P0320KIDNEY DAMAGE IN THE NON-HODGKIN LYMPHOMA/LEUKEMIA AND HODGKIN'S LYMPHOMA - CLINICAL AND PATHOLOGY SPECTRUM IN THE REAL PRACTICE

Abstract

Abstract Background and Aims Kidney damage in non-Hodgkin lymphoma/leukemia (NHL/CLL) and in Hodgkin’s lymphoma (HL) are caused by several mechanisms: tumor mass localization, clonal cell expansion, hormones, cytokines and growth factors secretion, metabolic, electrolyte and coagulation disturbances, infectious, drug-induced and radiation complications etc., which can affect urinary tract, renal arteries and veins and all renal parenchyma compartments. Clinical presentation of kidney involvement in the patients with NHL/CLL and HL include both acute kidney injury (AKI) and chronic kidney disease (CKD), the latter - with or without nephrotic syndrome (NS). Pre-renal AKI, tumor-lysis syndrome (TLS), or urinary tract compression by lymph nodes usually diagnosed on the clinical basis, but one cannot differentiate other conditions, particularly NS, in the clinical setting. Importantly, symptoms of kidney damage may dominate or even preclude overt NHL/CLL or HL, and only pathology data give the clue to the main diagnosis. Kidney biopsy or post-mortem pathology findings include various patterns of paraneoplastic glomerulonephritis (GN) as well as amyloidosis; as also as tubulointerstitial damages, mainly specific lymphoid interstitial infiltration and sometimes pyelonephritis Method In this retrospective study from a single nephrology centre, we retrieved charts of the patients with NHL/CLL and HL. Collected data were age, gender, main diagnosis, diagnosis of AKI or CKD, CKD stage, NS presence, the cause of AKI and CKD based on the clinical presentation, and pathology pattern, if available. Results Study group included 57 patients, 36 males and 21 females, median age 48 [18; 80] years. Kidney biopsy was performed in 22 (39%) of cases. Main clinical data and pathology shown in the Figure. Patients with B-cell NHL/HLL comprised almost ¾ of the study group, with AKI and CKD in a roughly equal proportion. Pathology showed specific infiltration in about ¼ of AKI and in a few CKD cases, and various paraneoplastic GN in every fifth case - minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous nephropathy (MN), membranoproliferative GN (MPGN), and IgA-nephropathy (IgAN); two cases of AA amyloidosis, and one case of tubulointerstitial nephritis. There were only three patients with T-cell NCL/CLL, pathology findings were MCD in one case and lymphoid infiltration in another. Four out of 13 cases of HL demonstrated paraneoplastic GN – MCD, FSGS and IgAN, with just one case of AA amyloidosis. Totally 17 cases of AKI - pre-renal and caused by TLS or urinary tract compression by lymph nodes diagnosed on the clinical basis. Interestingly, in five cases we found a combination of various clinical settings and pathology patterns – compression with lymph nodes and TLS or acute pyelonephritis, AA amyloidosis and lymphoid infiltration or acute pyelonephritis, and finally IgAN and lymphoid infiltration. In 14 (24.5%) of the study group, the cause pf CKD remained unknown, as kidney biopsy was not performed due to severe anaemia and/or thrombocytopenia. Conclusion It is impossible to decipher many of AKI and most of CKD causes in the patients with NCL/CLL and HL without pathology evaluation. Nephrologist must perform kidney biopsy in all patients with NCL/CLL of HL CKD, and those with AKI of unknown origin, unless contraindicated, especially if the hematological diagnosis is uncertain.