A case of bilateral renal masses: dilemmas in their evaluation and management

A 49-year-old woman underwent computed tomography (CT) examination of the chest and abdomen following a road traffic accident. This revealed bilateral solid renal masses. A subsequent CT examination with intravenous contrast demonstrated one solid enhancing lesion of 26 mm in the upper pole of the right kidney and two solid enhancing lesions of 27 mm each in the left kidney, one of which extended into the renal sinus fat (Figure 1). There was no evidence of vascular invasion or lymphadenopathy. Since these lesions were considered highly suspicious for renal cell carcinoma, the patient was scheduled for an open bilateral partial nephrectomy. A biopsy was not performed because of concerns about the potential for coexisting malignancy in patients with benign change identified on biopsy. The patient had Stage 4 chronic kidney disease as a result of anti-neutrophil cytoplasmic antibody (cANCA)-positive vasculitis treated 13 years previously but this was in remission on mycophenolate mofetil. Her creatinine concentration was 230 lmol/L (eGFR 1⁄4 20 mL/min) and she was aware that she would ultimately require renal replacement treatment. She was counselled about the possibility that partial nephrectomy might be inappropriate and therefore that bilateral nephrectomy might be necessary. She was familiar with the treatment of end-stage renal disease (ESRD) as her husband, father-in-law and sister-in-law had all undergone renal transplantation for ESRD caused by Adult Polycystic Kidney Disease. On the day of surgery, the kidneys were exposed via a midline incision. Multiple tumours were palpable throughout both kidneys. These were much more extensive and numerous than demonstrated by the CT examination, precluding nephron-sparing partial nephrectomy as previously planned. Bilateral nephrectomy was therefore performed after discussion in theatre with the renal physician responsible for her care. A Tenckhoff catheter was sited for peritoneal dialysis. Histopathology showed multiple oncocytic tumours present within both kidneys, comprising nests, tubules and solid sheets of cells with abundant eosinophilic cytoplasm and round monomorphic nuclei showing minimal nuclear atypia and no mitotic figures (Figure 2a). Immunohistochemical staining (CK8/18 diffuse 1, CK7 focal single cell cytoplasmic 1, c-kit diffuse 1, AMACR , Vimentin , RCC ) confirmed the tumours to be oncocytomas, with no evidence of renal cell carcinoma. Renal parenchyma around the tumours showed multiple microscopic foci of oncocytosis (Figure 2b). In addition, the renal cortex showed moderate chronic damage associated with focal segmental and global glomerulosclerosis and marked glomerulomegaly, indicative of hyperfiltration injury. There was no evidence of active glomerulonephritis or vasculitis. The patient made an uncomplicated recovery. After a brief period of haemodialysis, she performed automated peritoneal dialysis at home for 8 months before receiving a living donor kidney transplant from her mother.