allopurinol and Hyperkalemia

Tumour lysis syndrome (TLS) is a life-threatening emergency characterised by a massive cytolysis with the release of intracellular electrolytes, nucleic acids, and metabolites into the circulation. TLS comprises laboratory derangements (hyperuricaemia, hyperkalaemia, hyperphosphataemia, and hypocalcaemia) responsible for acute kidney injury. In patients with hematologic malignancies after cytotoxic therapy or spontaneously and also in advanced solid tumours. Assessment of disease specific risk level for TLS in patients receiving anti-tumoural therapy is essential for early diagnosis. Prophylaxis is the mainstay of management of TLS. It is important to routinely initiate a risk-adapted prophylactic strategy to correct metabolic alterations and preserve renal function. High and intermediate risk patients and patients with established TLS should be managed with multidisciplinary medical care in a hospital unit to receive monitoring and medical care. Renal replacement therapy should be considered in patients with refractory TLS.

Topics: Acute Kidney Injury; Allopurinol; Combined Modality Therapy; Fluid Therapy; Humans; Hyperkalemia; Hyperphosphatemia; Hyperuricemia; Hypocalcemia; Prognosis; Renal Replacement Therapy; Risk Factors; Severity of Illness Index; Tumor Lysis Syndrome; Urate Oxidase

Tumor lysis syndrome (TLS) is an oncologic emergency triggered by the rapid release of intracellular material from lysing malignant cells. Most common in rapidly growing hematologic malignancies, TLS has been reported in virtually every cancer type. Central to its pathogenesis is the rapid accumulation of uric acid derived from the breakdown of nucleic acids, which leads to kidney failure by various mechanisms. Kidney failure then limits the clearance of potassium, phosphorus, and uric acid leading to hyperkalemia, hyperphosphatemia, and secondary hypocalcemia, which can be fatal. Prevention of TLS may be more effective than treatment, and identification of at-risk individuals in whom to target preventative efforts remains a key research area. Herein, we discuss the pathophysiology, epidemiology, and treatment of TLS with an emphasis on the kidney manifestations of the disease.

Topics: Acute Kidney Injury; Allopurinol; Bicarbonates; Buffers; Calcium; Diuretics; Enzyme Inhibitors; Febuxostat; Fluid Therapy; Humans; Hyperkalemia; Hyperphosphatemia; Hyperuricemia; Hypocalcemia; Renal Dialysis; Thiazoles; Tumor Lysis Syndrome; Urate Oxidase

The tumor lysis syndrome (TLS) is a life-threatening complication caused by the massive release of nucleic acids, potassium and phosphate into the blood. This complication is the result of tumor cell lysis, which may occur due to treatment of drug sensitive and is characterized by rapid capacity of proliferation, that is often hematological origin. Moreover, the TLS can be observed before starting the treatment due to spontaneous tumor cell death, and frequently worsens when chemotherapy is initiated. TLS has high mortality, so that its prevention continues to be the most important therapeutic measure. In the intensive care unit (ICU), physicians should be aware of the clinical characteristics of TLS, which results in severe electrolyte metabolism disorders, especially hyperkalemia, hyperphosphatemia and hypocalcemia, and acute kidney injury which is a major cause of ICU mortality. An adequate strategy for the management of the TLS, combining hydration, urate oxidase, and an early admission to ICU can control this complication in most patients. The aim of this review is to provide diagnostic tools that allow to the ICU physician to recognize the population at high risk for developing the TLS, and outline a proper strategy for treating and preventing this serious complication.

