Comment on: Kidney disease in primary antiphospholipid antibody syndrome

Comment on: Kidney disease in primary antiphospholipid antibody syndrome Letters to the Editor Rheumatology 2018;57:403 to evidence of inflammatory-mediated tissue damage in doi:10.1093/rheumatology/kex401 APS, suggest that therapy should also be directed to- Advance Access publication 6 November 2017 wards preventing inflammation. At this point, we can speculate that steroids or immunosuppressives asso- Comment on: Kidney disease in primary ciated with anticoagulation or antiplatelet agents and antiphospholipid antibody syndrome ACE inhibitors might well contribute to preventing the pro- gression of renal involvement secondary to APS. SIR, we read with great interest the article by Gracia-Tello et al. [1]. The authors summarized potential mechanisms Funding: No specific funding was received from any involved in the pathogenesis of thrombosis in primary APS bodies in the public, commercial or not-for-profit sectors and provided information on new treatment modalities for to carry out the work described in this manuscript. APS. The authors especially focused on acute and chronic glomerular changes in APS. However, in primary APS, Disclosure statement: The authors have declared no tubulo-interstitial structures may be another affected conflicts of interest. part of kidney [2]. It has been reported that tubulo-inter- 1 1 stitial inflammation is frequently seen in primary APS pa- ¨ Cengiz Korkmaz and Dondu¨ U. Cansu tients. When taking into consideration the fact that 1 Department of Internal Medicine, Division of Rheumatology, interstitial involvement is of great importance in renal Eskis¸ehir Osmangazi University, Eskis¸ehir, Turkey prognosis, an attempt to prevent this might contribute Accepted 28 September 2017 positively to the prognosis of the disease [3]. Therefore Correspondence to: Cengiz Korkmaz, Department of Internal Medicine, Division of Rheumatology, Eskis¸ ehir Osmangazi the authors should have emphasized the inflammatory University, Eskis¸ ehir, Turkey. and fibrotic changes in the tubulo-interstitial structures E-mail: ckorkmaz@ogu.edu.tr seen in the course of APS and they should have also men- tioned how we approach these kinds of APS patients. References We do not exactly know why interstitium is involved in primary APS. It is possible that this interstitial cell prolif- 1 Gracia-Tello B, Isenberg D. Kidney disease in primary anti- eration could either be a reaction to the glomerular capil- phospholipid antibody syndrome. Rheumatology lary wall remodelling in the process of primary APS 2017;56:106980. nephropathy or due to inflammatory mediators. Recent 2 Korkmaz C, Kabukcuoglu S, Isiksoy S, Yalc ¸ in AU. Renal reports have shown that primary APS may have an involvement in primary antiphospholipid syndrome and its immuno-inflammatory aspect. It has been reported that response to treatment with immunosuppressive therapy. LA and/or aCL results in endothelial cell activation, in- Lupus 2003;12:7605. crease in some cytokines levels, complement system ac- 3 Remuzzi G, Bertani T. Pathophysiology of progressive tivation associated with hypocomplementaemia and nephropathies. N Engl J Med 1998;339:144856. increase in monocyte chemoattractant protein-1 levels 4 Mikawa K, Ikegaki J, Maekawa N et al. Perioperative effect [4, 5], which accounts for inflammation and fibrosis of of methylprednisolone given during lung surgery on renal interstitium. Aspirin and anticoagulants do not deal plasma concentration of C3a and C5a. Scand J Thorac with these inflammatory mediators. Targeted therapy for Cardivasc Surg 1990;24:22933. primary APS is in progress but there may be a long way to 5 Cho C-S, Cho M-L, Chen PP et al. Antiphospholipid anti- go into use. At this point, we should benefit from accumu- bodies induce monocyte chemoattractant protein-1 in lated experience regarding use of steroids and immuno- endothelial cells. J Immunol 2002;168:420915. suppressives in primary APS. It has been reported that 6 Cacoub P, Wechsler B, Piette JC et al. Malignant htper- steroids might play a role in the inhibition of C5a produc- tension in antiphospholipid syndrome without lupus tion or basal and aCL-induced monocyte chemoattractant nephritis. Clin Exp Rheumatol 1993;11:47985. protein-1 production and cytokines [4]. We and other au- 7 Sokunbi DO, Miller F, Wadhwa NK, Nord EP. Reversible thors [2, 6, 7] reported the beneficial effect of steroid and renal failure in primary antiphospholipid syndrome: a immunosuppressives in the treatment of APS-related report of two cases. J Am Soc Nephrol 1993;4:2835. nephropathy and hypertension. These studies, in addition ! The Author 2017. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oup.com Downloaded from https://academic.oup.com/rheumatology/article-abstract/57/2/403/4596654 by Ed 'DeepDyve' Gillespie user on 22 March 2018 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Rheumatology Oxford University Press

