Humans ; Tumor Lysis Syndrome/drug therapy* ; Leukemia, Myeloid, Acute/pathology* ; Bridged Bicyclo Compounds, Heterocyclic/therapeutic use* ; Sulfonamides/therapeutic use* ; Antineoplastic Combined Chemotherapy Protocols ; Antineoplastic Agents/therapeutic use*

Dramatic advances in the care of patients with cancer have led to significant improvement in outcomes and survival. However, renal manifestations of the underlying cancer as well as the effects of anti-neoplastic therapies leave patients with significant morbidity and chronic kidney disease risks. The most common renal manifestations associated with cancer include acute kidney injury (AKI) in the setting of multiple myeloma, tumor lysis syndrome, post-hematopoietic stem cell therapy, and AKI associated with chemotherapy. Knowledge of specific risk factors, modification of risk and careful attention to rapid AKI diagnosis are critical for improving outcomes.
Acute Kidney Injury ; Diagnosis ; Drug Therapy ; Humans ; Multiple Myeloma ; Renal Insufficiency, Chronic ; Risk Factors ; Stem Cells ; Tumor Lysis Syndrome

Tumor lysis syndrome is a serious complication of malignancy, resulting from the massive and rapid release of cellular components into the blood. Generally, it occurs after initiation of chemotherapy. The onset of spontaneous tumor lysis syndrome (STLS) before anti-cancer treatment is rare and occurs mostly in Burkitt lymphoma and non-Hodgkin's lymphoma. There are only a few case reports in children. Here, we report a case of STLS secondary to T-cell acute lymphoblastic leukemia (ALL), which presented with urinary stone and subsequent acute kidney injury with severe hyperuricemia. Occult malignancy should be considered in case of unexplained acute kidney injury with extreme hyperuricemia.
Acute Kidney Injury* ; Burkitt Lymphoma ; Child ; Drug Therapy ; Humans ; Hyperuricemia* ; Lymphoma, Non-Hodgkin ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; T-Lymphocytes ; Tumor Lysis Syndrome* ; Urinary Calculi*

Tumor lysis syndrome (TLS) is an oncologic emergency due to the rapid lysis of tumor cells and subsequent release of large amounts of intracellular potassium, phosphate, and uric acid into the bloodstream. Precipitation of uric acid and/or calcium phosphate crystals in the renal tubules can result in acute kidney injury. TLS is frequently observed in children with malignancy, which has high tumor burden, rapid cell turnover or high chemosensitivity (particularly, Burkitt's lymphoma and acute lymphoblastic leukemia), following the initiation of cytotoxic therapy. The current recommendations for prophylaxis and management are based on the TLS risk stratification. It is essential to administer adequate fluid and hypouricemic agents (allopurinol and/or rasburicase) to prevent acute kidney injury. In children susceptible to TLS, prompt diagnosis and aggressive treatment, such as renal replacement therapy, should be performed through close monitoring.
Acute Kidney Injury ; Burkitt Lymphoma ; Calcium ; Child ; Diagnosis ; Emergencies ; Humans ; Hyperkalemia ; Hyperphosphatemia ; Hyperuricemia ; Hypocalcemia ; Monitoring, Physiologic ; Potassium ; Primary Prevention ; Renal Replacement Therapy ; Tumor Burden ; Tumor Lysis Syndrome* ; Uric Acid

Tumor lysis syndrome is rare in hepatocellular carcinoma (HCC), but it has been reported more frequently recently in response to treatments such as transcatheter arterial chemoembolization (TACE), radiofrequency thermal ablation (RFTA), and sorafenib. Tumor lysis syndrome induced by low-dose steroid appears to be very unusual in HCC. We report a patient with hepatitis-C-related liver cirrhosis and HCC in whom tumor lysis syndrome occurred due to low-dose steroid (10 mg of prednisolone). The patient was a 90-year-old male who presented at the emergency room of our hospital with general weakness and poor oral intake. He had started to take prednisolone to treat adrenal insufficiency 2 days previously. Laboratory results revealed hyperuricemia, hyperphosphatemia, and increased creatinine. These abnormalities fulfilled the criteria in the Cairo-Bishop definition of tumor lysis syndrome. Although the patient received adequate hydration, severe metabolic acidosis and acute kidney injury progressed unabated. He finally developed multiple organ failure, and died 3 days after admission. This was a case of tumor lysis syndrome caused by administration of low-dose steroid in a patient with HCC.
Acute Kidney Injury/pathology ; Aged, 80 and over ; Antineoplastic Agents/therapeutic use ; Carcinoma, Hepatocellular/*pathology/therapy ; Chemoembolization, Therapeutic ; Creatinine/blood ; Humans ; Liver Neoplasms/*pathology/*therapy ; Male ; Niacinamide/analogs & derivatives/therapeutic use ; Phenylurea Compounds/therapeutic use ; Steroids/adverse effects/therapeutic use ; Tomography, X-Ray Computed ; Tumor Lysis Syndrome/*diagnosis/drug therapy

