Acute kidney injury secondary to thrombotic microangiopathy associated with idiopathic hypereosinophilic syndrome: a case report and review of the literature

Abstract

Background Renal involvement in idiopathic hypereosinophilic syndrome is uncommon. The mechanism of kidney damage can be explained as occurring via two distinct pathways: (1) thromboembolic ischemic changes secondary to endocardial disruption mediated by eosinophilic cytotoxicity to the myocardium and (2) direct eosinophilic cytotoxic effect to the kidney. Case presentation We present a case of a 63-year-old Caucasian man who presented to our hospital with 2 weeks of progressively generalized weakness. He was diagnosed with idiopathic hypereosinophilic syndrome with multiorgan involvement and acute kidney injury with biopsy-proven thrombotic microangiopathy. Full remission was achieved after 8 weeks of corticosteroid therapy. Conclusion Further studies are needed to investigate if age and absence of frank thrombocytopenia can serve as a prognostic feature of idiopathic hypereosinophilic syndrome, as seen in this case.

An Unusual Case of Immune Complex-Mediated Membranoproliferative Glomerulonephritis as Renal Manifestation of Idiopathic Hypereosinophilic Syndrome: A Case Report and Literature Review

“…Our patient presented general malaise, a fever, edema, fatigue, hyporexia, and a cough, coinciding with some other reported cases. Our patient did not present cardiac involvement, despite the heart being a frequently affected organ, as described in the minireview by Shehwaro et al [7] and in the case report by Curras-Martin et al [26]. Laboratory results showed anemia, also present in the report by Curras-Martin et al [26] and in almost half of the patients described by Dong et al [6].…”

“…Our patient did not present cardiac involvement, despite the heart being a frequently affected organ, as described in the minireview by Shehwaro et al [7] and in the case report by Curras-Martin et al [26]. Laboratory results showed anemia, also present in the report by Curras-Martin et al [26] and in almost half of the patients described by Dong et al [6]. In the reports of Ni H-F et al [25] and Curras-Martin et al [26], and in our case as well, there was a predominance of IgE, with it not being the same as the rest of the immunoglobulins.…”

Complement Factor I Gene Variant in an Atypical Hemolytic Uremic Syndrome Triggered by Hypereosinophilia Syndrome

“…Three cases of HES followed by renal TMA might be aHUS, especially since one case had low C3 [12]. However, genetic studies were not performed, so a definite diagnosis of aHUS cannot be made [2, 12]. Our patient had the fulfilled diagnostic criteria of HES (hypereosinophilia, urticaria, and facial angioedema) followed by the classic syndrome of aHUS.…”

“…However, there have been a few reports of the association; for example, aHUS with a coincidental finding of eosinophilia (but not HES), aHUS with Churg Strauss syndrome (eosinophilic granulomatosis with polyangiitis), HES followed by renal TMA (but not aHUS), and HES followed by thrombotic thrombocytopenic purpura [2,[9][10][11][12]. Three cases of HES followed by renal TMA might be aHUS, especially since one case had low C3 [12]. However, genetic studies were not performed, so a definite diagnosis of aHUS cannot be made [2,12].…”

Association of peripheral eosinophil count with chronic kidney disease progression risk: a retrospective cohort study

“…Makiya et al [28] observed a correlation between the eosinophilic granulocyte count and CD69 and granule protein concentration. Activated eosinophilic granulocytes lead to thrombotic microangiopathy [29]. Therefore, the eosinophilic granulocyte count may affect the severity of in ammation.…”