Topics: Acute Kidney Injury; Allopurinol; Antineoplastic Agents; Arrhythmias, Cardiac; Chelation Therapy; Clinical Trials as Topic; Combined Modality Therapy; Critical Care; Fluid Therapy; Humans; Hyperkalemia; Hyperphosphatemia; Hypocalcemia; Incidence; Multicenter Studies as Topic; Prognosis; Renal Replacement Therapy; Risk Factors; Severity of Illness Index; Tumor Lysis Syndrome; Urate Oxidase

Tumor lysis syndrome (TLS) is a serious complication of malignancies and can result in renal failure or death.. In tumors with a high proliferative rate with a relatively large mass and a high sensitivity to cytotoxic agents, the initiation of therapy often results in the rapid release of intracellular anions, cations and the metabolic products of proteins and nucleic acids into the bloodstream. The increased concentrations of uric acid, phosphates, potassium and urea can overwhelm the body's homeostatic mechanisms to process and excrete these materials and result in the clinical spectrum associated with TLS. Typical clinical sequelae include gastrointestinal disturbances, neuromuscular effects, cardiovascular complications, acute renal failure and death. Tumor lysis syndrome can also compromise the efficacy or administration of curative therapies. Available evidence suggests that the incidence of clinical TLS is approximately 3-7% for acute leukemias and 4-11% for lymphomas. Pediatric cancers are the leading cause of death by disease in children. The most common pediatric cancers include the leukemias, lymphomas, central nervous system tumors and neuroblastoma. Thus, TLS is a major concern to practitioners caring for pediatric oncology patients. Given the complexity of TLS prevention and treatment, a multidisciplinary approach involving the collaboration of medical oncologists/ hematologists and nephrologists has the greatest potential of ensuring optimal patient outcomes. Rehydration is fundamental in the management of TLS in addition to the current standard therapy for hyperuricemia which include rasburicase and allopurinol.. The early recognition and treatment of metabolic abnormalities often prevents the severe and life-threatening complications associated with tumor lysis syndrome.

Topics: Acute Kidney Injury; Allopurinol; Child; Fluid Therapy; Gout Suppressants; Humans; Hyperkalemia; Hyperphosphatemia; Hyperuricemia; Hypocalcemia; Tumor Lysis Syndrome; Urate Oxidase

Tumor lysis syndrome is an oncologic emergency that is characterized by severe electrolyte abnormalities. The syndrome occurs in patients with lymphoproliferative malignancies, most often after chemotherapy, but also spontaneously. The pathophysiology involves tumor cell lysis resulting in the release of potassium, phosphate and uric acid. The deposition of uric acid and calcium phosphate crystals in the renal tubules may lead to acute renal failure. The treatment consists in hydration, correction of the acidosis and hyperkalemia, use of allopurinol and recombinant urate oxidase (rasburicase) for preventing urate nephropathy and haemodialysis. The authors report a case of a patient with acute myeloid leukemia, who developed severe tumor lysis syndrome after chemotherapy.

Topics: Acidosis; Acute Kidney Injury; Allopurinol; Fluid Therapy; Humans; Hyperkalemia; Kidney Tubules; Recombinant Proteins; Renal Dialysis; Tumor Lysis Syndrome; Urate Oxidase; Uric Acid

Topics: Acute Kidney Injury; Allopurinol; Diagnosis, Differential; Fluid Therapy; Hemofiltration; Humans; Hyperkalemia; Hyperuricemia; Phosphorus; Renal Dialysis; Tumor Lysis Syndrome; Urate Oxidase

