Harutake Sawazaki

Incidentally discovered giant renal arteriovenous malformation

A case is presented of giant renal arteriovenous malformation (AVM). A 61‐year‐old woman was admitted to the National Defense Medical College Hospital for further evaluation of a renal cyst. Doppler ultrasonography and magnetic resonance imaging revealed a giant renal AVM, although the patient had no history nor clinical sign suggesting an AVM. Under the diagnosis of a right renal AVM, the patient underwent AVM resection.

Clear Cell Adenocarcinoma Arising From Abdominal Wall Endometriosis Mimicking Urachal Tumor

A 41-year-old woman presented with severe lower abdominal pain. She had a history of 2 cesarean deliveries. Magnetic resonance imaging (MRI) revealed a 4.3 × 4.6 × 4.8-cm mass on the urinary bladder dome. Preoperative diagnosis was invasive urachal tumor. Wide resection of the tumor was performed. The histopathological diagnosis was clear cell adenocarcinoma with endometriosis. MRI revealed normal-sized ovaries and uterus. The definite diagnosis of clear cell carcinoma arising from abdominal wall endometriosis was made. Adjuvant chemotherapy with paclitaxel and carboplatin (total 6 courses) was planned. The patient has thus far received 4 courses of this treatment.

Granulocyte colony-stimulating factor (G-CSF) producing bladder cancer subsequently developed from recurrent non-muscle invasive bladder cancer.

Bladder cancer producing granulocyte colony-stimulating factor (G-CSF) is rare. To our knowledge, approximately 50 cases have been reported in Japanese literature. A review of these cases showed bladder cancer producing G-CSF was the invasive or metastatic type at the initial diagnosis. Here, we present a very rare case of G-CSF producing bladder cancer that subsequently developed from recurrent noninvasive bladder cancer. A 91-year-old Japanese woman underwent TURBT seven times and intravesical therapy (mitomycin C, doxorubicin) from April 1993 to April 2004 for recurrence of non-muscleinvasive bladder cancer (pathology: urothelial carcinoma, grade 1–2, pTa-pT1a). For a renal pelvic tumor, left nephroureterectomy was performed in 1994 (pathology: urothelial carcinoma, grade 2, pTa). In September 2007, she underwent her eighth TURBT. The pathological diagnosis was carcinoma in situ (CIS), so intravesical Bacille de Calmette et Guerin (BCG) therapy was performed as the adjuvant therapy. However, the patient complained of macroscopic hematuria in February 2008. Cystoscopy and abdominal computed tomography revealed a large invasive tumor on the right bladder wall and right hydronephrosis (Fig. 1a). The patient underwent her ninth TURBT. The pathological diagnosis was urothelial carcinoma, grade 3, pT2 or more). Only a right cutaneous ureterostomy was performed. Three months later, she was referred to our hospital due to unconsciousness. The laboratory examination showed marked leukocytosis with a maximum of 52 600/ mm in the peripheral blood with no findings of inflammatory disease. Bone marrow puncture revealed no abnormal blood cells were found. A prominent elevation of G-CSF, 223 pg/mL (normal range: 3.7–32.3 pg/mL) was noted in the serum. Her general condition became worse and she died from the disease in June 2008. An autopsy was performed. A sample of the tumor showed urothelial carcinoma, grade 3 and positive immunostaining for G-CSF (Fig. 1b). G-CSF produced by non-hematopoietic malignant cells has been reported to be capable of inducing a leukemoid reaction in the host through intense stimulation of leukocyte production. Furthermore, this is frequently associated with aggressive tumor cell growth and a detrimental clinical outcome. Nishimura et al. have reported that acquisition of the G-CSF gene might accelerate the proliferation of cancer. Tachibana et al. have reported that bladder cancer cells producing G-CSF with expression of the G-CSF receptor, provides direct evidence of autocrine growth of bladder cancer cells induced by G-CSF. Chakraborty et al. have reported that the G-CSF/G-CSF receptor autocrine/ paracrine signaling loop significantly promotes survival and growth of bladder cancer and the G-CSF receptor autocrine signaling loop leads to b1-integrin-dependent increased adhesion and invasion of bladder carcinoma cells. In our patient, recurrent non-invasive bladder cancer developed CIS. The CIS subsequently developed into microinvasive bladder cancer, and the microinvasive bladder

Erythropoietin production in renal cell carcinoma and renal cysts in autosomal dominant polycystic kidney disease in a chronic dialysis patient with polycythemia: A case report

In patients undergoing chronic hemodialysis (HD), erythropoietin (EPO) production from the kidney generally decreases and renal anemia develops. Patients without anemia, but with high serum EPO (sEPO) levels are rare among HD patients. The current study presents the case of a 67-year-old female HD patient with autosomal dominant polycystic kidney disease (ADPKD) and renal cell carcinoma (RCC), manifesting polycythemia with elevated sEPO levels. A radical nephrectomy was performed, which diminished the polycythemia, but the sEPO levels remained high. To determine the origin of the EPO production, immunohistochemistry was performed to detect EPO in the RCC and the renal cysts of the surgically resected kidney. In addition, the sEPO and EPO levels in a renal cyst were determined by enzyme immunoassay. EPO expression was demonstrated in RCC and cyst epithelial cells using immunohistochemistry, revealing extremely high EPO levels in the cyst fluid. Due to the remission of polycythemia following the nephrectomy, EPO production from the resected kidney appeared to have been the cause of the polycythemia. Positive EPO staining of the renal cysts in the resected polycystic kidney and sustained sEPO elevation following nephrectomy led to the hypothesis of EPO production in the renal cysts of the contralateral polycystic kidney. Although the postoperative EPO level was higher than the normal range, the hematocrit (Hct) level gradually decreased and recombinant human EPO was required again three months following the nephrectomy. Eight months after the nephrectomy, the Hct level was 30.2% with the use of rHuEPO. In conclusion, EPO production from RCC and renal cysts in ADPKD appeared to cause polycythemia in the HD patient.

Massive Renal Replacement Lipomatosis With Foci of Xanthogranulomatous Pyelonephritis in a Horseshoe Kidney

Renal replacement lipomatosis (RRL) is a rare condition that occurs at the end of the spectrum of renal tissue replacement by fat. Xanthogranulomatous pyelonephritis (XGP) is a granulomatous inflammation characterized by destruction of renal parenchyma and replacement by lipid-laden macrophages. We present the case of a 75-year-old man who complained of severe anemia 34 years after right nephrolithotomy. Computed tomography revealed a huge low-density mass with renal parenchyma atrophy on the right side of horseshoe kidney. Right nephrectomy was performed. Pathological diagnosis was RRL with XGP. This is the first report of RRL with XGP in a horseshoe kidney.