alexa Clinical Presentation and Pathology Spectrum of Kidney Damage in Nonhodgkin Lymphoma/Leukemia and Lymphoplasmacytic Lymphomas
ISSN: 2329-6917

Journal of Leukemia
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Research Article

Clinical Presentation and Pathology Spectrum of Kidney Damage in Nonhodgkin Lymphoma/Leukemia and Lymphoplasmacytic Lymphomas

Zakharova EV1* and Stolyarevich ES2

1Nephrology Unit, City Clinical Hospital, Moscow, Russian Federation

2Pathology, City Nephrology Centre, Moscow, Russian Federation

*Corresponding Author:
Zakharova EV
Nephrology Unit, City Clinical Hospital
Moscow, Russian Federation
Tel: +7967-134-6936
E-mail: [email protected]

Received date: December 16, 2015 Accepted date: December 28, 2015 Published date: December 30, 2015

Citation: Zakharova EV, Stolyarevich ES (2015) Clinical Presentation and Pathology Spectrum of Kidney Damage in Non-hodgkin Lymphoma/Leukemia and Lymphoplasmacytic Lymphomas. J Leuk 3:201. doi:10.4172/2329-6917.1000201

Copyright: © 2015 Zakharova EV, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Kidney damage in non-Hodgkin lymphoma/leukemia (NHL/CLL) and lymphoplasmacytic lymphomas (LPCL) are caused by several mechanisms: tumor mass localization; clonal cell expansion; hormones, cytokines and growth factors secretion; metabolic, electrolyte and coagulation disturbances; deposition of paraproteins and treatment complications. Symptoms of kidney damage may dominate and even preclude overt NHL/CLL or LPCL, and only renal pathology findings give the clue to the diagnosis. We aimed to evaluate clinical presentation and pathology of kidney damage in patients with NHL/CLL or LPCL. Using electronic database and purposely designed chart, we searched data for 158 patients with lymphoproliferative disorders (LPD) and pathology proven kidney lesions. Patients with multiple myeloma, Hodgkin’s lymphoma, Castleman disease, “primary” AL amyloidosis and “primary” light chain deposition disease were excluded from further analysis. Study group consisted of 24 patients, 14 (58.3%) male and 10 (41.7%) female, median age 67 (17;76) years. 16 patients (66.6%) were diagnosed with NHL/CLL, 7 patients (29.1%) with Waldenström’s Macroglobulinemia (WM) and 1 (4.1%) with Franklin’s disease (FD). 10 (41.7%) of patients presented with nephrotic syndrome (NS), 17 (70.8%)–with impaired kidney function, and 6 (25.2%) with both NS and renal dysfunction. By pathology glomerulonephritis (GN) was found in 11 (45.8%) of patients, in 4 cases GN pattern was associated with monoclonal paraproteins, and in 7 cases GN was considered to be paraneoplastic. Interstitial nephritis was seen in 10 (41.6%) patients, in 8 of them due to specific lymphoid infiltration; and amyloidosis complicated only 3 (12.5%) cases. Patients with NHL/CLL or LPCL, presenting with renal abnormalities, show variety of pathology patterns hardly predictable on clinical basis. Most often in our patient series was specific lymphoid interstitial infiltration and paraneoplastic glomerulonephritis with MN and MPGN patterns. In many cases of NS and/or acute kidney injury (AKI) renal biopsy was crucial for the diagnosis of NHL/CLL and LPCL.


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