormally high reninemia, hyponatremia, and severe hypertension which were not controlled by large doses of beta-blockers in combination with dialysis. Their body weights were quite subnormal. Twelve patients out of 15 had essential hypertension (EH) as an underlying disease, and the remaining 3 had chronic glomerulonephritis (CN). Ten patients out of 15 died of hypertensive heart failure or hypertensive cerebrovascular accidents. Group B (6 patients) were treated by beta-blockers intermittently. They showed good results responding well to the treatment; high reninemia was brought down to normal level by the administration of beta-blockers and dialysis. Their underlying diseases were EH (3 patients) and CN (3 patients). Group C (9 patients) did not receive beta-blockers, because hypertension was easily controlled by dialysis alone. In the Group C patients, normoreninemia, normonatremia, and a favorable clinical course were characteristic. Their underlying disease was CN in all. From these results, it is concluded that the factors influencing the prognosis of te disease may be the existence of EH as an underlying disease, high reninemia, and hyponatremia which are not correctable either by administration of beta-blockers or by hemodialysis.
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PMID:Analysis of 30 patients with malignant hypertension treated with hemodialysis. 611 66

Activity of alanine aminopeptidase (AAP), aryl sulphatase A (ASA) beta-glucoronidase (beta-GA) and the concentration of beta 2-microglobulin in urine was determined in 12 patients with chronic diffuse glomerulonephritis and in 16 patients with essential hypertension. The control group consisted of 6 practically healthy persons. The AAP activity in urine of patients with chronic glomerulonephritis was significantly higher than that in healthy subjects. Renal excretion of lysosomal enzymes (ASA, beta-GA) appeared to be less expressed; no significant differences as regard to their excretion were noted between the above mentioned groups. Concentrations of beta 2-microglobulin in urine of patients with chronic glomerulonephritis 6 times exceeded its concentration in healthy persons and in hypertensive patients, more than 3 times as much. Determination of the enzyme activity and beta 2-microglobulin concentration in urine may serve a test in differential diagnosis, for evaluation of the treatment efficiency of patients with chronic glomerulonephritis accompanied by arterial hypertension and those suffering from essential hypertension.
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PMID:[Determination of enzyme activity and beta 2-microglobulin concentration in the urine in chronic diffuse glomerulonephritis and hypertension]. 617 19

In order to determine the influence of hypertension on the progression of chronic glomerulonephritis, we studied the renal lesions in Heymann nephritis (autologous immune complex nephritis) produced in SHR. Nephritic SHR treated by AHD, normal SHR, nephritic WKYR, and normal WKYR served as controls. Induction of Heymann nephritis did not alter the blood pressure in either SHR or WKYR as compared with each untreated control group. Administration of AHD normalized the blood pressure of SHR. Proteinuria, hypoproteinemia, hypercholesterolemia, and reduction in body weight were significantly greater in nephritic SHR than in nephritic SHR treated by AHD or nephritic WKYR, whereas BUN and serum creatinine were unchanged in all the nephritic rats. Histological findings such as glomerular basement membrane thickening, IgG and C3 deposits along capillary walls, and subepithelial electron-dense deposits were similar in all nephritic groups. Glomerular sclerosis and tubulointerstitial changes were more marked in nephritic SHR than in the other nephritic groups. Severe vascular thickening and necrosis, intravascular thrombosis, and perivascular cell infiltration were frequently observed in nephritic SHR. These lesions are characteristic of malignant hypertension. However, they were not found in control SHR, which maintained elevation of blood pressure equivalent to that of nephritic SHR throughout the study. It was concluded that hypertension may aggravate nephritic manifestations such as proteinuria, hypoproteinemia, and hypercholesterolemia but not excretory renal function and that the hypertensive vascular lesions are augmented by Heymann nephritis.
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PMID:Influence of hypertension on the progression of experimental autologous immune complex nephritis. 621 70

Hypertension frequently accompanies chronic glomerulonephritis. Mesangial injury and glomerulosclerosis are common in glomerulonephritis and are often harbingers of progressive glomerular destruction. Thus, in a model of mesangial immune injury we studied the relationship between hypertension, mesangial injury, and glomerulosclerosis. We induced mesangial ferritin-antiferritin immune complex disease (FIC) in Dahl salt-sensitive (S) and salt-resistant (R) rats. S and R rats with FIC were fed chow containing 0.3% NaCl until 14 weeks of age and then switched to 8.0% NaCl chow until 28 weeks of age. Groups of control S and R rats (no FIC) were either fed 0.3% NaCl for 28 weeks or switched to 8.0% NaCl chow at 14 weeks of age. Blood pressure, serum creatinine, urinary protein, and glomerular injury (assessed by semiquantitative morphometric analysis) were determined at 14 and 28 weeks of age. R rats with or without FIC did not develop hypertension; mesangial injury was minimal. At 14 weeks of age, only S FIC rats developed hypertension, proteinuria, significant mesangial expansion and early glomerulosclerosis. At 28 weeks of age, proteinuria, mesangial expansion, and glomerulosclerosis were significantly more severe in hypertensive S rats with FIC than in those without FIC. These studies show that despite a normal salt intake, mesangial injury hastened the onset of hypertension, but only in rats genetically predisposed to hypertension (S FIC at 14 weeks). High dietary salt further aggravated hypertension, which, in turn, magnified both mesangial injury and glomerulosclerosis. Clinically, the different rates of progression of human glomerulonephritis associated with hypertension may be in part dependent on similar mechanisms.
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PMID:Mesangial immune injury, hypertension, and progressive glomerular damage in Dahl rats. 623 58

The qualitative and quantitative morphological evaluation of the juxtaglomerular apparatus (JGA) is given on the basis of electron microscopic examinations of JGA in renal biopsies of the patients with mesangio-proliferative and mesangiocapillary glomerulonephritis with or without hypertension. An increase in the total number of JGA cells including granular ones is observed in chronic glomerulonephritis. In hypertensive forms of glomerulonephritis, particularly those with high proteinuria, rhomboidal protogranules were prevalent in the cytoplasm of epithelioid cells, in glomerulonephritis without hypertension and marked proteinuria spheric and lipofuscin-like granules were predominant. In glomerulonephritis with hypertension, an analysis of granule formation in JGA epithelioid cells by formparameter revealed a significant predominance of elongated granules (rhomboidal protogranules), and a lineal correlation analysis demonstrated a strong association between the degree of JGA activation assessed by formparameter values and the duration of the disease. An increase in the number of granulated cells in JGA correlated with the increased activities of glomerular mesangial cells and the appearance of epithelioid cells in the afferent arteriolar wall. The dystrophic changes of adrenergic nerves and their endings developing in glomerulonephritis may be a manifestation of overcharge of nervous apparatuses, particularly in the presence of arterial hypertension.
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PMID:[The juxtaglomerular apparatus in chronic glomerulonephritis]. 626 33


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