A Case of Chronic Myeloid Leukemia Complicated with Minimal Change Nephrotic Syndrome

Talwar, Rashmi; Dash, Swetaleena; Kucheria, Kiran

doi:10.1159/000068492

Cited by 12 publications

(4 citation statements)

References 6 publications

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“…In addition to immune-related pathways, we found GSEA enriched in acute and chronic myeloid leukemia pathways. Similar to our results, several studies claim a direct or indirect causal relationship between leukemic pathogenesis and renal pathology; and con rm that the pathological type is MCD by biopsy [30][31][32].…”

Section: Discussionsupporting

confidence: 92%

Identification of key biomarkers and immune infiltration in Minimal Change Disease: Novel Insights from bioinformatics analysis

Tang

Yang

et al. 2022

Preprint

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Background Minimal change disease (MCD) is not a simple immune disease, and its pathogenesis has not been elucidated because of its complexity in terms of the glomerular microenvironment and genetic susceptibility. Hence the therapeutic approach is equally imprecise. Methods We downloaded GSE108109 from the Gene Expression Omnibus (GEO) database for bioinformatic analyses. Genome-wide expression analysis (GSEA) and functional enrichment analysis of differentially expressed genes (DEGs) were performed. Single sample gene set enrichment analysis (ssGSEA) was applied to assess the level of immune infiltration patterns of diseases. Protein-Protein Interaction (PPI) network was constructed to identify hub genes. Hub genes were intersected with immune-related genes downloaded from the Immunology Database and Analysis Portal (ImmPort) to obtain key genes. In addition, the expression levels of key genes were validated in the Kidney Interactive Transcriptomics webpage and Nephroseq database. Receiver operating characteristic (ROC) analysis and principal component analysis (PCA) was performed to explore the value of key genes for MCD diagnosis. Results 1029 DEGs were screened, of which 493 were up-regulated, and 536 were down-regulated. GSEA analysis revealed that DEGs were significantly enriched in three pathways, including T-cell receptor signaling pathway, natural killer cell-mediated cytotoxicity, and B-cell receptor signaling pathway. In addition, 17 of the 21 immune cell types were significantly different in MCD compared to the normal group. A total of five key genes (ISG15, IRF1, OAS1, RSAD2, BST2) were shown to play essential roles in the immune response. Among them, IRF1, OAS1, RSAD2, and BST2 were highly expressed in podocytes. Conclusions In this study, bioinformatics analysis revealed new insights into MCD: (1) Immune cell infiltration analysis provided new evidence and clues to the molecular mechanisms of MCD. (2) Key genes such as ISG15, IRF1, OAS1, RSAD2 and BST2 may contribute to the immunopathological process of MCD development.

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Section: Discussionsupporting

confidence: 92%

Identification of key biomarkers and immune infiltration in Minimal Change Disease: Novel Insights from bioinformatics analysis

Tang

Yang

et al. 2022

Preprint

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“…The abnormal cooperation of donor T cells and recipient B cells in GVHD may release cytokines, causing effacement of foot process of glomerular epithelial cells and hyperfiltration 3,8,12,31 . It should be noted that MCD is also known to be associated with non‐Hodgkin lymphoma and leukaemia, 32 including CML 33 . After HSCT, recurrent nephrotic syndrome due to MCD associated with GVHD and relapse of acute myeloid leukaemia has been reported 22 .…”

Section: Discussionmentioning

confidence: 99%

“…3,8,12,31 It should be noted that MCD is also known to be associated with non-Hodgkin lymphoma and leukaemia, 32 including CML. 33 After HSCT, recurrent nephrotic syndrome due to MCD associated with GVHD and relapse of acute myeloid leukaemia has been reported. 22 Hence, it is prudent to exclude paraneoplastic syndrome owing to disease recurrence in cases of MCD and MGN.…”

Section: Discussionmentioning

confidence: 99%

Clinicopathologic analysis of renal biopsies after haematopoietic stem cell transplantation

Chan¹,

Lam²,

Au³

et al. 2008

Nephrology

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Among the various renal lesions after HSCT, membranous glomerulonephritis and thrombotic microangiopathy were the most common. Mechanisms of renal injury varied from graft-versus-host disease-associated immune complex deposition to non-immune complex injury on endothelial cells, glomerular epithelial cells and tubular epithelium. Pathologists and clinicians should attend to the histological and temporal heterogeneity of renal injury when managing patients after HSCT.