To identify patients with lymphoma at risk for tumor lysis after chemotherapy.. The case records of 102 patients receiving combination chemotherapy for non-Hodgkin's lymphoma (intermediate to high-grade histology) were reviewed. Patients were considered to have "laboratory tumor lysis" if two of the following metabolic changes occurred within 4 days of treatment: a 25% increase in the serum phosphate, potassium, uric acid, or urea nitrogen concentrations, or a 25% decline in the serum calcium concentration. "Clinical tumor lysis" was defined as laboratory tumor lysis plus one of the following: a serum potassium level greater than 6 mmol/L, a creatinine level greater than 221 mumol/L, or a calcium level less than 1.5 mmol/L, the development of a life-threatening arrhythmia, or sudden death.. Laboratory tumor lysis occurred in 42% of patients and clinical tumor lysis in 6%. There was no statistical difference in the frequency of either tumor lysis syndrome among lymphoma subgroups. Clinical tumor lysis occurred more frequently in patients with pretreatment renal insufficiency (serum creatinine level greater than 132 mumol/L) than in patients with normal renal function (36% versus 2%; p = 0.01). The development of azotemia correlated with high pretreatment serum lactate dehydrogenase concentrations (p < 0.01; r2 = 0.11).. Clinically significant tumor lysis is a rare occurrence in patients with lymphoma when they are receiving allopurinol. However, tumor lysis can occur in patients with all types of moderate to high-grade non-Hodgkin's lymphoma. Patients with a high serum lactate dehydrogenase level or renal insufficiency are at increased risk for metabolic complications after chemotherapy and should be closely monitored.

Topics: Acute Disease; Allopurinol; Antineoplastic Combined Chemotherapy Protocols; Blood Urea Nitrogen; Burkitt Lymphoma; Creatinine; Humans; Hyperkalemia; Hypocalcemia; L-Lactate Dehydrogenase; Leukemia, Lymphocytic, Chronic, B-Cell; Lymphoma, Large B-Cell, Diffuse; Lymphoma, Non-Hodgkin; Lymphoma, T-Cell; Phosphates; Renal Insufficiency; Retrospective Studies; Risk Factors; Tumor Lysis Syndrome; Uric Acid

A small proportion of patients with acute or chronic leukemia has an extraordinarily high blood leukocyte count. These high counts can result in a very high fractional volume of leukocytes (leukocrit), which is also a function of the mean leukocyte volume in different types of leukemia. Despite a high fractional volume of leukocytes, bulk viscosity of blood is usually not increased because a decrement in the fractional volume of erythrocytes accompanies the increase in leukocytes. Nevertheless, the excessive numbers of leukocytes present two major problems: first, they can seriously affect flow in the circulation of the lung, brain, and less often, other organs by obstructing microchannels or by forming aggregates and white thrombi in small veins. Moreover, leukemic blasts may compete for oxygen in the microcirculation and they may be invasive, damaging vessel walls. Second, their rapid destruction in response to cytotoxic drugs causes metabolic disturbances, especially uric acid accumulation, which can lead to obstructive uropathy.

Topics: Adolescent; Allopurinol; Antineoplastic Agents; Blood Flow Velocity; Blood Viscosity; Cerebrovascular Circulation; Child; Child, Preschool; Exchange Transfusion, Whole Blood; Hematocrit; Humans; Hyperkalemia; Leukapheresis; Leukemia; Leukocyte Count; Leukocytosis; Microcirculation; Oxygen Consumption; Pulmonary Circulation; Uric Acid

Flavopiridol, a cyclin-dependent kinase inhibitor, is cytotoxic to leukemic blasts. In a Phase II study, flavopiridol 50 mg/m(2) was given by 1-h infusion daily x 3 beginning day 1 followed by 2 g/m(2)/72 h ara-C beginning day 6 and 40 mg/m(2) mitoxantrone on day 9 (FLAM) to 45 adults with newly diagnosed acute myelogenous leukemia (AML) with multiple poor-risk features. Thirty patients (67%) achieved complete remission (CR) and 4 (9%) died. Twelve (40%) received myeloablative allogeneic bone marrow transplant (BMT) in first CR. Median OS and DFS are not reached (67% alive 12.5-31 months, 58% in CR 11.4-30 months), with median follow-up 22 months. Sixteen received FLAM in CR, with median OS and DFS 9 and 13.1 months, and 36% alive at 21-31 months. Short OS and DFS correlated with adverse cytogenetics, regardless of age or treatment in CR. The addition of allogeneic BMT in CR translates into long OS and DFS in the majority of eligible patients.