Comment on: Kidney disease in primary antiphospholipid antibody syndrome

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© The Author 2017. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oup.com
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1462-0324
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10.1093/rheumatology/kex401
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Abstract

Letters to the Editor Rheumatology 2018;57:403 to evidence of inflammatory-mediated tissue damage in doi:10.1093/rheumatology/kex401 APS, suggest that therapy should also be directed to- Advance Access publication 6 November 2017 wards preventing inflammation. At this point, we can speculate that steroids or immunosuppressives asso- Comment on: Kidney disease in primary ciated with anticoagulation or antiplatelet agents and antiphospholipid antibody syndrome ACE inhibitors might well contribute to preventing the pro- gression of renal involvement secondary to APS. SIR, we read with great interest the article by Gracia-Tello et al. [1]. The authors summarized potential mechanisms Funding: No specific funding was received from any involved in the pathogenesis of thrombosis in primary APS bodies in the public, commercial or not-for-profit sectors and provided information on new treatment modalities for to carry out the work described in this manuscript. APS. The authors especially focused on acute and chronic glomerular changes in APS. However, in primary APS, Disclosure statement: The authors have declared no tubulo-interstitial structures may be another affected conflicts of interest. part of kidney [2]. It has been reported that tubulo-inter- 1 1 stitial inflammation is frequently seen in primary APS pa- ¨ Cengiz Korkmaz and Dondu¨ U. Cansu tients. When taking into consideration the fact that 1 Department of Internal Medicine, Division of Rheumatology, interstitial involvement is of great importance in renal Eskis¸ehir Osmangazi University, Eskis¸ehir, Turkey prognosis, an attempt to prevent this might contribute Accepted 28 September 2017 positively to the prognosis of the disease [3]. Therefore Correspondence to: Cengiz Korkmaz, Department of Internal Medicine, Division of Rheumatology, Eskis¸ ehir Osmangazi the authors should have emphasized the inflammatory University, Eskis¸ ehir, Turkey. and fibrotic changes in the tubulo-interstitial structures E-mail: ckorkmaz@ogu.edu.tr seen in the course of APS and they should have also men- tioned how we approach these kinds of APS patients. References We do not exactly know why interstitium is involved in primary APS. It is possible that this interstitial cell prolif- 1 Gracia-Tello B, Isenberg D. Kidney disease in primary anti- eration could either be a reaction to the glomerular capil- phospholipid antibody syndrome. Rheumatology lary wall remodelling in the process of primary APS 2017;56:106980. nephropathy or due to inflammatory mediators. Recent 2 Korkmaz C, Kabukcuoglu S, Isiksoy S, Yalc ¸ in AU. Renal reports have shown that primary APS may have an involvement in primary antiphospholipid syndrome and its immuno-inflammatory aspect. It has been reported that response to treatment with immunosuppressive therapy. LA and/or aCL results in endothelial cell activation, in- Lupus 2003;12:7605. crease in some cytokines levels, complement system ac- 3 Remuzzi G, Bertani T. Pathophysiology of progressive tivation associated with hypocomplementaemia and nephropathies. N Engl J Med 1998;339:144856. increase in monocyte chemoattractant protein-1 levels 4 Mikawa K, Ikegaki J, Maekawa N et al. Perioperative effect [4, 5], which accounts for inflammation and fibrosis of of methylprednisolone given during lung surgery on renal interstitium. Aspirin and anticoagulants do not deal plasma concentration of C3a and C5a. Scand J Thorac with these inflammatory mediators. Targeted therapy for Cardivasc Surg 1990;24:22933. primary APS is in progress but there may be a long way to 5 Cho C-S, Cho M-L, Chen PP et al. Antiphospholipid anti- go into use. At this point, we should benefit from accumu- bodies induce monocyte chemoattractant protein-1 in lated experience regarding use of steroids and immuno- endothelial cells. J Immunol 2002;168:420915. suppressives in primary APS. It has been reported that 6 Cacoub P, Wechsler B, Piette JC et al. Malignant htper- steroids might play a role in the inhibition of C5a produc- tension in antiphospholipid syndrome without lupus tion or basal and aCL-induced monocyte chemoattractant nephritis. Clin Exp Rheumatol 1993;11:47985. protein-1 production and cytokines [4]. We and other au- 7 Sokunbi DO, Miller F, Wadhwa NK, Nord EP. Reversible thors [2, 6, 7] reported the beneficial effect of steroid and renal failure in primary antiphospholipid syndrome: a immunosuppressives in the treatment of APS-related report of two cases. J Am Soc Nephrol 1993;4:2835. nephropathy and hypertension. These studies, in addition ! The Author 2017. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oup.com Downloaded from https://academic.oup.com/rheumatology/article-abstract/57/2/403/4596654 by Ed 'DeepDyve' Gillespie user on 22 March 2018

Journal

RheumatologyOxford University Press

Published: Feb 1, 2018

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