Renal Involvement in Non-Hodgkin Lymphoma: Proven by Renal Biopsy

Abstract

AimsTo determine the spectrum of renal lesions in patients with kidney involvement in non-Hodgkin's lymphoma (NHL) by renal biopsy.MethodsThe clinical features and histological findings at the time of the renal biopsy were assessed for each patient.ResultsWe identified 20 patients with NHL and renal involvement, and the diagnosis of NHL was established following the kidney biopsy in 18 (90%) patients. The types of NHL include the following: chronic lymphocytic leukemia/small lymphocytic lymphoma (n = 8), diffuse large B-cell lymphoma (n = 4), T/NK cell lymphoma (n = 3), lymphoplasmacytic lymphoma (n = 2), cutaneous T-cell lymphoma (n = 1), mucosa-associated lymphoid tissue lymphoma (n = 1) and mantle cell lymphoma (n = 1). All presented with proteinuria, and 15 patients had impaired renal function. The pathological findings included (1) membranoproliferative glomerulonephritis-like pattern in seven patients; (2) crescent glomerulonephritis in four; (3) minimal-change disease in three, and glomeruli without specific pathological abnormalities in three; (4) intraglomerular large B-cell lymphoma in one; (5) intracapillary monoclonal IgM deposits in one; (6) primary diffuse large B-cell lymphoma of the kidneys in one; and (7) lymphoma infiltration of the kidney in eight patients.ConclusionA wide spectrum of renal lesions can be observed in patients with NHL, and NHL may be first proven by renal biopsies for evaluation of kidney injury or proteinuria. Renal biopsy is necessary to establish the underlying cause of renal involvement in NHL.

Exosomes released by chronic lymphocytic leukemia cells induce the transition of stromal cells into cancer-associated fibroblasts

“…The accumulation of MEC-1-eGFP cells in mice kidneys ( Figure 7E) also confirmed the renal involvement observed in CLL patients. 40,41 Our data demonstrate a protumorigenic effect of CLL-derived exosomes in vivo and their importance in the early onset of the disease when tumor cells impact the microenvironment to proliferate and promote angiogenesis, which is similar to previous studies. 19,20,42,43 In summary, our in vitro and in vivo data show that CLL exosomes harbor an oncogenic potential by stimulating stromal cells to induce an inflammatory and protumorigenic milieu, including increased angiogenesis, thus supporting the survival and outgrowth of CLL cells.…”

Clinical, laboratory, and morphological characteristics of kidney damage in lymphoproliferative disorders

“…Генез возникновения лимфоидной пролифера-ции в почечной ткани недостаточно ясен. Возможно, играют роль индуцируемые при НХЛ провоспалитель-ные молекулы, способствующие проникновению лим-фоидных клеток в воспалительный инфильтрат [12]. Диффузная лимфоидная инфильтрация интерстиция почек разрушает нормальную почечную архитектуру, вызывает интраренальную обструкцию микроцирку-ляции и канальцев, способствуя развитию склероза клубочков, атрофии канальцев, и тем самым приводит к дисфункции почек.…”

Glomerulonephritis With Masked Monotypic Immunoglobulin Deposits and Concurrent Lymphomatous Infiltration

“…It is often the presenting feature of disease. 1,7 Direct kidney infiltration has been reported in virtually all lymphomas and/or plasma cell dyscrasias and typically results in decreased kidney function. 2,5, [8][9][10] The presence of hematopoietic/inflammatory cells within the interstitium raises a broad differential diagnosis.…”

“…[1][2][3][4] In some instances, these mechanisms can occur concurrently and result in a mixed clinical picture with multiple histologic findings. 5 Recently, an unusual pattern of glomerular injury has been described in which routine immunofluorescence performed on frozen tissue shows dominant C3 staining; however, immunofluorescence performed on paraffin-embedded tissue following antigen retrieval demonstrates monotypic immunoglobulin staining.…”