A 57-year-old man was admitted to our nephrology department with complaints of pitting edema, anorexia, fatigue, and oliguria. Two years ago he had been diagnosed as squamous cell cancer of the lung and had been treated with 8 cycles of cisplatin and paclitaxel, followed by 5-day long radiation therapy. Afterwards he had stable disease and was regularly followed-up by oncology department. After completion of chemotherapy, his serum creatinine was within normal range and urinalysis was totally normal.The patient did not describe vasculitic symptoms such as arthritis, skin lesions, neuropathy, and others. He noticed decreased urinary output and macroscopic hematuria for 10 days. In physical examination there was a mild pretibial edema and blood pressure was normal, being 130/85 mmHg on admission. Blood count findings were within normal limits. On admission, marked renal dysfunction was noted with blood urea nitrogen: 53 mg/dL and serum creatinine: 4.87 mg/dL. Serum creatinine level increased gradually, up to 5.93 mg/dL and 3.4 gr per 24 hour proteinuria was also detected. Urinalysis testing revealed numerous dysmorphic red blood cells, granular and red blood cell casts. Ultrasonography showed two normal-sized kidneys and normal blood flow in renal arteries and veins. Autoantibodies, such as anti-glomerular basement membrane (GBM) antibody, perinuclear antineutrophil cytoplasmic autoantibodies (p-ANCA), cytoplasmic antineutrophil cytoplasmic autoantibodies (c-ANCA), antinuclear antibodies (ANA), and anti-double strand DNA (anti-ds DNA) were negative. Cryoglobulin, and markers of hepatitis B and C were negative. Complement levels and serum immunoglobulin levels were also within normal ranges.During follow-up, urine output decreased gradually and renal functions worsened progressively. A kidney biopsy was performed. Histopathologic findings of biopsy showed diffuse necrotizing crescentic GN. In biopsy specimen, twenty-six glomeruli were present; 10 glomeruli were globally sclerosed, 6 glomeruli showed cellular crescents, 4 glomeruli showed fibrocellular crescents and well-defined chronic tubulo-interstistial scarring. Direct immunofluorescence studies did not show any linear staining for IgG, IgM, IgA and complements along the glomerular capillary walls. In differential diagnosis, ANCA associated vasculitis, acute tubular necrosis and acute interstitial nephritis were ruled out and a diagnosis of crescentic GN was rendered based on the above findings.He was not treated with immunosuppressive therapy because he had a tumoral mass in chest X ray and he was taken under an oncological evaluation presuming lung cancer activation.Additionally, tumor treatment is essential for correcting paraneoplastic syndromes, therefore the primary treatment should be directed to the cancer in such cases.1,2
