Serum Levels of Neutrophil Gelatinase–Associated Lipocalin Are Associated With Microalbuminuria in HIV-Infected Patients

Damås, Jan Kristian; Bækken, Morten; Ueland, Thor; Manner, Ingjerd W.; Os, Ingrid; Yndestad, Arne; Flo, Trude Helen; Øktedalen, Olav; Aukrust, Pål

doi:10.1097/qai.0b013e31823f35a7

Cited by 3 publications

(2 citation statements)

References 19 publications

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“…Plasma and urinary Lcn2/Ngal levels have been proposed as biomarkers for early identification of AKI in a variety of experimental and clinical settings [28,29]. Most studies have highlighted tubular expression of Lcn2/Ngal, but its expression also increases in glomerular diseases, including diabetes [64,65,66,67], hemolytic uremic syndrome [68], HIV nephropathy [69,70], systemic lupus erythematosus [71,72] and chronic kidney disease [73]. Using a transgenic Lcn2/Ngal-luciferase reporter mouse, Paragas et al [27] elegantly showed that ischemia-reperfusion, cisplatin and lipid A induce distal tubular expression of Lcn2/Ngal.…”

Section: Discussionmentioning

confidence: 99%

Podocytes Express IL-6 and Lipocalin 2/ Neutrophil Gelatinase-Associated Lipocalin in Lipopolysaccharide-Induced Acute Glomerular Injury

Lee

Borsting

Declèves

et al. 2012

Nephron Exp Nephrol

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Background/Aims: Acute kidney injury (AKI) contributes to significant morbidity and mortality in the intensive care unit (ICU). Plasma levels of interleukin (IL)-6 predict the development of AKI and are associated with higher mortality in ICU patients with AKI. Most studies in AKI have focused on the tubulo-interstitium, despite evidence of glomerular involvement. In the following study, our goals were to investigate the expression of IL-6 and its downstream mediators in septic-induced AKI. Methods: Podocytes were treated in vitro with lipopolysaccharide (LPS) and mice were treated with LPS, and we evaluated IL-6 expression by real-time PCR, ELISA and in situ RNA hybridization. Results: Following LPS stimulation, IL-6 is rapidly and highly induced in cultured podocytes and in vivo in glomeruli and infiltrating leukocytes. Surprisingly, in direct response to exogenous IL-6, podocytes produce lipocalin-2/neutrophil gelatinase-associated lipocalin (Lcn2/Ngal). LPS also potently induces Lcn2/Ngal expression in podocytes in culture and in glomeruli in vivo. Intense Lcn2/Ngal expression is also observed in IL-6 knockout mice, suggesting that while IL-6 may be sufficient to induce glomerular Lcn2/Ngal expression, it is not essential. Conclusions: The glomerulus is involved in septic AKI, and we demonstrate that podocytes secrete key mediators of AKI including IL-6 and Lcn2/Ngal.

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Section: Discussionmentioning

confidence: 99%

Podocytes Express IL-6 and Lipocalin 2/ Neutrophil Gelatinase-Associated Lipocalin in Lipopolysaccharide-Induced Acute Glomerular Injury

Lee

Borsting

Declèves

et al. 2012

Nephron Exp Nephrol

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“…6 Another study has shown the correlation with serum neutrophil gelatinase-associated lipocalin (NGAL), an inflammatory marker produced by neutrophils and other cells. 20 In the present study we hypothesized that in HIV-infected individuals whose disease was well controlled with combination antiretroviral therapy (cART), albuminuria is associated with chronic inflammation independent of traditional risk factors and toxicity from antiretroviral therapy. We chose to study whether a relationship existed between biomarkers of CVD and albuminuria.…”

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confidence: 99%

Albuminuria Is Associated with Elevated Acute Phase Reactants and Proinflammatory Markers in HIV-Infected Patients Receiving Suppressive Combination Antiretroviral Therapy

