Captopril effect on prostaglandin E2, thromboxane B2 and proteinuria in lupus nephritis patients

Daza, Leonel; Kornhauser, Carlos; Zamora, Lurdes; Flores, Jorge

doi:10.1016/j.prostaglandins.2005.08.001

Cited by 13 publications

(7 citation statements)

References 33 publications

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“…The inhibition of this axis using an angiotensin-converting-enzyme (ACE) inhibitor, captopril, has been shown to be effective in improving survival, glomerular damage, proteinuria, lymphoid hyperplasia, dermatitis and hypergammaglobulinemia in 2 mouse models of spontaneous lupus, MRL. lpr and NZW/NZB (38–40), with parallel findings in human lupus nephritis (41, 42). Increased renal renin activity has also been reported in patients with lupus nephritis(43, 44).…”

Section: Discussionsupporting

confidence: 62%

Urine Proteome Scans Uncover Total Urinary Protease, Prostaglandin D Synthase, Serum Amyloid P, and Superoxide Dismutase as Potential Markers of Lupus Nephritis

Brekken

et al. 2010

The Journal of Immunology

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To identify potential biomarkers in immune-mediated nephritis, urine from mice subjected to an augmented passive model of anti-glomerular basement membrane-induced experimental nephritis was resolved using 2D-gels. The urinary proteome in these diseased mice was comprised of at least 71 different proteins. Using orthogonal assays, several of these molecules, including serum amyloid P, prostaglandin D synthase, superoxide dismutase, renin and total protease were validated to be elevated in the urine and kidneys of mice during anti-GBM disease, as well as in mice with spontaneously arising lupus nephritis. Among these, urinary protease was the only marker that appeared to be exclusively renal in origin, whereas the others were partly serum-derived. Longitudinal studies in murine lupus demonstrated that total urinary protease had better predictive value for histologically active nephritis (r = 0.78), compared to proteinuria (r = −0.04) or azotemia (r = 0.28), or the other markers examined, while urine SAP emerged as the single most predictive marker of histological GN. Collectively, these studies uncover total urinary protease, PGDS, SAP and SOD as novel biomarkers of anti-GBM disease and lupus nephritis, with stronger correlation to renal disease compared to currently employed biomarkers. These findings could have important diagnostic and prognostic ramifications in the management of these renal diatheses.

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Section: Discussionsupporting

confidence: 62%

Urine Proteome Scans Uncover Total Urinary Protease, Prostaglandin D Synthase, Serum Amyloid P, and Superoxide Dismutase as Potential Markers of Lupus Nephritis

Brekken

et al. 2010

The Journal of Immunology

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“…Specific studies in lupus nephritis are, however, very few. Daza et al [15], for example, have reported that lupus nephritis patients treated with prednisone and cyclophosphamide plus captopril showed a decrease in the rate of proteinuria and in urine prostanglandin E2 at 6 months of treatment and Tse et al [16] have shown that lupus nephritis patients with persistent proteinuria (>1 g/day) treated with ACE inhibitors (n ¼ 12) or angiotensin II receptor blockers (ARBs) (n ¼ 2) diminished their proteinuria and improved their serum albumin from baseline. Furthermore, De Albuquerque et al [17] have shown that captopril treatment delays the onset of proteinuria in lupus mice and this improvement correlates with reduced expression of TGF-in the kidneys and of splenic levels of type 2 cytokines (IL-4 and IL-10).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme inhibitors delay the occurrence of renal involvement and are associated with a decreased risk of disease activity in patients with systemic lupus erythematosus--results from LUMINA (LIX): a multiethnic US cohort

et al. 2008

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“…At the same time, we also can’t deny the bad consequence caused by PGE 2 and TXB 2 in the LN. High levels of PGE 2 and TXB 2 promoted the activation of T cells and the production of IL-4 and IL-10 cytokines, which in turn leads to glomerulosclerosis in LN [84].…”

Section: Mechanism Of Aa-induced Renal Inflammationmentioning

confidence: 99%

Arachidonic Acid Metabolism and Kidney Inflammation

Wang

Chen

et al. 2019

IJMS

217

151

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As a major component of cell membrane lipids, Arachidonic acid (AA), being a major component of the cell membrane lipid content, is mainly metabolized by three kinds of enzymes: cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP450) enzymes. Based on these three metabolic pathways, AA could be converted into various metabolites that trigger different inflammatory responses. In the kidney, prostaglandins (PG), thromboxane (Tx), leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs) are the major metabolites generated from AA. An increased level of prostaglandins (PGs), TxA2 and leukotriene B4 (LTB4) results in inflammatory damage to the kidney. Moreover, the LTB4-leukotriene B4 receptor 1 (BLT1) axis participates in the acute kidney injury via mediating the recruitment of renal neutrophils. In addition, AA can regulate renal ion transport through 19-hydroxystilbenetetraenoic acid (19-HETE) and 20-HETE, both of which are produced by cytochrome P450 monooxygenase. Epoxyeicosatrienoic acids (EETs) generated by the CYP450 enzyme also plays a paramount role in the kidney damage during the inflammation process. For example, 14 and 15-EET mitigated ischemia/reperfusion-caused renal tubular epithelial cell damage. Many drug candidates that target the AA metabolism pathways are being developed to treat kidney inflammation. These observations support an extraordinary interest in a wide range of studies on drug interventions aiming to control AA metabolism and kidney inflammation.

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Captopril effect on prostaglandin E2, thromboxane B2 and proteinuria in lupus nephritis patients

Cited by 13 publications

References 33 publications

Urine Proteome Scans Uncover Total Urinary Protease, Prostaglandin D Synthase, Serum Amyloid P, and Superoxide Dismutase as Potential Markers of Lupus Nephritis

Urine Proteome Scans Uncover Total Urinary Protease, Prostaglandin D Synthase, Serum Amyloid P, and Superoxide Dismutase as Potential Markers of Lupus Nephritis

Angiotensin-converting enzyme inhibitors delay the occurrence of renal involvement and are associated with a decreased risk of disease activity in patients with systemic lupus erythematosus--results from LUMINA (LIX): a multiethnic US cohort

Arachidonic Acid Metabolism and Kidney Inflammation

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