Development of tumor lysis syndrome (TLS) may occur after chemotherapy or spontaneously in bulky or rapidly growing tumors. This syndrome is frequent but preventable in patients with hematologic malignancies. TLS following therapy has been reported infrequently in various types of solid tumors. TLS associated with oxaliplatin containing chemotherapy in a solid tumor has never been reported. A 59-year-old man received 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX) chemotherapy for metastatic colon cancer. Development of TLS occurred three days after administration of chemotherapy. Two days later, his abnormal laboratory findings were recovered with appropriate management. To the best of our knowledge, the current case is the first report on development of acute TLS following oxaliplatin containing chemotherapy in a patient with colon cancer. We also review the literature on tumor lysis syndrome in patients with colorectal cancer.
Colon ; Colonic Neoplasms* ; Colorectal Neoplasms ; Drug Therapy ; Fluorouracil ; Hematologic Neoplasms ; Humans ; Leucovorin ; Middle Aged ; Tumor Lysis Syndrome*

Tumor lysis syndrome (TLS) has rarely been observed in solid tumors. We report on a case of a patient with advanced invasive thymoma who developed tumor lysis syndrome after chemotherapy. The potential complications of TLS should be considered in treatment of extensive thymoma.
Acute Kidney Injury ; Drug Therapy ; Humans ; Hyperuricemia ; Thymoma* ; Tumor Lysis Syndrome*

Antineoplastic Agents ; adverse effects ; Child ; Child, Preschool ; Hematopoietic Stem Cell Transplantation ; adverse effects ; Humans ; Kidney Diseases ; etiology ; pathology ; therapy ; Kidney Neoplasms ; etiology ; pathology ; therapy ; Neoplasms ; complications ; therapy ; Paraneoplastic Syndromes ; etiology ; pathology ; therapy ; Radiotherapy ; adverse effects ; Risk Factors ; Tumor Lysis Syndrome ; etiology ; pathology ; therapy

OBJECTIVETo investigate risk factors associated with acute tumor lysis syndrome (ATLS) in children with B-cell lymphoma and to explore feasible means for the prophylaxis and treatment.

METHODData from 18 children with ATLS in B-cell lymphoma were collected to assess their tumor burden at diagnosis and before chemotherapy. Evaluation was performed at the 8th day, 3 month, and the end of chemotherapy and follow up. The incidence of ATLS in B-cell lymphoma, and the relationship between the incidence of ATLS and whether the kidney was involved and large tumor burden were analyzed respectively. All patients received hydration, alkalinization and received allopurinol routinely. Urate oxidase and hemodialysis treatment were administered in some cases.

RESULTOf the 103 children with B-cell lymphoma, 18 were diagnosed as having ATLS (17.5%). All the 18 cases with ATLS were histopathologically confirmed as having Burkitt's lymphoma. All the patients were at stage III or IV and all had large tumor sizes, and 7 were found to have blasts in the bone marrow>25% (38.9%). Lactate dehydrogenase (LDH) levels≥1000 U/L were found in 11 (61.1%) cases. All patients had developed metabolic abnormalities, including hyperuricemia, hyperphosphatemia, hypocalcemia, and uremia. In terms of clinical features and prognosis, all cases had nausea, vomiting, anorexia, oliguria, and anuria at different levels. One had gastrointestinal bleeding, 7 patients experienced seizures. The etiology in five was hypocalcemia and two had reversible posterior encephalopathy syndrome and all responded well to treatment. Nine cases of ATLS responded to supportive care, 4 required hemodialysis, and the other 4 responded to urate oxidase. Ten cases survived and 8 died. The major cause of death was severe complications and treatment was given up in 5 cases and recurrence occurred in 3 cases.

CONCLUSIONATLS was commonly seen in Burkitt's subtype of B-cell lymphoma. Higher LDH and large tumor sizes and kidney involvement were important risk factors for the development of ATLS in children with B-cell lymphoma. Treatments with hydration, alkalinization and allopurinol were safe and effective. Urate oxidase and hemodialytic treatments should be given timely.

Child ; Humans ; Kidney ; physiopathology ; L-Lactate Dehydrogenase ; analysis ; Lymphoma, B-Cell ; complications ; diagnosis ; drug therapy ; Risk Factors ; Tumor Burden ; Tumor Lysis Syndrome ; diagnosis ; drug therapy ; etiology

Antineoplastic Agents ; adverse effects ; therapeutic use ; Diarrhea ; chemically induced ; Drug Delivery Systems ; methods ; Exanthema ; chemically induced ; Humans ; Leukopenia ; chemically induced ; Lung Diseases, Interstitial ; chemically induced ; Myocardial Infarction ; chemically induced ; Neoplasms ; drug therapy ; Tumor Lysis Syndrome ; etiology