PURPOSE: It is to examine clinical manifestations, early biochemical indicators, and risk factors for non-oliguric hyperkalemia (NOHK) in extremely low birth weight infants (ELBWI). MATERIALS AND METHODS: We collected clinical and biochemical data from 75 ELBWI admitted to Ajou University Hospital between Jan. 2008 and Jun. 2011 by reviewing medical records retrospectively. NOHK was defined as serum potassium > or =7 mmol/L during the first 72 hours of life with urine output > or =1 mL/kg/h. RESULTS: NOHK developed in 26.7% (20/75) of ELBWI. Among NOHK developed in ELBWI, 85% (17/20) developed within postnatal (PN) 48 hours, 5% (1/20) experienced cardiac arrhythmia and 20% (4/20) of NOHK infants expired within PN 72 hours. There were statistically significant differences in gestational age, use of antenatal steroid, and serum phosphorous level at PN 24 hours, and serum sodium, calcium, and urea levels at PN 72 hours between NOHK and non-NOHK groups (p-value <0.050). However, there were no statistical differences in the rate of intraventricular hemorrhage, arrhythmia, mortality occurred, methods of fluid therapy, supplementation of amino acid and calcium, frequencies of umbilical artery catheterization and urine output between the two groups. CONCLUSION: NOHK is not a rare complication in ELBWI. It occurs more frequently in ELBWI with younger gestational age and who didn't use antenatal steroid. Furthermore, electrolyte imbalance such as hypernatremia, hypocalcemia and hyperphosphatemia occurred more often in NOHK group within PN 72 hours. Therefore, more use of antenatal steroid and careful control by monitoring electrolyte imbalance should be considered in order to prevent NOHK in ELBWI.
Gestational Age ; Humans ; Hyperkalemia/diagnosis/drug therapy/*epidemiology ; *Infant, Extremely Low Birth Weight ; Infant, Newborn ; Infant, Premature ; Infant, Premature, Diseases/diagnosis/drug therapy/*epidemiology ; Republic of Korea ; Risk Factors

The acute tumor lysis syndrome is an acute illness caused by massive cell lysis after chemotherapies. This syndrome is characterized by hyperuricemia, hyperphosphatemia with hypocalcemia and hyperkalemia. Among these electrolyte abnormalities, the most serious complication is the severe hyperphosphatemia (greater than 14mg/dL) that could result in sudden cardiac arrest or respiratory failure. In order to correct the severe hyperphosphatemia, hemodialysis has been used commonly as the renal replacement therapy . However the hemodialysis can make posthemodialysis serum phosphate rebounded unless the patient take this treatment for more than 6 hours. Therefore it is not sufficient to use hemodialysis treatment alone. To solve this problem, hemodialysis has been used with or replaced by the uninterrupted dialysis technique such as CRRT (continuous renal replacement therapy). We report a 33-year-old man with Burkitt lymphoma who showed severe hyperphosphatemia (peak phosphate value was 18.6mg/dL) during the course of chemotherapy. used with 5 day CAVH (continuous arteriovenous hemofiltration) his phosphate level could be maintained without any rebound. Therefore we concluded that CAVH in conjunction with hemodialysis would be a successful way to control severe hyperphosphatemia associated with tumor lysis syndrome.
Adult ; Burkitt Lymphoma ; Death, Sudden, Cardiac ; Dialysis ; Drug Therapy ; Hemofiltration* ; Humans ; Hyperkalemia ; Hyperphosphatemia* ; Hyperuricemia ; Hypocalcemia ; Renal Dialysis* ; Renal Replacement Therapy ; Respiratory Insufficiency ; Tumor Lysis Syndrome*

Colonic necrosis is known as a rare complication following the administration of Kayexalate (sodium polystryrene sulfonate) in sorbitol. We report a rare case of colonic mucosal necrosis following Kalimate (calcium polystryrene sulfonate), an analogue of Kayexalate without sorbitol in a 34-yr-old man. He had a history of hypertension and uremia. During the management of intracranial hemorrhage, hyperkalemia developed. Kalimate was administered orally and as an enema suspended in 20% dextrose water to treat hyperkalemia. Two days after administration of Kalimate enema, he had profuse hematochezia, and a sigmoidoscopy showed diffuse colonic mucosal necrosis in the rectum and sigmoid colon. Microscopic examination of random colonic biopsies by two consecutive sigmoidoscopies revealed angulated crystals with a characteristic crystalline mosaic pattern on the ulcerated mucosa, which were consistent with Kayexalate crystals. Hematochezia subsided with conservative treatment after a discontinuance of Kalimate administration.
Adult ; Colon/*pathology ; Gastrointestinal Hemorrhage/etiology ; Humans ; Hyperkalemia/drug therapy ; Intestinal Mucosa/*pathology ; Male ; Necrosis/*chemically induced/complications/pathology ; Polystyrenes/*adverse effects/therapeutic use ; Uremia/*physiopathology

