Serum Angiotensin-Converting Enzyme Level Is Elevated in Patients With Human Immunodeficiency Virus Infection

Ouellette, Daniel R.; Kelly, Joan; Anders, G

doi:10.1001/archinte.1992.00400140069016

Cited by 23 publications

(9 citation statements)

References 29 publications

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“…High levels of ACE are detected in the circulation of HIV-infected patients [165], but these changes may be related to lung endothelial injury rather than systemic activation of the renin-angiotensin system. Overall, the reduction of proteinuria or hypertension during the late stages of HIVAN may be the most relevant beneficial effects of these drugs [162,163,164].…”

Section: Angiotensin-converting Enzyme Inhibitorsmentioning

confidence: 99%

A 20-year history of childhood HIV-associated nephropathy

Ray

Rakusan

et al. 2004

Pediatr Nephrol

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In 1984, physicians in New York and Miami reported HIV-infected adult patients with heavy proteinuria and rapid progression to end-stage renal disease. These patients showed large edematous kidneys with a combination of focal segmental glomerulosclerosis (FSGS) and tubulointerstitial lesions. This renal syndrome, named HIV-associated nephropathy (HIVAN), was found predominantly in African Americans. Subsequent studies confirmed the presence of HIVAN in children, who frequently develop nephrotic syndrome in association with FSGS and/or mesangial hyperplasia with microcystic tubular dilatation. Since then, substantial progress has been made in our understanding of the etiology and pathogenesis of HIVAN. This article reviews 20 years of research into the pathogenesis of HIVAN and discusses how these concepts could be applied to the treatment of children with HIVAN. HIV-1 infection plays a direct role in the pathogenesis of childhood HIVAN, at least partially by affecting the growth and differentiation of glomerular and tubular epithelial cells and enhancing the renal recruitment of infiltrating mononuclear cells and cytokines. An up-regulation of renal heparan sulfate proteoglycans seems to play a relevant role in this process, by increasing the recruitment of heparin-binding growth factors (i.e., FGF-2), chemokines, HIV-infected cells, and viral proteins (i.e., gp120, Tat). These changes enhance the infectivity of HIV-1 in the kidney and induce injury and proliferation of intrinsic renal cells. Highly active anti-retroviral therapy (HAART) appears to be the most promising treatment to prevent the progression of childhood HIVAN. Hopefully, in the near future, better education, prevention, and treatment programs will lead to the eradication of this fatal childhood disease.

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Section: Angiotensin-converting Enzyme Inhibitorsmentioning

confidence: 99%

A 20-year history of childhood HIV-associated nephropathy

Ray

Rakusan

et al. 2004

Pediatr Nephrol

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“…The possibility of intrapontine and prepontine tumor should also be considered [27]. Because one of the most frequently entertained diagnoses when examining a patient with bilateral facial Bell palsy is sarcoidosis, it should be recalled that angiotensin-converting enzyme levels can also be increased in acute retroviral syndrome [28], as patient 2 exemplifies. To our knowledge, there have been no controlled studies of antiretroviral therapy in HIV-1-related facial paralysis to demonstrate efficacy.…”

mentioning

confidence: 99%

Bilateral Bell Palsy and Acute HIV Type 1 Infection: Report of 2 Cases and Review

Serrano

Hernández

Arroyo

et al. 2007

Clinical Infectious Diseases

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Two adult patients who presented to a hospital with bilateral facial Bell palsy who were also experiencing human immunodeficiency virus type 1 seroconversion are described. Ten additional cases retrieved from the literature are also reviewed. Bell palsy appeared a median of 15 days after the beginning of the clinical disease, and aseptic meningitis was an invariable concomitant of facial neuropathy. All but 1 patient (8.3%) recovered without sequelae.

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“…MMPs are produced by many cell types including lymphocytes, granulocytes, astrocytes, and activated macrophages. There is an increased concentration of MMPs 1,3,7,8,9,25, and 26 in the saliva and gingival tissue of HIV-infected patients. 74,75 Gingival mast cells have also been shown to strongly express MMP-1 and MMP-8 in HIV-infected patients.…”

Section: The Non-genetic Role Of Thiamine In Hivmentioning

confidence: 99%

The role of thiamine in HIV infection

Lương

Nguyễn

2013

International Journal of Infectious Diseases

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Patients infected with HIV have a high prevalence of thiamine deficiency. Genetic studies have provided the opportunity to determine which proteins link thiamine to HIV pathology, i.e., renin-angiotensin system, poly(ADP-ribosyl) polymerase 1, Sp1 promoter gene, transcription factor p53, apoptotic factor caspase 3, and glycogen synthetase kinase 3β. Thiamine also affects HIV through non-genomic factors, i.e., matrix metalloproteinase, vascular endothelial growth factor, heme oxygenase 1, the prostaglandins, cyclooxygenase 2, reactive oxygen species, and nitric oxide. In conclusion, thiamine may benefit HIV patients, but further investigation of the role of thiamine in HIV infection is needed.

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Serum Angiotensin-Converting Enzyme Level Is Elevated in Patients With Human Immunodeficiency Virus Infection

Cited by 23 publications

References 29 publications

A 20-year history of childhood HIV-associated nephropathy

A 20-year history of childhood HIV-associated nephropathy

Bilateral Bell Palsy and Acute HIV Type 1 Infection: Report of 2 Cases and Review

The role of thiamine in HIV infection

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