We present a 66-year-old patient with a medical history of subtotal gastrectomy for gastric adenocarcinoma four years ago and arterial hypertension on treatment with spironolactone. The patient was referred by the Digestive Service for a long-standing condition characterised by: anorexia, loss of 12 kilos in 6 months (current weight 42 kilos), hypochromic anaemia and constipation. Physical examination revealed a large, firm, painless, mobile tumour that occupied three quarters of the abdomen.

Given the history of gastric adenocarcinoma, the severe deterioration of the general condition, the constipation and the anaemia, the first clinical suspicion suggested was: ascites due to carcinomatosis, tumoural intestinal obstruction or abdominal tumour. The analytical data showed haemoglobin 7.5 g/dl, 3.35 million haematitis, 27% haematocrit, MCV 71.3, RDW 18, ESR 37 mm/h, CRP 0.7, PSA 2.6 ng/ml, creatinine 0.89 and urea 24. Liver and digestive tumour markers were unremarkable. Gastroscopy revealed an inflammatory polyp in the gastric stump, with no evidence of tumour recurrence. Colonoscopy was impossible due to intestinal displacement and intolerance of the patient. The abdominopelvic ultrasound revealed the presence of a cystic tumour with incomplete septa, of mixed anechoic content, which occupied the entire abdominal cavity. The left kidney was identified as normal, with no evidence of the presence of the right kidney.
In view of the finding of a voluminous intra-abdominal cystic lesion, the patient was referred to our clinic where intravenous urography was performed with the result of right functional annulment, contralateral normofunction and a large mass effect that displaced the digestive lumen towards the left hypochondrium and impressed the right lateral wall of the cystogram. The CT scan showed a large cystic mass measuring 29.5 cm x 27.5 cm x 16 cm, with multiple septa and well-defined walls occupying almost the entire abdomen. A calcific image was identified in the theoretical renal pelvis area of the hydronephrotic kidney with compression and displacement of all abdominal structures.

Given the diagnostic suspicion of giant hydronephrosis secondary to obstructive lithiasic uropathy, the possibility of percutaneous drainage and subsequent nephrectomy was evaluated. Simple right nephrectomy was performed by subcostal lumbotomy, evacuating 7,800 millilitres of serohaematic content. An extended hilar lymphadenectomy was performed due to the finding of lymphadenopathies at this level. The fluid culture was negative and cytology was not performed as there was no clinical or radiological suspicion of urothelial tumour.
Histological examination revealed the presence of a multicystic kidney, with marked dilatation of the pyelocaliceal system and severe parenchymal atrophy (thickness 0.5 cm). The epithelial lining showed changes of dysplasia of different degrees, with areas of papillary pattern and areas of infiltration of the renal parenchyma.

In other areas, solid nests of cells with large, clear cytoplasm and high nuclear grade (Fuhrman grade 3) were identified, as well as nodal infiltration of clear cell type renal cell carcinoma.

The subsequent evolution was unfavourable, with the appearance of liver metastases and the eventual death of the patient two months later.