O-charoen

Ndhlovu

Gangcuangco

et al. 2014

AIDS Research and Human Retroviruses

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Albuminuria among HIV-infected individuals has been found to be associated with cardiovascular disease (CVD) and mortality. Inflammation has been associated with albuminuria. The pathophysiology of albuminuria in HIV-infected individuals is poorly understood. We investigated the association of albuminuria with inflammatory biomarkers among HIV-infected individuals on combination antiretroviral therapy (cART). This is a cross-sectional analysis of participants enrolled in the Hawaii Aging with HIV-Cardiovascular Cohort. Plasma inflammatory biomarkers were assessed using the Milliplex Human Cardiovascular disease multiplex assays. A random urine sample was collected for albumin measurement. Albuminuria was defined as urine albumin-tocreatinine ratio of ‡ 30 mg/g. Framingham risk score was calculated and divided into three classes. Simple and multivariable logistic regression analyses were utilized to assess the correlation between plasma inflammatory biomarkers and albuminuria and were adjusted for Framingham risk category. Among 111 HIV-infected patients [median (IQR) age of 52 (46-57) years, 86% male, median (IQR) CD4 count of 489 (341-638) cells/ mm 3 , 85% with HIV RNA < 50 copies/ml], 18 subjects (16.2%) had moderately increased albuminuria (albuminuria range between 30 and 300 mg/g) and 2 subjects (1.8%) had severely increased albuminuria (albuminuria more than 300 mg/g). In multivariable logistic models, sE-selectin, sVCAM-1, CRP, SAA, and SAP remained significantly associated with albuminuria after adjustment of CVD risk factors. This study showed an association between inflammation and albuminuria independent of previously reported risk factors for albuminuria in HIV-infected subjects who were on combination antiretroviral therapy (cART). Chronic inflammation despite potent antiretroviral treatment may contribute to higher rates of albuminuria among HIVinfected patients.

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Serum Lipocalin 2 (Neutrophil Gelatinase–Associated Lipocalin) in Relation to Biomarkers of Inflammation and Cardiac Stretch During Activation of the Renin-Angiotensin-Aldosterone System in Human Immunodeficiency Virus

Bogorodskaya

Fitch

Burdo

et al. 2019

The Journal of Infectious Diseases

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Purpose To evaluate the relationship of lipocalin 2 to inflammation and cardiac injury with increased aldosterone in human immunodeficiency virus (HIV). Methods A standardized 6-day low-sodium diet was used to stimulate renin-angiotensin-aldosterone system (RAAS) activation, and serum lipocalin 2 and biomarkers of inflammation and cardiac stretch were assessed among persons with or without HIV. Results Lipocalin 2 levels increased with RAAS activation compared with suppression in the HIV group (median level [interquartile range], 71.3 [59.2–99.7] vs 67.0 [51.8–86.3] ng/mL; P = .01). During RAAS activation, lipocalin 2 was related to biomarkers of inflammation (tumor necrosis factor α [P = .007]), monocyte/macrophage activation (soluble CD163 [P = .005] and chemokine [C-C motif] ligand 2 [P = .03]), and markers of cardiac stretch (brain natriuretic peptide [P < .001] and N-terminal fragment of the prohormone brain natriuretic peptide [P = .001]) in HIV. Conclusion Lipocalin 2 may be important in modulating aldosterone-induced inflammation, monocyte activation, and cardiac stretch during RAAS activation in HIV. Clinical Trial Registration NCT01407237

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Serum Levels of Neutrophil Gelatinase–Associated Lipocalin Are Associated With Microalbuminuria in HIV-Infected Patients

Cited by 3 publications

References 19 publications

Podocytes Express IL-6 and Lipocalin 2/ Neutrophil Gelatinase-Associated Lipocalin in Lipopolysaccharide-Induced Acute Glomerular Injury

Podocytes Express IL-6 and Lipocalin 2/ Neutrophil Gelatinase-Associated Lipocalin in Lipopolysaccharide-Induced Acute Glomerular Injury

Albuminuria Is Associated with Elevated Acute Phase Reactants and Proinflammatory Markers in HIV-Infected Patients Receiving Suppressive Combination Antiretroviral Therapy

Serum Lipocalin 2 (Neutrophil Gelatinase–Associated Lipocalin) in Relation to Biomarkers of Inflammation and Cardiac Stretch During Activation of the Renin-Angiotensin-Aldosterone System in Human Immunodeficiency Virus

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