Acute Renal Failure Due to a Primary Renal B-Cell Lymphoma

Clinical History 

A 77-year-old retired physician with a serum creatinine level of 1.0 mg/dL (88.4 μmol/L) underwent lumbosacral surgery at another institution. Three months after surgery, he was noted to have anorexia, a 20-pound weight loss, and a serum creatinine level of 4.5 mg/dL (398 μmol/L) that increased to 9.8 mg/dL (866 μmol/L) within 1 week. Ultrasonography showed his kidneys to be large (left, 13.5 cm; right, 12.5 cm) with no obstruction. The patient had no history of sicca syndrome or Sjögren disease. Because his doctors believed the anorexia and weight loss were caused by renal failure, he started dialysis therapy and then was discharged to a nursing facility. Because of continued anorexia and weakness, he was transferred to our hospital for additional examination and treatment.

Physical examination on admission showed blood pressure of 154/86 mm Hg, but otherwise normal vital signs. No lymphadenopathy or edema was identified, and no abnormality was noted on physical examination other than the healed lumbosacral scar. Admission laboratory studies showed the following values: hemoglobin, 11.6 g/dL (116 g/L); leukocytes, 7,600/μL; serum creatinine, 7.3 mg/dL (645 μmol/L); normal electrolytes with corrected serum calcium of 9.3 mg/dL (2.32 mmol/L); uric acid, 2.6 mg/dL (155 μmol/L); and potassium, 5.3 mEq/L (mmol/L). A 24-hour urine measurement showed creatinine clearance of 3 mL/min (0.05 mL/s) and 880 mg of protein. Although serum protein electrophoresis showed a slight increase in γ-globulin level at 1.8 g/dL (18 g/L), no abnormal protein level was found. Sedimentation rate was 31 mm/h with a C-reactive protein level of 8.2 mg/dL. All test results for antinuclear, anti-DNA, anti–glomerular basement membrane, and antineutrophil cytoplasmic antibodies were negative, with normal complement and angiotensin-converting enzyme levels. Percutaneous biopsy of the right kidney guided by computed tomography was performed.

Kidney Biopsy 

Light microscopic evaluation showed 2 cores of renal medulla and 2 cores of cortex with 7 glomeruli. There was moderately increased mesangial matrix with no proliferation; capillary basement membranes were unremarkable with silver stain. There was dense lymphocytic infiltration throughout the cortex (Fig 1A) and focally in the medulla, consistent with PRL. Tumor cells were large with atypical nuclear features, and numerous mitoses were noted (Fig 1B). Periodic acid-Schiff hematoxylin and trichrome stains showed tubular atrophy with no tubulitis. An immunohistochemical stain for CD20 was strongly positive in most neoplastic cells throughout the cortex and focally in the medulla (Fig 2A). Staining for CD3 showed only occasional cells with positive staining (Fig 2B).

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Figure 1. ▲Diffuse dense lymphomatous infiltration in the cortex (hematoxylin and eosin; original magnification [A] ×40; [B] ×200).

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Figure 2. Immunochemical stains for (A) CD20 and (B) CD3 (anti-CD20; original magnification ×200).

Immunofluorescence sections contained 3 glomeruli. There was diffuse 1+ mesangial staining for C3, but stains for immunoglobulin G, immunoglobulin M, immunoglobulin A, C1q, and light chains were negative. There was 2+ staining for C3 in vessels and focally in tubular basement membranes.

Ultrastructural examination confirmed marked expansion of the interstitium by tumor cells. Nuclei were irregularly shaped with dispersed chromatin and 1 or more small nucleoli. There were relatively few organelles; scattered mitochondria and rare lysosomes were noted. No intercellular junctions were identified.

Diagnosis 

The final diagnosis was poorly differentiated large B-cell lymphoma.

Clinical Follow-Up 

The patient underwent an extensive search for extrarenal lymphoma. Additional computed tomography of the chest, head, abdomen, and pelvis showed a 2-cm mass in the right kidney that was believed to be a more localized area of the lymphoma (Fig 3), with no evidence of hematoma from the biopsy. However, no lymphadenopathy or other organ involvement was identified. The diagnosis was PRL with no extrarenal involvement.

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Figure 3. Computed tomographic scan of the abdomen shows no lymphadenopathy, but a 2-cm mass (white line) in the right kidney believed to be a more localized form of the diffuse lymphomatous involvement.

The patient began treatment with cyclophosphamide (1,000 mg intravenously), vincristine (2 mg intravenously), prednisone (80 mg/d for 5 days), and rituximab (675 mg intravenously). Within 1 week, urine output improved, with a serum creatinine level of only 2.6 mg/dL (230 μmol/L) and an estimated glomerular filtration rate by means of the Modification of Diet in Renal Disease Study equation of 26 mL/min/1.73 m2 (0.43 mL/s/1.73 m2). Six months after initiation of chemotherapy, he remained free of dialysis therapy, had a serum creatinine level of 2.4 mg/dL (212 μmol/L), gained 15 pounds, and was considered to be in remission.