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)

Net fluxes of sodium and potassium ions were determined in sodium-loaded, potassium-depleted erythrocytes from 370 white subjects, 194 of whom had essential hypertension or had been born to parents with essential hypertension. Findings were compared with those in 86 controls who were normotensive and did not have a family history of hypertension. Compared with controls all patients with essential hypertension had a low sodium to potassium ratio secondary to a deficit in the sodium-potassium cotransport system. A similar abnormality was found in subjects born to parents with essential hypertension, the prevalences of a deficient cotransport system in such subjects being 53.6% (52 out of 97) among those with one hypertensive parent and 73.7% (14 out of 19) among those with two hypertensive parents. Both sexes were equally affected. Studies in 14 families over two or three generations showed the erythrocyte cation abnormality in one or more members of each consecutive generation. No close association was evident between the deficient erythrocyte sodium-potassium cotransport system and either blood groups ABO, Rh, Kidd, Duffy, P, and MNS or the major histocompatibility HLA antigens. Out of 90 consecutive unrelated and normotensive white blood donors, 36 showed a low erythrocyte sodium-potassium net flux ratio. It is concluded that in white people abnormal erythrocyte cation transport is a biochemical disorder characteristic of essential hypertension and transmitted by a dominant and autosomal mode expressing a single abnormal gene.
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PMID:Inheritance of abnormal erythrocyte cation transport in essential hypertension. 678 58

Oral cyclosporin A was used as prophylaxis against graft-versus-host disease in (a) 31 patients with acute leukaemia or aplastic anaemia given transplants of HLA-matched bone marrow and (b) five patients with inborn errors of metabolism given transplants of haplotype-identical (parental) bone marrow. Twenty-six patients survived longer than two months after the operation. Despite the cyclosporin A, 31 patients (86%) suffered an acute form of graft-versus-host disease and 22 (61%) a chronic form. Nevertheless, the disease was usually treatable with immunosuppressive agents and caused the death of only one patient. Cyclosporin A caused renal toxicity in all cases; occasionally this was associated with a "capillary leak" syndrome, fatal in two patients. In children hypertension, fits, and fluid retention were common side effects. Blood concentrations of cyclosporin A correlated with blood urea values and blood pressure but did not predict the occurrence of graft-versus-host disease. Four different dose schedules were used to find the optimum way to administer this drug. Oral cyclosporin A is extremely effective at reducing the severity of graft-versus-host disease, but prevention of the disease is limited by toxicity of the drug and variable absorption. Better results might be achieved with parenteral administration or by using the drug in combination with other methods.
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PMID:Cyclosporin A as prophylaxis against graft-versus-host disease in 36 patients. 680 91

The frequency of 40 HLA antigen specificities was determined in 44 patients with end-stage renal disease secondary to reflux nephropathy and compared with those observed in 526 control subjects. Higher than normal frequencies were observed for HLA-B12 in female patients, and HLA-B8 in combination with HLA-A9 or HLA-BW15 in male patients, and HLA-BW15 in patients of both sexes. A comparison of the frequency of HLA antigens in the reflux patients with a history of hypertension versus those without a history of hypertension revealed that HLA-A3 was found with higher frequency and HLA-A1 and HLA-B8 with lower frequency in association with hypertension. These results suggest that the major histocompatibility antigens might be in linkage disequilibrium wih a gene (or genes) determining the susceptibility to renal damage by vesicoureteral reflux and that this linkage, or the clinical expression of this linkage, might be influenced by variations in relation to the sex of the patients.
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PMID:In search of marker for genetic susceptibility to reflux nephropathy. 693 14

1. Human leucocyte AB antigens were determined by means of a lymphocyte toxicity test in 84 patients with essential hypertension and in 1000 blood donors. 2. The prevalence of HLA B8 was 16.4% in hypertensive patients and 8.9% in controls (P = 0.07). 3. The prevalence of HLA B12 was 34.5% in hypertensive patients and 26.9% in the control group (N.S.). In WHO stage III hypertension HLA B12 was found in six out of 10 patients. 4. The prevalence of HLA B15 was 1.2% in hypertensive patients and 6.4% in controls (P less than 0.05). 5. In view of a previous report of HLA antigens in Spanish diabetic population, this study does not support the suggestion of a genetic and possibly HLA-linked connection between essential hypertension and diabetes mellitus among the Spanish population. 6. A positive family history of hypertension tended to be more common in those patients with essential hypertension associated with HLA B8.
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PMID:HLA antigens in Spanish patients with essential hypertension. 694 68

Serum antinuclear antibody (ANA) and HLA phenotype frequency were studied in 100 black subjects with essential hypertension and 100 normotensive black controls matched for age and sex. 11% of hypertensive individuals had a positive serum ANA test compared with 2% of controls (p less than 0.01). Among the hypertensive patients, positive serum ANA test was seen exclusively in patients who were receiving treatment with methyldopa. Although ANA also correlated with hypertensive vascular damage as assessed by retinal and EKG abnormalities, this was believed to have been due to the higher dose of methyldopa that may have been required to treat hypertension in these more severe cases. A statistically significant correlation of HLA-A11 and HLA-B12 with hypertension was observed, but only studied when uncorrected for the number of HLA specificities. It was concluded that autoantibody formation in essential hypertension is most likely to have been a consequence of antihypertensive drug therapy. In addition, further studies using larger number of patients and controls might more clearly establish the question of whether or not HLA is associated with essential hypertension.
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PMID:Immunogenetic studies in essential hypertension among black patients. I. Correlative studies of serum autoantibody formation. 697 42