Addison's disease is a rare disorder resulted from a chronic deficiency of the adreanl cortical hormone. The clinical manifestations are general weakness, weight loss, hyperpigmentation, hypovolemia with hyponatremia and hyperkalemia. We report a case of Addison's disease in a 60-year-old woman who has experienced slowly progressive weakness, weight loss and generalized cutaneous pigmentation, especially sun exposed area, extensor surface and nail bed for the last, 2 years. On a hormonal assay of the adrenal glands, basal plasma cortisol level was decreased and basal plasma ACTH level was markedly elevated. A chest X-ray showed streaky tuberculous infiltration in left, upper lobe field and adrenal CT scan showed calcific densities of both adrenal glands with nodular enlargement of right adrenal gland. There was a clinical improvement with steroid replacement therapy and anti-tuber- culosis chemotherapy. A nearly normal appearance was obtained after 5 months' treatment.
Addison Disease ; Adrenal Glands ; Adrenocorticotropic Hormone ; Drug Therapy ; Female ; Humans ; Hydrocortisone ; Hyperkalemia ; Hyperpigmentation ; Hyponatremia ; Hypovolemia ; Middle Aged ; Pigmentation ; Plasma ; Solar System ; Thorax ; Tomography, X-Ray Computed ; Weight Loss

BACKGROUND: Acute tumor lysis syndrome(TLS) has been defined as the metabolic abnormalities that occur after rapid tumor breakdown. In this study, we have evaluated the types or degrees of metabolic abnormalities and clinical characteristics in patients with non-Hodgkin's lymphoma(NHL) who developed TLS. METHODS: Patients were considered to have 'laboratory TLS(LTLS)' if any two of the following metabolic abnormalities occurred spontaneously or within 4 days of treatment: hyperphosphatemia, hyperkalemia, hyperuricemia, azotemia, and hypocalcemia. 'Clinical TLS(CTLS)' was defined as LTLS plus one of the following: a serum potassium level greater than 6.0mEq/L, a creatinine level greater than 2.5mg/dL, a calcium level less than 6.0mg/dL, the development of a life-threatening arrhythmia, or sudden death. RESULTS: Of 111 cases with NHL, TLS occurred in 16(14.4%), LTLS in 11(9.9%), and CTLS in 5(4.5%). There was a significant difference of gender, histologic type, clinical stage, performance status, extranodal involvement, serum lactate dehydrogenase(LDH), LDH index, beta2-microglobulin, uric acid, and blood urea nitrogen(BUN) level in the TLS versus control group. In multiple regression analysis, TLS occurred more frequently in patients with pre-treatment azotemia, aggressive histologic type, and elevated serum LDH level(p< 0.05, respectively). Pre-treatment and post-treatment TLS occurred in 8 cases(50%) respectively. The common metabolic abnormalities included hyperphosphatemia(87.5%), azotemia(81.3%), and hypocalcemia(75%). Of 11 cases with conservative care, 8 cases recovered within several days, but 3 cases died with multi-organ failure from disease progression. All 5 cases after hemodialysis for TLS recovered without any significant complications. CONCLUSION: The current study suggests that all patients with high-grade lymphomas and pre-treatment azotemia or a high serum LDH level be carefully monitored for at least 4 days after chemotherapy.
Arrhythmias, Cardiac ; Azotemia ; Calcium ; Creatinine ; Death, Sudden ; Disease Progression ; Drug Therapy ; Humans ; Hyperkalemia ; Hyperphosphatemia ; Hyperuricemia ; Hypocalcemia ; Lactic Acid ; Lymphoma, Non-Hodgkin* ; Potassium ; Renal Dialysis ; Tumor Lysis Syndrome* ; Urea ; Uric Acid

