Miroslav Podhola

Long-term survival after radical surgery for renal cell carcinoma with tumour thrombus extension into the right atrium.

Whats known on the subject? and What does the study add?

Is rat liver affected by non-alcoholic steatosis more susceptible to the acute toxic effect of thioacetamide?

Non‐alcoholic fatty liver disease (NAFLD) is the most common chronic condition of the liver in the western world. There is only little evidence about altered sensitivity of steatotic liver to acute toxic injury. The aim of this project was to test whether hepatic steatosis sensitizes rat liver to acute toxic injury induced by thioacetamide (TAA). Male Sprague–Dawley rats were fed ad libitum a standard pelleted diet (ST‐1, 10% energy fat) and high‐fat gelled diet (HFGD, 71% energy fat) for 6 weeks and then TAA was applied intraperitoneally in one dose of 100 mg/kg. Animals were sacrificed in 24‐, 48‐ and 72‐h interval after TAA administration. We assessed the serum biochemistry, the hepatic reduced glutathione, thiobarbituric acid reactive substances, cytokine concentration, the respiration of isolated liver mitochondria and histopathological samples (H+E, Sudan III, bromodeoxyuridine [BrdU] incorporation). Activities of alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase and concentration of serum bilirubin were significantly higher in HFGD groups after application of TAA, compared to ST‐1. There were no differences in activities of respiratory complexes I and II. Serum tumour necrosis factor alpha at 24 and 48 h, liver tissue interleukin‐6 at 72 h and transforming growth factor β1 at 24 and 48 h were elevated in TAA‐administrated rats fed with HFGD, but not ST‐1. TAA‐induced centrilobular necrosis and subsequent regenerative response of the liver were higher in HFGD‐fed rats in comparison with ST‐1. Liver affected by NAFLD, compared to non‐steatotic liver, is more sensitive to toxic effect of TAA.

Susceptibility of rat non-alcoholic fatty liver to the acute toxic effect of acetaminophen

Background and Aim:  Acetaminophen overdose is the most frequent cause of acute liver failure. Non‐alcoholic fatty liver disease is the most common chronic condition of the liver. The aim was to assess whether non‐alcoholic steatosis sensitizes rat liver to acute toxic effect of acetaminophen.

Low-Grade Cribriform Cystadenocarcinoma of the Parotid Gland: A Neoplasm With Favorable Prognosis, Distinct From Salivary Duct Carcinoma

Low-grade cribriform cystadenocarcinoma of salivary glands is a recently described rare tumor with favorable prognosis. This study reports the case of 50-year-old woman with swelling lasting for 9 months in the right parotideomasseteric area. Grossly, the tumor was well circumscribed and dominated by cystic space. Microscopically, the neoplasm consisted of well-demarcated islets, some of them cystically dilated. The architecture of islets varied from solid to cribriform and micropapillary without comedo-type necroses. The tumor cells featured no significant cytologic atypia. Immunohistochemically, luminal cells showed expression of cytokeratins (CK), CK7, CK18, and S100 protein. In addition, immunostains for CK5/6, CK14, p63 protein, and smooth muscle actin displayed a continuous rim of myoepithelial cells around all tumor nests. In contrast, detection of CK20, hormonal receptors (androgen, estrogen, and progesterone), epidermal growth factor receptor and Her-2/neu oncoprotein was negative. The patient is free of disease for 2 years. The relationship between low-grade cribriform cystadenocarcinoma and salivary duct carcinoma is discussed.

The leiomyomatous stroma in renal cell carcinomas is polyclonal and not part of the neoplastic process

Some renal epithelial neoplasms, such as renal angiomyoadenomatous tumor, clear cell papillary renal cell carcinoma and renal cell carcinoma with smooth muscle stroma, contain a variably prominent smooth muscle stromal component. Whether or not this leiomyomatous stroma is part of the neoplastic proliferation has not been firmly established. We studied the clonality status of 14 renal cell carcinomas with a prominent smooth muscle stromal component (four renal angiomyoadenomatous tumors/clear cell papillary carcinomas, five clear cell carcinomas, two papillary carcinomas, and three renal cell carcinomas with smooth muscle rich stroma) using the human androgen receptor assay (HUMARA). We found the leiomyomatous stromal component in all analyzable (8/14) cases to be polyclonal and therefore reactive rather than neoplastic. Based on morphological observations, we propose that the non-neoplastic leiomyomatous stromal component is likely derived from smooth muscle cells of large caliber veins located at the peripheral capsular region or within the collagenous septae of the tumors.

Case 1-2012: ANCA associated glomerulonephritis in combination with IgG4-positive mediastinal mass in a patient with ankylosing spondylitis treated with TNF alpha inhibitors.

