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LETTERS TO THE EDITORTurk J Hematol 2021;38:155-174Figure 1. Lymph node biopsy: (a) markedly hyperplastic follicles with reactive germinal centers, (b) well-defined peripheral mantle zone,and (c) intense diffuse eosinophilia with formation of eosinophilic microabscesses. Paracortical plasma cells were also present. IgG4 wasincreased with a value of 0.8%, which was below the 40% threshold for IgG4-related disease.the steroid was tapered slowly. Abdominal CT performed inthe fourth month showed significant decrease in the numberand size of lymph nodes. Steroid treatment was discontinuedat the seventh month. To date, the patient has no symptomsand is being followed recurrence-free.There are many reports of renal involvement in Kimura disease.A review of 175 patients with Kimura disease found renalinvolvement in 12% [3]. Renal biopsies of patients with renalinvolvement of Kimura disease showed mesangioproliferativeglomerulonephritis, minimal change disease, focalsegmental glomerulosclerosis, membranous nephropathy,membranoproliferative glomerulonephritis, and acute tubularnecrosis [4]. The treatment, however, remains unclear. Whileexcision is considered adequate in patients without renalinvolvement, systemic steroids are recommended in patientswho have renal involvement or relapse after excision [5].Here, we have presented a patient who was diagnosed withminimal change disease and Kimura disease and respondedto steroid treatment. Kimura disease should be considered inpatients investigated for lymphadenopathies in the presence ofelevated serum IgE levels and renal disease.Keywords: Kimura disease, Lymphadenopathy, Eosinophilia,Minimal change diseaseAnahtar Sözcükler: Kimura hastalığı, Lenfadenopati, Eozinofili,Minimal değişiklik hastalığıAuthorship ContributionsSurgical and Medical Practices: R.E., E.C., G.K.; Concept: E.E.D.;Design: R.E., İ.M.; Data Collection or Processing: E.C., E.E.D.;Analysis or Interpretation: R.E., İ.M.; Literature Search: R.E., G.K.;Writing: R.E., G.K.Conflict of Interest: No conflict of interest was declared by theauthors.Financial Disclosure: The authors declared that this studyreceived no financial support.References1. Kumar V, Mittal N, Huang Y, Balderracchi J, Zheng HX, Li Z, Xu Y. A case seriesof Kimura’s disease: a diagnostic challenge. Ther Adv Hematol 2018;9:207-211.2. Yu B, Xu G, Liu X, Yin W, Chen H, Sun B. Kimura’s disease affecting multiplebody parts in a 57-year-old female patient: a case report. Allergy AsthmaClin Immunol 2019;15:84.3. Yamada A, Mitsuhashi K, Miyakawa Y, Kosaka K, Takehara K, Iijima M, TanakaK, Shibata S. Membranous glomerulonephritis associated with eosinophiliclymphfolliculosis of the skin (Kimura’s disease): report of a case and reviewof the literature. Clin Nephrol 1982;18:211-215.4. Chen Y, Wang J, Xu F, Zeng C, Liu Z. Clinicopathological features andprognosis of Kimura’s disease with renal involvement in Chinese patients.Clin Nephrol 2016;85:332-339.5. Su S, Chen X, Li J, Yu J, Zhang L. Kimura’s disease with membranoproliferativeglomerulonephritis: a case report with literature review. Ren Fail2019;41:126-130.EthicsInformed Consent: The patient provided informed consent forthis publication.©Copyright 2021 by Turkish Society of HematologyTurkish Journal of Hematology, Published by Galenos Publishing HouseAddress for Correspondence/Yazışma Adresi: Rafet Eren, M.D., University of Health Sciences Turkey, Prof.Dr. Cemil Taşcıoğlu City Hospital, Department of Hematology, İstanbul, TurkeyPhone : +90 531 996 18 42E-mail : drrafeteren@gmail.com ORCID: orcid.org/0000-0003-0973-6279Received/Geliş tarihi: August 14, 2020Accepted/Kabul tarihi: September 29, 2020DOI: 10.4274/tjh.galenos.2020.2020.0477166