Idiopathic mesangial glomerulonephritis with IgA deposits was observed in two relatives, father and son, in a family of 5 members. In the father the disease started at age 43 with relapsing macroscopic hematuria, proteinuria, renal failure and hypertension, with a progressive course in the ensuing four years. The affected son, the oldest of three brothers, developed relapsing macroscopic hematuria at age 16; two years later renal function was normal and there was no hypertension, but microhematuria persisted without proteinuria. The mother and the other two brothers had no clinical or biological signs of renal disease. Serum immunoglobulins (IgG, IgA, and IgM) and complement (C3, C4, C3 proactivator) were normal in the patients and their relatives. Histocompatibility typing demonstrated the presence of HLA-Bw35 in the father and the two unaffected sons, being negative in the mother and the affected son. The analysis of HLA-Bw35 in 23 patients with IgA mesangial glomerulonephritis gave positive results in 30% of them, while the control group had a positivity of 15% (p non significant with the X2 test). The present observations suggest that IgA mesangial glomerulonephritis is a potentially familial and hereditary renal disease. HLA-Bw35 antigen appears not to be a genetic marker of the disease in our geographical area.
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PMID:[Familial and hereditary mesangial glomerulonephritis with IgA deposits (author's transl)]. 701 69

Three of five siblings developed a steroid-resistant nephrotic syndrome with focal segmental glomerulosclerosis within a four-month period. Two of the siblings with nephrotic syndrome (Patients 1 and 2) also have sickle cell anemia; the third (Patient 3) carries the thalassemia trait. The dizygotic twin brother of Patient 2 has sickle cell anemia, but does not have the nephrotic syndrome. The nephrotic syndrome of patient 1 was resistant to corticosteroid and cyclophosphamide therapy and she developed severe renal failure 14 months after onset. The nephrotic syndrome of Patients 2 and 3 was steroid resistant but was partially responsive to cyclophosphamide therapy. They have persistent proteinuria with mild elevation of serum creatinine concentration and hypertension 5 1/2 years after diagnosis. In this family, the nephrotic syndrome appeared unrelated to the specific hemoglobinopathy, HLA type or mixed lymphocyte culture responsiveness despite the similarity of the renal disease.
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PMID:Familial nephrotic syndrome and focal segmental glomerulosclerosis. 719 18

This study was designed to investigate whether isolated genetic factors, controlled by genes in the HLA chromosomal region, could be indicted as independent contributing influences in the genesis of premature coronary artery disease (CAD). Nineteen patients with fixed obstructive CAD documented by coronary angiography had no coronary risk factors with respect to age; levels of serum cholesterol, fasting triglycerides, and blood glucose; blood pressure; obesity; history of diabetes mellitus or hypertension; and cigarette-smoking history. Sixteen patients had a family history of CAD. HLA typing was restricted to antigens of the A and B loci. Control subjects (n = 1,157) were normal. At the A locus, no antigens demonstrated an observed frequency significantly higher than that expected from the control population. At the B locus, BW 38 had a statistically significant greater frequency (p less than 0.01) in the study group with CAD (21 percent) than in the control population (4 percent). The association between BW 38 and premature CAD lost its statistical significance when conservatively corrected for the number of HLA antigens tested by the Bonferroni adjustment. The relative risk for CAD if a patient had antigen BW 38 was 6.2. Our data suggest a statistically significant trend between the presence of HLA BW 38 and premature CAD. Whether the HLA tissue antigens are involved directly in the pathogenesis of CAD, act as markers for immune response genes, or serve as markers of other yet undefined genetic factors needs further study.
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PMID:Correlation of HLA types in premature coronary artery disease: an attempt to define independent genetic risk factors. 719 67

Glomerulonephritis with mesangial deposition of IgA was diagnosed in 31 patients. In Spain this disease is the second more frequent primary glomerulonephritis, representing 27% of them. One out of every four patients with IgA mesangial glomerulonephritis ends the clinical course in renal failure. Such bad evolution might be predicted by the existence of arterial hypertension, severe proteinuria, degree of glomerular sclerosis, presence of HLA Bw35, and increased polymeric IgA in serum. The present pathogenetic concepts are reviewed.
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PMID:[IgA mesangial glomerulonephritis (author's transl)]. 725 41

Essential hypertension is a common disorder with potentially life-threatening sequelae. Hypertension among black persons may have characteristics different from hypertension among white persons. It has been estimated that up to 60% of population variance in blood pressure may be attributable to genetic differences. We studied the distribution of HLA antigens in 100 black hypertensives and 100 normotensive controls. Hypertension was not significantly associated with any of the 25 HLA antigens identified. We conclude that HLA-A and HLA-B locus antigens are not associated with essential hypertension in the black patient.
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PMID:Histocompatibility antigens in black patients with essential hypertension. 728 93


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