47 ‐year ‐old man with ankylosing spondylitis was admit‐ ted with fever of unknown origin. diagnosis of ankylosing spondylitis was made 14 years ago based on occurrence of inflammatory back pain, bilateral sacroileitis and HLA B27 positivity. the patient was treated with non ‐steroidal anti‐inflammatory drugs; treatment with TNF alpha inhibi‐ tor (adalimumab 40 mg s.c. every other week) had been started ten months before admission. four months ago the patient started to be subfebrile or febrile (38 °c, sometimes with chills), he suffered from night swelling, fatigue, weight loss (5 kg during the last month) with normal appetite and without changes of bowel movements. the treatment with adalimumab was stopped two months ago. Before admis‐ sion, several tests and imaging methods were performed, however, the origin of the fever remained unclear (normal chest X ‐ray, abdominal ultrasonography, scintigraphy of the skeleton, otorhinolaryngologic examination, antinuclear fac‐ tor and anti dsdna antibodies as well as quantiferon tB gold were negative). with persistent fever he was admitted to our department of Rheumatology. Laboratory markers of inflammation were elevated (eryth‐ rocyte sedimentation rate 101mm/hour, cRp 110 mg/l), blood count and differential leukocyte count were nor mal, urine examination showed significant microsco‐ pic erythrocyturia (++++) and increasing proteinuria (0.74 g/day...1.2 g/day...2.64 g/day), serum creatinine was ini tially normal, subsequently the values were increasing (83...113...146...189...212 μmol/l). Paraprotein was not detected either in blood or in urine. infectious aetiology was not found (blood cultures repeatedly negative, as well as other cultures, also Mycobacterium species pcR in serum and urine negative). However, a significant titre of PRO3 anca antibodies (136.8 U/ml) was detected. high resolution ct (hRct) of the lung excluded a pneu‐ mopathy, but displayed a mediastinal mass in posterior mediastinum (190 × 32 × 53 mm), located perivertebrally, saddle shaped, in contact with dorsal aortic wall. fluoro‐ dexyglucose pet/ct revealed hypermetabolism of this mediastinal mass (figs. 1–3); another similar mass was found in the aortic arch area (20 × 8 mm, fig. 4), and still another under the bifurcation of abdominal aorta (30 × 35 × 10 mm, fig. 5). a ct ‐guided biopsy of the mediastinal mass was performed, followed by a kidney biopsy.

Mesalazine-Induced Interstitial Nephritis

5-aminosalicylate compounds (mesalazine, sulfasalazine) are widely used in therapy of inflammatory bowel diseases. Mesalazine-induced interstitial nephritis is a rare complication; however, the morbidity in an affected individual is high. Regular renal screening in patients treated with 5-aminosalicylate compounds is important. A 15-year-old boy with treated idiopathic proctocolitis, consequent mesalazine-induced nephritis, and a favorable response to corticotherapy is presented.

Spontaneous regression of renal cell carcinoma lung metastases in a patient with psoriasis

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Metastatic colorectal carcinoma and kidney tumors: a report of four cases

AIMS AND BACKGROUND The prognosis of patients with metastatic colorectal carcinoma (CRC) has improved substantially over the last two decades. Longer patient survival comes at a price of more complications, including second primary neoplasms and metastases at unusual sites. METHOD Retrospective chart review. RESULTS We present 4 patients with metastatic CRC who developed kidney tumors. In 2 cases, partial nephrectomy or nephrectomy was performed for second primary renal cell carcinoma. The patients survived 2.5 and more than 6 years after kidney surgery. In the other 2 patients the kidney tumors were diagnosed as CRC metastases, histologically verified in one case; these two patients died within two years of diagnosis of kidney involvement. CONCLUSION The diagnostic approach to kidney tumors in CRC patients should include a biopsy because only patients with primary renal cell carcinoma and selected patients with metastatic CRC benefit from nephrectomy.

Plasmapheresis-induced clinical improvement in a patient with steroid-resistant nephrotic syndrome due to podocin (NPHS2) gene mutation.

Podocin mutations (NPHS2 gene) are mostly responsible for steroid-resistant nephrotic syndrome (SRNS) of childhood onset. Patients with NPHS2 gene mutations do not respond to corticoids and other immunosuppressive agents; partial remission can be rarely induced by cyclosporin A. We present a boy, where SRNS was diagnosed within first year of life. By the age of 15 years, proteinuria reached 9000 mg/24 h, cholesterolemia 15 mmol/L, albuminemia 19.6 g/L, in spite of combined therapy with cyclosporine A, methylprednisolone, enalapril and losartan. At that time a combined heterozygous form of two NPHS2 gene mutations (p.R138Q and p.V290M) was diagnosed, methylprednisolone was discontinued and patient underwent ten plasmapheresis procedures. This resulted in clinical improvement (proteinuria 3000 mg/24 h, S-cholesterol 6 mmol/L, albumin 30g/L) lasting for three years. In conclusion, plasmapheresis can result in clinical improvement and stabilization of SRNS caused by podocine mutation, before renal replacement therapy is initiated.