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)

A 33-year-old man is described with hyperkalaemia, hypertension and acidosis. The blood pressure was 160 to 200 mmHg systolic and 90 to 110 mmHg diastolic and the plasma potassium was between 6.0 and 7.0 mmole per litre. There was no renal disease and creatinine clearance was 103 ml per minute. Plasma renin activity was low and plasma aldosterone was at the lower limit of normal. Sodium deprivation or oral frusemide had little effect on blood pressure, plasma potassium, renin, aldosterone or arginine vasopressin. However, bendrofluazide caused a rapid fall of blood pressure and plasma potassium, and rise of plasma renin, aldosterone and plasma arginine vasopressin. Hypertension and hyperkalaemia is rare in the absence of renal failure. Four similar patients reported previously are reviewed. We suggest that our patient, and perhaps some of those reported earlier had primary abnormality of renal tubular function with impaired secretion of potassium and excessive tubular reabsorption of sodium. The plasma renin activity could be due to volume expansion and the low plasma aldosterone was probably caused by the antagonistic effects of low renin depressing synthesis and hyperkalaemia increasing it. A minor similar tubular abnormality might be the explanation in some of the patients with essential hypertension who have low plasma renin activity.
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PMID:Hypertension and hyperkalaemia responding to bendrofluazide. 50 50

Minoxidil, a potent vasodilator antihypertensive agent, was given to 14 patients with severe hypertension uncontrolled by conventional agents. Thirteen patients had elevated serum creatinine levels. Over a period of 20 months (mean duration of administration) minoxidil lowered blood pressure from 194/124 to 147/90 mm Hg (mean values), in combination with furosemide and a sympathetic inhibitor (usually propranolol). Progression of preexisting renal disease was halted in all but three patients. Fluid retention, cardiac failure, and angina were troublesome side effects. The occurrence of hypertrichosis also limited the usefulness of minoxidil, particularly in female patients.
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PMID:Minoxidil therapy for refractory hypertension and chronic renal failure. 50 78

Three children with renal disease, hypertension, and the Cockayne syndrome were evaluated. All patients had severe hypertension; peripheral vein renin was elevated in two patients. Renal biopsy specimens from two patients were studied by light microscopy, electron microscopy, and immunofluoresence. Immunohistologic studies demonstrated deposits of immunoglobulin and complement in the vessels and glomeruli of the first patient; deposits of immunoglobulin and complement were seen in the glomeruli of the third patient. Also electron-dense deposits were seen in the glomerular basement membrane of the third patient. Circulating immune complexes were detected by the Raji cell and Clq binding techniques in this child as well. Both hypertension and renal disease are frequent complications of the Cockayne syndrome.
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PMID:The Cockayne syndrome: an evaluation of hypertension and studies of renal pathology. 51 20

This study describes the levels of urinary kininase activity in hypertension. Urinary kininase activity in essential and secondary hypertensive patients was higher than in controls (1010.2 +/- 102.7 versus 114.4 +/- 23.1 ng destroyed bradykinin/min.; p less than 0.001). In a group of hypertensive diabetics without nephropathy kininase activity in urine was decreased (46.0 +/- 12.7 ng destroyed bradykinin/min.). This investigation shows that in hypertension urinary kininase activity reaches higher levels. An inverse correlation was found between urinary kallikrein and urinary kininase activity from essential hypertensive patients.
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PMID:Altered urinary excretion of human kininase activity in hypertension. 51 58

Classical sex-linked hemophilia (Hemophilia A) has been described as due to deficiency in the synthesis of Factor VIII procoagulant activity (VIII:C). The availability of immunological techniques provided the means of identifying Factor VIII-Related Antigen(VI-IIR:Ag) detectable by rabbit antibodies to F VIII, which is distinct from VIII:C detected by human anti-F VIII available from multitransfused patients. Hemophilia A is lacking in VIII:C but not VIIIR:Ag. Recently, a third function of the F VIII "complex" was discovered with the help of ristocetin (von Willebrand's Factor, VIIIR: RCo). This activity is reduced in von Willebrand's syndrome. Estimation of the titers of VIII:C and VIIIR:Ag provides a method for more accurate detection of hemophilic carriers. Newly available chromogenic substrates perhaps will give rise to more simplified assays of VIII:C. The development of cryoprecipitates and stable lyophilized concentrates of F VIII has greatly simplified and intensified maintenance therapy, and has opened a new era in treatment. Prophylactic therapy has been shown to be very helpful in certain "high risk" cases. The impact and benefits of home care and self-administration has been tremendous. However, the varying quality of cryoprecipitates and the high cost of more purified concentrates are still stumbling blocks in treatment regimes. Other problems exist. Spontaneous bleeding, especially central nervous system bleeding, account for the majority deaths by haemorrhage. Inhibitor kinetics have been well characterized. It is clear that there exists "low" and "high" responders. For the "high" responders, plasmapheresis, immunosuppressives and the infusion of Factor IX concentrates have been utilized with varying success. The prevention of hemophilic arthropathy and its progression by maintenance therapy seems to be still inadequate. The results of trials with more vigorous regimes are awaited. The complications of therapy still remain to be solved. Apart from the well-known complications wuch as hepatitis, haemolytic disease and F VIII inhibitors, the existence of previously unnoticed complications as splenomegaly, hypertension, renal disease and paradoxal bleeding have been recently realized. The role of altered fibrinogen, fibrin degradation products (FDP) and unclassified fibrinogen derivatives (UFD) present in cryoprecipitates and F VIII concentrates in the above complications needs to be further clarified. In conclusion, tremendous progress in various aspects of hemophilia has been achieved in developed countries. Comprehensive care can now be carried out in various centers. On the other hand, developing countries still face a number of basic problems. The concept that hemophilia is a "manageable" disease and that chronic crippling and death from exsanguination can be prevented, should be disseminated widely by various means...
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PMID:Recent advances in hemophilia. 52 46