Topics: Adult; Aged; Allopurinol; Antineoplastic Combined Chemotherapy Protocols; Bone Marrow Transplantation; Combined Modality Therapy; Cytarabine; Disease-Free Survival; Female; Flavonoids; Follow-Up Studies; Heart Diseases; Humans; Hyperkalemia; Kaplan-Meier Estimate; Leukemia, Myeloid, Acute; Male; Middle Aged; Mitoxantrone; Piperidines; Polyamines; Premedication; Remission Induction; Risk; Sepsis; Sevelamer; Transplantation, Homologous; Treatment Outcome; Tumor Lysis Syndrome; Young Adult

The prevalence of chronic kidney disease (CKD) is increasing worldwide; black patients have an increased risk of developing CKD and end stage kidney disease (ESKD) at significantly higher rates than other races.. A cross sectional study was carried out on black patients with CKD attending the kidney outpatient clinic at Charlotte Maxeke Johannesburg Academic Hospital (CMJAH) in South Africa, between September 2019 to March 2020. Demographic and clinical data were extracted from the ongoing kidney outpatient clinic records and interviews, and were filled in a questionnaire. Patients provided blood and urine for laboratory investigations as standard of care, and data were descriptively and inferentially entered into REDcap and analysed using STATA version 17. Multivariable logistic regression analysis was used to identify demographic and clinical variables associated with advanced CKD.. A total of 312 black patients with CKD were enrolled in the study with a median age of 58 (IQR 46-67) years; 58% patients had advanced CKD, 31.5% of whom had grossly increased proteinuria, 96.7% had hypertension, 38.7% had diabetes mellitus and 38.1% had both hypertension and diabetes mellitus. In patients with advanced CKD, the median age was 61 (IQR 51-69) years, eGFR 33 (30-39) mL/min/1.73 m2, serum bicarbonate 22 (IQR 20-24), haemoglobin 12.9 (IQR 11.5-14.0) g/dl and serum uric acid 0.43 (IQR 0.37-0.53). The prevalence of metabolic acidosis was 62.4%, anemia 46.4% and gout 30.9% among those with advanced CKD, while the prevalence of metabolic acidosis and anaemia was 46.6% and 25.9% respectively in those with early CKD. Variables with higher odds for advanced CKD after multivariable logistic regression analysis were hypertension (OR 3.3, 95% CI 1.2-9.2, P = 0.020), diabetes mellitus (OR 1.8, 95% CI 1.1-3.3, P = 0.024), severe proteinuria (OR 3.5, 95% CI 1.9-6.5, P = 0.001), angina (OR 2.5, 95% CI 1.2-5.1, P = 0.008), anaemia (OR 2.9, 95% CI 1.7-4.9, P = 0.001), hyperuricemia (OR 2.4, 95% CI 1.4-4.1, P = 0.001), and metabolic acidosis (OR 2.0, 95% CI 1.2-3.1, P = 0.005). Other associations with advanced CKD were loss of spouse (widow/widower) (OR 3.2, 95% CI 1.4-7.4, P = 0.006), low transferrin (OR 2.4, 95% CI 1.1-5.1, P = 0.028), hyperkalemia (OR 5.4, 95% CI 1.2-24.1, P = 0.029), use of allopurinol (OR 2.4, 95% CI 1.4-4.3, P = 0.005) and doxazosin (OR 1.9, 95% CI 1.2-3.1, P = 0.006).. Hypertension and diabetes mellitus were strongly associated with advanced CKD, suggesting a need for primary and secondary population-based prevention measures. Metabolic acidosis, anemia with low transferrin levels, hyperuricemia and hyperkalemia were highly prevalent in our patients, including those with early CKD, and they were strongly associated with advanced CKD, requiring clinicians and dietitians to be proactive in supporting the needs of CKD patients in meeting their daily dietary requirements towards preventing and slowing the progression of CKD.