Turk J Hematol 2021;38:155-174LETTERS TO THE EDITORAcute Kidney Injury Due to Leukemic Infiltration in a Patient withChronic Lymphocytic LeukemiaKronik Lenfositik Lösemide Lösemik İnfiltrasyona Bağlı Akut Böbrek YetmezliğiGizem Kumru Şahin 1 , Hasan Emre Kocabay 2 , Saba Kiremitçi 3 , Osman İlhan 4 , Kenan Keven 11Ankara University Faculty of Medicine, Department of Nephrology, Ankara, Turkey2Ankara University Faculty of Medicine, Department of Internal Medicine, Ankara, Turkey3Ankara University Faculty of Medicine, Department of Medical Pathology, Ankara, Turkey4Ankara University Faculty of Medicine, Department of Hematology, Ankara, TurkeyTo the Editor,The kidneys are among the organs most affected by leukemicinvolvement in chronic lymphocytic leukemia (CLL) patients inpostmortem autopsy series (63%-90%) [1,2]. However, leukemicinfiltration (LI) of the kidneys has been a rare cause of renalimpairment in CLL patients [3,4]. Here we describe a case of CLLpresenting with severe acute kidney injury (AKI) due to LI.A 72-year-old white male without any renal disease presentedwith general malaise and weight loss. He had been diagnosedwith stage B(1) B-CLL four years before and was treated witha bendamustine and rituximab protocol. Physical examinationrevealed general lymphadenopathy and hepatomegaly.Complete blood count findings were as follows: hemoglobin,11.3 g/dL; leukocytes, 411.4x10 9 /L (lymphocytes: 60%); platelets,247x10 9 /L. The blood film appearances were suggestive of CLL.The following biochemical tests were abnormal: blood ureanitrogen, 44 mg/dL (normal: 8-22); serum creatinine (sCr),6.16 mg/dL (normal: 0.7-1.3); CKD-EPI estimated-glomerularfiltration rate, 8 mL/min/1.73 m 2 (normal: >60). His urine hadno leukocytes or casts, with 3 erythrocytes/field and proteinuriain the non-nephrotic range (1779 mg/24 h). Serological testsfor hepatitis B, hepatitis C, HIV, and autoimmune kidneydisorders were negative. Serum-free light chain (sFLC) kappawas 317.5 mg/dL (normal: 3.3-19.4) and sFLC lambda was22.2 mg/dL (normal: 5.71-26.3), but no monoclonal bandsin serum or urine immunofixation were detected. Renalultrasound showed normal-sized kidneys with no evidenceof obstructive nephropathy. A renal biopsy was performed,which demonstrated heavy infiltration of diffuse monomorphicneoplastic lymphocytes in the interstitium (Figure 1A). Six of21 glomeruli were globally sclerotic and acute tubular necrosisand disruption were seen. Immunohistochemistry revealed thatthese infiltrative cells were positive for CD20 and CD5 (Figures1B and 1C) without any amyloid or light chain deposition.The clinical picture was consistent with AKI due to LI of thekidneys. Therapeutic leukapheresis and treatment with highdosemethylprednisolone and rituximab were administered.His renal functions were restored with no need to performhemodialysis and complete response in CLL was achieved(leukocytes: 10.3x10 9 /L). After a year of follow-up, his renalfunction had improved to sCr of 2.04 mg/dL, and a completeblood count revealed hemoglobin of 14.7 g/dL, leukocytes of9.15x10 9 /L, and platelets of 294x10 9 /L.Besides LI, renal impairment in CLL patients can be associatedwith prerenal azotemia, thrombotic microangiopathy,acute tubular necrosis, acute interstitial nephritis, uric acidnephropathy, light chain nephropathy, amyloidosis, obstructivenephropathy, glomerulonephritis, and cryoglobulinemia [5]. LI ofthe kidneys is common in CLL, but it is unlikely to be associatedwith severe AKI [4]. Although the mechanism of this clinicalpresentation is unclear, it was suggested that the compression ofthe tubular lumen and microvasculature by CLL cells may causeintrarenal obstruction and ischemia [6]. No clear associationwas demonstrated between CLL stage, intensity of interstitialinfiltration, and severity of renal impairment [7]. Relapsed orrefractory CLL and presentation with AKI are supportive for LIFigure 1. (A) Diffuse monomorphic neoplastic lymphocyticinfiltrate in the renal tissue (H&E, 200 x ). (B) Lymphocytic infiltrationshowing immunopositivity for CD20 (immunohistochemistry,300 x ). (C) Lymphocytic infiltration showing immunopositivity forCD5 (immunohistochemistry, 300 x ).167
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