1 The effect of an intravenous bolus of labetalol (0.6--1.6 mg/kg body weight) on central and peripheral haemodynamics was studied in nine subjects with essential hypertension and in eleven subjects with chronic renal disease and hypertension. 2 The BP reduction amounting to 20/13 mmHg was entirely due to the lowering of the total peripheral vascular resistance. This also included the vascular resistance in the muscles. 3 This peripheral vasodilatation was not counteracted by a reflex increase of the cardiac output. 4 The reflex tachycardia and overshoot of BP in Valsalva's manoeuvre were largely abolished. 5 Central and peripheral venous BPs, vascular volume of the forearm and venous distensibility did not show any significant change after treatment with labetalol. 6 In spite of the lowering of the vascular resistance of the forearm by labetalol, forearm blood flow was not significantly affected due to the parallel decrease in the perfusion pressure. 7 Plasma renin activity fell after labetalol in all instances.
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PMID:Effect of an alpha- and beta-adrenoceptor-blocking agent (labetalol) on haemodynamics in hypertension. 52 90

A case-control study was conducted of the deaths from subarachnoid haemorrhage (SAH) in women aged 15-44 in England and Wales in 1976. There was a small excess of oral contraceptive use by the women who died from SAH compared with their generally healthy practice-matched controls; this was not, however, statistically significant. Out of 134 women who died from SAH, 34 had a history of hypertension compared with only six of their controls. Renal disease and pre-eclamptic toxaemia were more commonly associated with hypertension in the dead women than in controls. No change in the annual mortality from SAH has been observed in the past 20 years such as might have been expected if the risks were high. Although current or past use of oral contraceptives may have increased the blood pressure and risk of SAH in a few women, the most important factor in determining this risk was hypertension. SAH should thus probably not be regarded as serious cause for concern in healthy non-hypertensive women using oral contraceptives.
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PMID:Oral contraceptives and fatal subarachnoid haemorrhage. 52 13

For the judgment of the peripheral blood supply 16 insulin-dependent diabetics with necrobiosis lipoidica at the lower extremities were compared with 15 insulin-dependent diabetics without necrobiosis lipoidica. The vascular changes in form of retinopathy, nephropathy, neuropathy, hypertension, the results of the radiologically provable vascular changes, oscillograms and impedance plethysmograms as well as the results of the muscle and skin clearance and angioscintigraphy were evaluated. The at last mentioned methods give an insight into the microangiopathy. The apparantly contradicting findings of the muscle clearance (smaller blood supply) and of the skin clearance (increased blood flow) find their explanation by the angioscintigraphically proved different regional parameters of blood flow in the necrobiotic regions. The angiopathic findings are characterized by the enrichment of activity in the marginal seam as a sign of hyperemia and decreased accumulation in the centre as an expression of necrobiosis. The changes of the connective tissue and their causes of development are discussed. Angiopathic and traumatic influences conditioned by metabolism, apart from local peculiarities are taken into consideration.
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PMID:[Peripheral blood flow in patients with necrobiosis lipoidica (diabeticorum)]. 54 2

The efficacy of correlating the L/S ratio in the amniotic fluid with fetal lung maturity has been substantiated in normal pregnancies. In gestations complicated by fetomaternal diseases, however, the assay is less reliable. This study involves 555 pregnancies in which there was a significant maternal, fetal, or placental disorder. The L/S ratio was related to fetal respiratory maturity as measured by Dubowitz criteria and the occurrence of RDS. The results show that pre-eclampsia, chronic hypertension, diabetes (Class D, E, F), significant cardiovascular disease, severe hemoglobinopathies, various congenital anomalies, chronic placental insufficiency, and prolonged ruptured membranes accelerated the L/S ration. Conversely, mild diabetes (Class B, C), intrinsic renal disease, hepatitis, collagen disease, hydrops fetalis, syphilis, and toxoplasmosis were associated with a delay in the L/S ratio. A significant increase in erroneous responses was noted in these patients when the L/S ratio was correlated to infant maturity and to the incidence of RDS. Possible mechanisms for these findings are discussed.
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PMID:The lecithin/sphingomyelin ratio in cases associated with fetomaternal disease. 57 73

This report describes a case of Laurence-Moon-Biedl syndrome identified in a 24-month-old boy. Significant renal involvement was present with right-sided vesicoureteral reflux, cystocele, urinary tract infections, and growth arrest of the right kidney. After the development of hypertension a left renal biopsy was performed to determine if bilateral renal disease was present. Histopathological and ultrastructural changes in the left kidney are described. These changes appear to be unrelated to pyelonephritis or hypertension and to be most consistent with the nephropathy of Laurence-Moon-Biedl syndrome.
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PMID:Renal histopathological changes in a child with Laurence-Moon-Biedl syndrome. 59 46


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