A 75-year-old man with stage IV CKD on a background of previously poorly controlled type 2 diabetes mellitus (T2DM) was reviewed in his routine renal outpatient appointment. His renal function had been slowly worsening for the past 2 years; however, on this occasion a marked increase in creatinine and proteinuria was noted despite excellent blood glucose control during the preceding 6 months, with an average glycated haemoglobin (HbA1c) of 5% ().\nApart from the T2DM complicated by neuropathy and nephropathy, his past medical history also included hypertension.\nHe was compliant with all of his medications with no significant recent medication changes and his regular medications included gliclazide, moxonidine, telmisartan/amlodipine, oral iron sulfate and vadadustat (an oral prolyl hydroxylase inhibitor).\nHe was an ex-smoker having smoked during his teenage years and he consumed less than 3 units of alcohol/week.\nThere was no family history of renal disease or haematological malignancies.\nExamination revealed moderate lymphadenopathy in the left cervical region. There was no other peripheral lymphadenopathy and no hepatosplenomegaly. The remainder of the examination was normal.\nPlans for renal replacement therapy were made, including commencement of work-up to determine suitability for renal transplantation and to investigate the lymphadenopathy. A subsequent CT of his abdomen revealed extensive lymphadenopathy. Due to progressive fluid overload and worsening biochemical parameters, he was commenced on haemodialysis.
A 19-year-old male patient was admitted to the Nephrology Department of Ankara University Faculty of Medicine due to painless hematuria, bilateral renal masses, and acute kidney injury for further investigations. He was first evaluated at another center for hematuria. There was one episode of hematuria, which had subsided spontaneously. Abdominal ultrasonography had revealed bilateral diffuse renal masses and the patient was referred to our center for further examination.\nOn admission, there was no history of fever, weight loss, night ssweats and any other health problem. The patient’s physical examination findings were unremarkable. In particular, there was no peripheral lymphadenopathy or hepatosplenomegaly. Also the kidneys were not palpable. Laboratory tests revealed white blood cell count of 7.7x109/L, hemoglobin of 11.6 g/dL, platelet count of 315x109/L, serum blood urea nitrogen of 17 mg/dL, serum creatinine of 1.5 mg/dL (normal range: 0.5-0.9), serum uric acid of 7.6 mg/dL (normal range: 2.4-5.7), serum lactate dehydrogenase of 1042 U/L (normal range: 125-220), and serum ferritin of 749 ng/mL (normal range: 11-307). Erythrocyte sedimentation rate was 52 mm/h and C-reactive protein level was 27.5 mg/L (normal: <3). Urinalysis showed density of 1010, pH of 5.5, protein of 15 mg/dL, and glucose negative, and urine microscopy showed 4 leukocytes and 3 erythrocytes per high-power field. Viral serology tests were negative. C3 and C4 as well as quantitative immunoglobulin levels were all within normal limits with negative antinuclear antibody and anti-neutrophil cytoplasmic antibody tests. Urinary ultrasonography demonstrated bilaterally enlarged kidneys without obstruction (right: 16x8 cm, left: 15.5x8 cm) and numerous solid hypoechoic nodular cortical masses in both kidneys (largest of 6.5x5.5 cm in size, numerous variably sized masses) with perirenal and paraaortic multiple enlarged lymph nodes (largest <2.5 cm in size).\nContrast-enhanced computerized tomography (CT) scanning of the abdomen confirmed bilaterally enlarged kidneys, bilateral variably sized multiple hypodense renal masses, and paraaortic, paracaval multiple enlarged lymph nodes (). In addition, the liver was slightly enlarged with normal parenchyma while the size of the spleen and parenchyma was normal.\nThereafter, 18F-fluorodeoxyglucose positron emission tomography-computed tomography (18F-FDG PET-CT) was performed for staging and its role in the differential diagnosis. It was performed to examine the entire body, revealing an abnormal accumulation in the thyroid gland, anterior mediastinum, bilateral hilar, right parasternal lymph node, left subdiaphragmatic lymph node, bilateral renal cortices, and multiple abdominal paraaortic, paracaval, and aortocaval lymph nodes ( and ).\nA percutaneous tru-cut biopsy of the kidney was performed and histopathological examination showed extensive infiltration of the renal parenchyma by atypical lymphoid cells ( and ). Immunohistochemical studies demonstrated positive staining of the neoplastic cells for CD20, CD10, bcl-6 (, , , and ) and negative results for MUM1 () and Bcl-2. The ki-67 proliferation index of neoplastic cells was 80% (). EBER in situ hybridization was negative. A diagnosis of diffuse large B-cell non-Hodgkin lymphoma (NHL) was made. To exclude lymphoma involvement of the bone marrow, the patient underwent bone marrow biopsy and there was not bone marrow infiltration.\nSubsequently, the patient was transferred to the department of hematology for treatment and chemotherapy regimen as well; cyclophosphamide, adriamycin, vincristine, prednisolone, and rituximab (CHOP+R) were started. After a cycle of chemotherapy, the patient’s renal functions returned to normal.