PURPOSE: Tacrolimus (FK-506) represents a major advance in the prevention of rejection following solid organ transplantation. Previous clinical trials in Japan, Europe, and the US suggest that tacrolimus is an effective primary immunosuppressive agent in kidney transplantation. This prospective, non-randomized single center study was done to confirmed the efficacy of tacrolimus in kidney transplantation. METHODS: A total of 50 renal transplant recipients who followed-up at least one year after transplantation was included in this study. Thirty six cases (72%) recived triple drug therapy consists of tacrolimus, mycophenolate mofetil (MMF), and low dose steroid. RESULTS: The overall incidence of acute rejection was 10%, all episodes of rejection were treated effectively with steroid pulse therapy. The incidence of treatment failure was six percent. One and two year graft survival were 98% and 96%, respectively. Adverse effects of tacrolimus therapy included tremor of the hand (56%), diarrhea (34%), alopecia (26%), hyperkalemia (22%), nephrotoxicity (18%), post transplant diabetes mellitus (14%), hypertension (14%), and hypercholesterolemia (10%). However, the incidence of gum hypertrophy and hirsutism were 6% and 2%, respectively. CONCLUSION: This short-term study indicates that tacrolimus appears to provide safe and effective primary immunosuppression in kidney transplantation.
Alopecia ; Diabetes Mellitus ; Diarrhea ; Drug Therapy ; Europe ; Gingiva ; Graft Survival ; Hand ; Hirsutism ; Hypercholesterolemia ; Hyperkalemia ; Hypertension ; Hypertrophy ; Immunosuppression* ; Incidence ; Japan ; Kidney Transplantation* ; Organ Transplantation ; Prospective Studies ; Tacrolimus* ; Transplantation ; Transplants ; Treatment Failure ; Tremor

Tumor lysis syndrome (TLS) defines the metabolic derangements that occur with tumor breakdown following the initiation of cytotoxic therapy. TLS results from the rapid destruction of malignant cells and the abrupt release of intracellular materials and their metabolites into the extracellular space. The syndrome causes hyperuricemia, hyperkalemia, hyperphosphatemia, secondary hypocalcemia and uremia. It can result in acute renal failure and be fatal. Early recognition of patient at risk and preventive measures are important. There is a high incidence of TLS in tumors with high proliferative rates and large burden such as acute lymphoblastic leukemia and Burkitt's lymphoma. It less commonly occurs in solid tumors such as testicular cancer, breast cancer and small cell lung cancer. There are only a few reports on TLS complicated in CML in blast crisis. So we report a 45-yr-old woman presenting with TLS associated with CML in lymphoblastic crisis after the initiation of cytotoxic chemotherapy.
Acute Kidney Injury ; Blast Crisis ; Breast Neoplasms ; Burkitt Lymphoma ; Drug Therapy ; Extracellular Space ; Female ; Humans ; Hyperkalemia ; Hyperphosphatemia ; Hyperuricemia ; Hypocalcemia ; Incidence ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Small Cell Lung Carcinoma ; Testicular Neoplasms ; Tumor Lysis Syndrome* ; Uremia

Cyclosporin A (CsA)-induced hyperkalemia is caused by alterations in transepithelial K(+) secretion resulting from the inhibition of renal tubular Na(+), K(+) -ATPase activity. Thyroxine enhances renal cortical Na(+), K(+) -ATPase activity. This study investigated the effect of thyroxine on CsA-induced hyperkalemia. Sprague-Dawley rats were treated with either CsA, thyroxine, CsA and thyroxine, or olive-oil vehicle. CsA resulted in an increase in BUN and serum K(+), along with a decrease in creatinine clearance, fractional excretion of potassium, and renal cortical Na(+), K(+) -ATPase activity, as compared with oil vehicle administration. Histochemical study showed reduced Na(+), K(+) -ATPase activity in the proximal tubular epithelial cells of the CsA-treated compared with the oil-treated rats. Histologically, isometric intracytoplasmic vacuolation, disruption of the arrangement and swelling of the mitochondria, and a large number of lysosomes in the tubular epithelium were characteristic of the CsA-treated rats. Co-administration of thyroxine prevented CsA-induced hyperkalemia and reduced creatinine clearance, Na(+), K(+) -ATPase activity, and severity of the histologic changes in the renal tubular cells when compared with the CsA-treated rats. Thyroxine increased the fractional excretion of potassium via the preservation of Na(+), K(+) -ATPase activity in the renal tubular cells. Thus, the beneficial effects of thyroxine may be suited to treatment modalities for CsA-induced hyperkalemia.
Animals ; Cyclosporine/antagonists & inhibitors/*toxicity ; Hyperkalemia/chemically induced/*drug therapy/metabolism/prevention & control ; Immunosuppressive Agents/antagonists & inhibitors/*toxicity ; Kidney Cortex/*drug effects/*enzymology/pathology ; Male ; Microsomes/enzymology ; Potassium/blood/metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium-Potassium-Exchanging ATPase/*metabolism ; Thyroxine/*pharmacology