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“…Renal involvement with peripheral eosinophilia can occur in a number of conditions like drugs [16], myeloproliferative disorders [17], parasitic manifestation [18], cholesterol embolization [19] or necrotizing vasculitis. No such cause was obvious from history and investigations in our case.…”

Section: Discussionmentioning

confidence: 99%

Idiopathic Hypereosinophilic Syndrome Presenting as IgA Nephropathy with Nephrotic Range Proteinuria

Shah¹,

Koul²,

Shah³

et al. 2013

OJNeph

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Idiopathic hypereosinophilic syndrome (IHES) is a disorder characterized by increased eosinophil count (eosinophilia) along with organ dysfunction secondary to organ infiltration of eosinophils and release of inflammatory markers [1][2][3][4], with no obvious cause for eosinophilia. The onset of symptoms is insidious in most of the cases and eosinophilia is detected incidentally. However, in others, the initial manifestations are severe and life-threatening due to the rapid evolution of cardiac or neurologic complications [5]. Renal involvement is rarely reported [6] in IHES. Herein we reported a case of IHES with predominant renal involvement as nephrotic syndrome with focal necrotizing IgA nephropathy.Keywords: Idiopathic Hypereosinophilic Syndrome; Eosinophilia; Renal Involvement; Nephrotic Syndrome Case ReportA 50-year old male presented with a 3-week history of a non-productive cough, associated with intermittent low grade fever, periorbital puffiness and lower extremity edema. Patient denied any history of breathlessness, chest-pain, hemoptysis, orthopnea, paroxysmal nocturnal dyspnea, drop in urine output, skin rash or arthritis. His past history was insignificant and he denied any history of drug intake.Hisexamination revealed mild pallor, with periorbitalpuffiness, lower extremity pitting edema and mild splenomegaly. He had hemoglobin of 11 g/dL with a total leucocyte count of 9.2 × 10 9 /cumm and an ESR of 23 mmhr. His differential count included 46% polymorphs 11% lymphocytes and 41% eosinophils with AEC count of 3800 which repeatedly was high and ranged from 3800 to 5500. A peripheral blood film showed features of normochromic normocytic anaemia with no abnormal cells. His serum creatinine was 1.7 mg/dL with a creatinine clearance of 44 ml/min. Liver functions showed hypoporoteinemia with hypoalbuminemia. He had an active urinary sedimentand urine which showed presence of eosinophils on wright's staining. 24 hours urinary protein was 5.04 g/24hours which was reproduced twice. Repeated stool examination for the presence of ova/parasite was negative.Radiograph of the chest was normal. High resolution computerized tomography of the chest did not reveal any abnormality. His electrocardiograph and echocardiography were normal. Ultrasonography of abdomen was normal as well.Patient was investigated further to look for eosinophilic infiltration of other organ systems in view of persistant hypereosinophilia.Patient was subjected to bronchoscopy to obtain bronchoalveolar lavage for eosinophils which revealed 62% eosinophils. Bone marrow aspiration and biopsy revealed 56% eosinophils with no dysplasia and blasts. p-ANCA andc-ANCA were within normal limits. Serum tryptase levels were within normal limits.Patient was subjected to percutaneous renal biopsy to look for the etiology of nephrotic range proteinuria. Renal biopsy revealed, marked interstitial edema and patchy inflammation including aggregates of eosinophils admixed with mononuclear cells and occasional neutrophils. An eosinophilic infiltrate wa...

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A Case of Chronic Myeloid Leukemia Complicated with Minimal Change Nephrotic Syndrome

Cited by 12 publications

References 6 publications

Identification of key biomarkers and immune infiltration in Minimal Change Disease: Novel Insights from bioinformatics analysis

Identification of key biomarkers and immune infiltration in Minimal Change Disease: Novel Insights from bioinformatics analysis

Clinicopathologic analysis of renal biopsies after haematopoietic stem cell transplantation

Idiopathic Hypereosinophilic Syndrome Presenting as IgA Nephropathy with Nephrotic Range Proteinuria

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