s-1743 and Kidney-Neoplasms

s-1743 has been researched along with Kidney-Neoplasms* in 2 studies

Other Studies

2 other study(ies) available for s-1743 and Kidney-Neoplasms

ArticleYear
An evaluation of the protective effect of esomeprazole in an experimental model of renal ischemia-reperfusion.
    International urology and nephrology, 2018, Volume: 50, Issue:2

    The ischemia and subsequent reperfusion (IR) which occurs in partial nephrectomy used in the treatment of renal tumors causes loss of parenchyma in the damaged kidney. The aim of this study is to evaluate, both biochemically and histologically, the efficacy of esomeprazole in an ischemia-reperfusion model in rat kidneys.. The rats were randomized into three groups of seven animals each, referred to as the sham, control, and PPI groups. In the sham group, only a laparotomy was performed. In the control group, following laparotomy the left renal artery was dissected and tied for 30-min ischemia. In the PPI group, a vascular route to the tail vein was opened, and 10 mg/kg esomeprazole was administered. After 1 h, the same procedures described for the control group were performed. All the animals were killed 24 h after the procedure. Biochemical analyses were applied for evaluation of oxidant and antioxidant agents in the blood and left kidney of each subject (oxidative markers: malondialdehyde, myeloperoxidase; antioxidant marker: superoxide dismutase). In the histological examination of the kidney tissues stained with hematoxylin-eosin, the TUNEL method was applied in the evaluation of apoptosis.. No statistically significant biochemical difference was determined in the blood and tissue samples. In the histological and apoptosis evaluations, a statistically significant difference was determined between the sham, control, and PPI groups. The median (IQR) values of the TUNEL-positive cells were counted as 1.50 (4) in the sham group, 11.50 (12) in the control group, and 6.00 (9) in the PPI group (p < 0.001).. A protective effect of esomeprazole was confirmed in renal ischemia-reperfusion damage created in an experimental rat model.

    Topics: Animals; Apoptosis; Enzyme Inhibitors; Esomeprazole; Kidney; Kidney Neoplasms; Malondialdehyde; Models, Theoretical; Nephrectomy; Oxidative Stress; Rats; Reperfusion Injury; Superoxide Dismutase; Treatment Outcome

2018
Clinical case report: a rare cause of acute kidney failure - tissue is the issue.
    Acta clinica Belgica, 2017, Volume: 72, Issue:3

    A patient was admitted to the medical emergency department by his family physician. His complaints were weakness and fatigue for more than one week. Four days before admission, he went to his general practitioner for these complaints and also for painful elbows. His physician prescribed diclofenac and esomeprazole. Upon presentation, he had high systolic/diastolic blood pressure (>180/>90 mm Hg, measured repeatedly), and otherwise normal parameters. He had gained 6.5 kg in body weight. Clinical examination was normal, except for very mild bilateral malleolar edema. Routine blood tests showed a strongly elevated serum creatinine, hyperkalemia, and elevated lactate dehydrogenase. Haptoglobin levels were normal. Urinalysis showed a normal sediment, urine and blood cultures remained sterile. Ophthalmoscopy was completely normal, as was a routine chest X-ray. Renal ultrasound demonstrated kidneys with a diameter of 13 cm. Due to uncontrollable hypertension, our patient was hospitalized at the intensive care department where intravenous nifedipine was started, with good instantaneous control of blood pressure. Because of increasing potassium levels acute hemodialysis was started within 24 h after admission. Differential diagnosis consisted of diclofenac- or esomeprazole-induced interstitial nephritis or rapidly progressive glomerulonephritis. A renal biopsy was performed within 72 h after admission. The kidney biopsy showed an overwhelming inflammatory cell infiltrate consisting of a monoclonal lymphocytic cell population. However, the numerous mitotic figures, polyploidy, and prominent nucleoli present, were indicative of a lymphoma. Additional stainings confirmed a non-Hodgkin diffuse large-cell B-cell lymphoma. Treatment with R-CHOP (rituximab, cyclophosphamide, doxorubicine, vincristine, and prednisolone) was initiated with very good clinical and biochemical response, yet only mild recovery of kidney function. Occasionally the kidney is involved as an extranodal non-Hodgkin lymphoma (NHL) localization. However, a primary presentation of acute kidney failure due to lymphoma localization is extremely rare. Our case demonstrates that early renal biopsy is indispensable for fast and adequate diagnosis and treatment.

    Topics: Acute Kidney Injury; Anti-Inflammatory Agents, Non-Steroidal; Antibodies, Monoclonal, Murine-Derived; Antineoplastic Combined Chemotherapy Protocols; Cyclophosphamide; Diagnosis, Differential; Diclofenac; Doxorubicin; Esomeprazole; Glomerulonephritis; Humans; Kidney Neoplasms; Lymphoma, Large B-Cell, Diffuse; Male; Middle Aged; Nephritis, Interstitial; Prednisone; Proton Pump Inhibitors; Rituximab; Vincristine

2017