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Letters to Editor
24 (
5
); 331-332

Authors’ reply

Department of Nephrology, Seth G.S. Medical College and K.E.M. Hospital, Acharya Donde Marg, Parel, Mumbai, Maharashtra, India
Address for correspondence: Dr. V. S. Keskar, Department of Nephrology, Seth G.S. Medical College and K.E.M. Hospital, Acharya Donde Marg, Parel, Mumbai - 400 012, Maharashtra, India. E-mail: vaibhavsrikeskar@gmail.com

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This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Disclaimer:
This article was originally published by Medknow Publications & Media Pvt Ltd and was migrated to Scientific Scholar after the change of Publisher.

Sir,

We thank M. D. Al-Mendalawi.[1] for their interest in our case report[2] and the insightful comments. We agree that association of malaria and hemolytic uremic syndrome-thrombotic thrombocytopenia purpura (HUS-TTP) may not be causal and only a few cases have been described hitherto. However, ADAMTS13 activity and antigen levels have been reported to be reduced in patients with falciparum as well as vivax malaria.[3] This evidence of endothelial injury in malarial infections is intriguing and needs to be explored. Furthermore, given the vivax malaria increasingly being reported as a cause of severe malaria,[4] it will be interesting to study what proportion of them have HUS-TTP.

Thrombotic microangiopathy is a histologic description that is characteristic of several diverse disorders, such as malignant hypertension and scleroderma, as well as TTP and HUS.[56] When the patients with microangiopathic hemolytic anemia and thrombocytopenia are initially evaluated, the comprehensive term TTP-HUS can probably be the best one to describe the clinical entity seen in our patient.

We agree that a complete evaluation including assessment of ADAMTS13 activity and genetic and autoimmune tests to identify a complement-related defect is required, which could not be done in our case. In absence of such a detailed evaluation, there remains a possibility of presence of underlying complement disorder where HUS was triggered by malarial infection. Infections, including diarrhea, are known as a trigger to develop HUS in patients having complement dysregulation.[78]

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