Renal involvement in non-Hodgkin lymphoma: proven by renal biopsy

Abstract

Aims: To determine the spectrum of renal lesions in patients with kidney involvement in non-Hodgkin's lymphoma (NHL) by renal biopsy.

Methods: The clinical features and histological findings at the time of the renal biopsy were assessed for each patient.

Results: We 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.

Conclusion: A 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.

Figure 1. Representative renal histological change in patients with NHL.

A Light microscopy showed increased cellularity in glomeruli and the accentuation of the lobular architecture (patient 9 PAS×400). B Immunofluorescence showed granular staining in a lobular pattern for IgG (patient 9 IF×400). C Electron microscopy showed fine subendothelial electron-dense deposits (patient 9 EM). D Glomeruli with focal segmental necrosis and lymphoid cell infiltration around glomeruli (patient 8 Masson×400). E Glomeruli without pathological abnormalities visualized by LM with lymphocyte-like cell infiltration in the interstitial tissue (patient 5 PAS×200). F Mononuclear cell infiltration in the peritubular capillaries (patient 5 PAS×400).

Figure 2. Diffuse infiltration into the renal parenchyma and intraglomerular lymphoma in DLBCL.

A. Accumulation of large atypical lymphoid cells was observed in renal specimens (patient 13 PAS×400). B. Immunohistochemical staining showing strong staining for CD20 in the lymphoid cells (patient 13 IH×400). C. Glomerular capillary lumina containing atypical large cells in the enlarged glomeruli (patient 14 PAS ×400). D Immunohistochemistry showing strong staining for CD20 in lymphoid cells localized within the glomerular capillary lumina (patient 14 IH×400).

Figure 3. Intracapillary monoclonal deposition disease in an NHL patient (patient 12).

A PAS-positive intracapillary thrombi in glomerulus (PAS, ×200). B Immunofluorescence showed bright staining of the intraglomerular thrombi for IgM. C Immunofluorescence showed bright staining of the intraglomerular thrombi for κ LC.D Electron microscopy showed that the glomerular capillary lumen was filled with granular electron-dense material. No organized structure was observed.