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)

The case of a renal transplant recipient with a known history of iv drug abuse but unknown human immunodeficiency virus (HIV) status who presents after having a stable renal allograft function for 4 yr, with acute/subacute advanced renal failure, nephrotic syndrome, and hypertension, as well as clinical and histologic findings of thrombotic microangiopathy, is reported. He was subsequently found to have a positive serology for HIV-1 with a low CD4 count but no clinical manifestations of the acquired immunodeficiency syndrome. He was treated conservatively with zidovudine (AZT). The patient never regained graft function and was ultimately discharged from the hospital on maintenance dialytic therapy. This is, to our knowledge, the first report of thrombotic microangiopathy in an HIV-1-infected patient presenting late in the course as acute/subacute renal allograft failure.
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PMID:Late renal allograft failure secondary to thrombotic microangiopathy-human immunodeficiency virus nephropathy. 801 72

HIV infection has been associated with a variety of renal diseases, although the pathogenesis of such dysfunction is unknown. To determine whether HIV-infection is associated with glomerular permeability defects, and if so, the prevalence of the finding, we studied patients with various stages of HIV infection. Urine samples from 505 outpatients with HIV infection (without hypertension, azotemia, or dipstick proteinuria), 41 normal controls and 40 febrile non-HIV positive, hospitalized patients with infectious diseases were analyzed for the urinary microalbumin/creatinine ratio (U microA/Cr), a sensitive indicator of incipient renal disease in diabetes mellitus and hypertension, and the urinary beta 2-microglobulin/creatinine ratio (U beta 2/Cr), an indicator of renal tubular function. Microalbumin concentration was measured by ELISA. Beta 2-microglobulin concentration was measured by an enzyme immunoassay. HIV-infected outpatients had higher mean U microA/Cr than normal subjects, but not febrile hospitalized controls. The prevalence of an increased U microA/Cr was 29.8% in the HIV-infected outpatient population. There was no difference in the ratio between Black and White HIV-infected outpatients, HIV-infected outpatients treated or untreated with zidovudine (AZT), or HIV infected outpatients untreated with any drug. There was no difference between U microA/Cr in stage II, III or IV HIV-infected patients when assessed by analysis of variance. A similar pattern was noted with U beta 2/Cr. The prevalence of an increased U beta 2/Cr ratio was 37.7% in HIV-infected outpatients. Increased urinary albumin and beta 2-microglobulin excretion, not associated with drug therapy, is present in patients with early HIV infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal urinary protein excretion in HIV-infected patients. 813 71

At an international think tank in Washington, D.C., HIV experts presented evidence showing that combination therapy used early in the course of infection has suppressed HIV in patients to undetectable levels. The new combinations are using older nucleoside analogues, such as zidovudine (AZT), lamivudine (3TC), and didanosine (ddI), and combining them with protease inhibitors or with nevirapine, a non-nucleoside analogue. This type of treatment has reduced the amount of virus to levels too low to be detected by the most sensitive tests in some individuals. AIDS researchers are hopeful that these combinations will turn HIV infection into a chronic, yet manageable, disease similar to hypertension and diabetes. Despite these developments, surveys and interviews indicate that many treatment providers have not changed their practices, either because they are not aware of the new data, or because they want more definitive studies before putting their patients at risk. Additionally, obstacles to these new therapies include patient compliance with the treatment regimen, adverse reactions to the combination therapies, and cost.
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PMID:Breakthroughs in HIV treatment not yet embraced by clinicians. 1136 53

Epoietin alfa (EPO) is a synthetic version of erythropoietin. Initially approved by the Food and Drug Administration (FDA) for treating anemia in patients on kidney dialysis, the approval was later expanded to include people with AZT-related anemia, those undergoing chemotherapy, and those undergoing surgery that requires blood transfusions. In clinical studies, EPO raised hematocrit, which indicates increased red blood cells, and therefore decreased the number of blood transfusions needed. For patients with high blood pressure, or for patients who have anemia from iron or folate insufficiency, EPO should not be used.
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PMID:Epoietin alfa (EPO) for anemia. 1136 62

The objective of this study was to determine the effects of highly active antiretroviral therapy (HAART) drugs on pulmonary endothelial function. Porcine pulmonary arteries or human pulmonary arterial endothelial cells (HPAECs) were incubated with eight HAART drugs [ritonavir, indinavir, lopinavir, zidovudine (AZT), abacavir, stavudine, didanosine (ddI), and lamivudine] individually or in combination [three HAART drugs (3-plex; indinavir, stavudine, and ddI)] at their clinical plasma concentrations for 24 hours. Endothelium-dependent vasorelaxation in response to bradykinin was reduced significantly by the ritonavir in a concentration-dependent manner. Five other HAART drugs (indinavir, lamivudine, abacavir, AZT, and ddI) and the 3-plex significantly also impaired endothelium-dependent vasorelaxation in response to bradykinin. Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs. Furthermore, both ritonavir and AZT substantially activated ERK2 in HPAECs. Additionally, the antioxidants ginsenoside Rb1 and ginkgolide A effectively reversed HAART drug-induced vasomotor dysfunction and eNOS down-regulation. Inhibition of ERK1/2 also partially blocked ritonavir- and AZT-induced down-regulation of eNOS and vasomotor dysfunction. Thus, HAART drugs significantly impair endothelial functions of porcine pulmonary arteries and HPAECs, which may be mediated by eNOS down-regulation, oxidative stress, and ERK1/2 activation. These findings suggest that HAART drugs may contribute to the high incidence of pulmonary artery hypertension in human immunodeficiency virus-infected patients.
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PMID:Roles and mechanisms of human immunodeficiency virus protease inhibitor ritonavir and other anti-human immunodeficiency virus drugs in endothelial dysfunction of porcine pulmonary arteries and human pulmonary artery endothelial cells. 1921 43