Topics: Acidosis; Aged; Allopurinol; Anemia; Bicarbonates; Cross-Sectional Studies; Diabetes Mellitus; Doxazosin; Hemoglobins; Humans; Hyperkalemia; Hypertension; Hyperuricemia; Middle Aged; Prevalence; Proteinuria; Renal Insufficiency, Chronic; South Africa; Tertiary Care Centers; Transferrins; Uric Acid

The potassium content of University of Wisconsin solution (UW) is 125 mEq/L and that of histidine-tryptophan-ketoglutarate solution (HTK) only 9 mEq/L. The aim of the present study was to analyze their effects to change potassium levels on reperfusion among patients undergoing living-donor liver transplantation.. Anesthesia records of adult living-donor liver transplant patients were reviewed retrospectively. Patients received liver graft preserved in UW were grouped in group I (GI) and HTK in group II (GII). The potassium levels in the anheptic phase were compared with those 5 minutes after reperfusion using paired Student t tests. P values of <.05 were regarded to be significant.. Eighty-five GI patients showed the potassium significantly decreased from 3.76±0.70 to 3.60±0.74, whereas the change among 355 GII patients was almost unremarkable: 4.00±0.57 to 3.96±0.06 mEq/L.. Although UW contains a higher potassium content, it seems to have no negative impact on changes in serum potassium levels; in contrast it decreased the potassium level significantly at 5 minutes after reperfusion. Both preservation solutions maintain the patients' potassium levels within the normal range.

Topics: Adenosine; Adult; Allopurinol; Biomarkers; Glucose; Glutathione; Hepatectomy; Humans; Hyperkalemia; Insulin; Liver Transplantation; Living Donors; Mannitol; Middle Aged; Organ Preservation; Organ Preservation Solutions; Potassium; Potassium Chloride; Procaine; Raffinose; Reference Values; Reperfusion; Retrospective Studies; Risk Factors; Taiwan; Time Factors; Treatment Outcome

Topics: Allopurinol; Causality; Fluid Therapy; Gout Suppressants; Humans; Hyperkalemia; Hyperphosphatemia; Hypocalcemia; Neoplasms; Nurse's Role; Nursing Assessment; Oncology Nursing; Patient Education as Topic; Risk Assessment; Tumor Lysis Syndrome; Urate Oxidase

Topics: Acute Kidney Injury; Aged; Aged, 80 and over; Allopurinol; Amiloride; Aspirin; Drug Combinations; Drug Therapy, Combination; Humans; Hydrochlorothiazide; Hyperkalemia; Indomethacin; Male; Nifedipine; Sulfamethoxazole; Trimethoprim; Trimethoprim, Sulfamethoxazole Drug Combination

A patient with acute lymphoblastic leukemia with a large tumor burden is presented. Following successful chemotherapy, the patient experienced a cardiac arrest presumably due to hyperkalemia in association with hyperuricemia. The implication of these findings for patients with responsive hematological malignancies is discussed.

Topics: Adolescent; Allopurinol; Daunorubicin; Drug Therapy, Combination; Heart Arrest; Humans; Hyperkalemia; Leukemia, Lymphoid; Male; Prednisone; Uric Acid; Vinblastine; Vincristine

Topics: Adolescent; Allopurinol; Drug Therapy, Combination; Humans; Hyperkalemia; Leukemia, Lymphoid; Leukocyte Count; Male; Potassium; Prednisone; Vincristine

Topics: Acute Disease; Allopurinol; Child, Preschool; Humans; Hyperkalemia; Hypocalcemia; Leukemia, Lymphoid; Male; Methotrexate; Prednisone; Uric Acid

Topics: Adolescent; Adult; Allopurinol; Animals; Ascitic Fluid; Blood Urea Nitrogen; Burkitt Lymphoma; Child; Cyclophosphamide; Death, Sudden; Female; Humans; Hyperkalemia; Injections, Intravenous; Leukemia L1210; Male; Maryland; Mice; Nitrogen Mustard Compounds; Potassium; Retrospective Studies