Caffeine-induced hypokalemia: a case report.

BACKGROUND: With an increase in the global popularity of coffee, caffeine is one of the most consumed ingredients of modern times. However, the consumption of massive amounts of caffeine can lead to severe hypokalemia. CASE PRESENTATION: A 29-year-old man without a specific past medical history was admitted to our hospital with recurrent episodes of sudden and severe lower-extremity weakness. Laboratory tests revealed low serum potassium concentration (2.6-2.9 mmol/L) and low urine osmolality (100-130 mOsm/kgH2O) in three such prior episodes. Urinary potassium/urinary creatinine ratio was 12 and 16 mmol/gCr, respectively. The patient was not under medication with laxatives, diuretics, or herbal remedies. Through an in-depth interview, we found that the patient consumed large amounts of caffeine-containing beverages daily, which included > 15 cups of coffee, soda, and various kinds of tea. After the cessation of coffee intake and concomitant intravenous potassium replacement, the symptoms rapidly resolved, and the serum potassium level normalized. CONCLUSIONS: An increased intracellular shift of potassium and increased loss of potassium in urine due to the diuretic action have been suggested to be the causes of caffeine-induced hypokalemia. In cases of recurring hypokalemia of unknown cause, high caffeine intake should be considered.

Influence of Daily Fluid Balance prior to Continuous Renal Replacement Therapy on Outcomes in Critically Ill Patients.

Positive fluid balance is a risk factor for mortality in critically ill patients, especially those requiring continuous renal replacement therapy (CRRT). However, the association between daily fluid balance and various organ impairments remains unclear. This study investigated the impacts of daily fluid balance prior to CRRT on organ dysfunction, as well as mortality in critically ill patients. We identified daily fluid balance between intensive care unit (ICU) admission and CRRT initiation. According to daily fluid balance, the time to CRRT initiation and the rate of organ failure based on the sequential organ failure assessment (SOFA) score were assessed. We recruited 100 patients who experienced CRRT for acute kidney injury. CRRT was initiated within 2 [0, 4] days. The time to CRRT initiation was shortened in proportion to daily fluid balance, even after the adjustment for the renal SOFA score at ICU admission (HR 1.14, P = 0.007). Based on the SOFA score, positive daily fluid balance was associated with respiratory, cardiovascular, nervous, and coagulation failure, independent of each initial SOFA score at ICU admission (HR 1.36, 1.26, 1.24 and 2.26, all P < 0.05). Ultimately, we found that positive fluid balance was related with an increase in the rate of 28-day mortality (HR 1.14, P = 0.012). Positive daily fluid balance may accelerate the requirement for CRRT, moreover, it can be associated with an increased risk of multiple organ failure in critically ill patients.

A Case of Osmotic Demyelination Presenting with Severe Hypernatremia.

Osmotic demyelination syndrome is a demyelinating disorder associated with rapid correction of hyponatremia. But, it rarely occurs in acute hypernatremia, and it leads to permanent neurologic symptoms and is associated with high mortality. A 44-year-old woman treated with alternative medicine was admitted with a history of drowsy mental status. Severe hypernatremia (197mEq/L) with hyperosmolality (415mOsm/kgH2O) was evident initially and magnetic resonance imaging revealed a high signal intensity lesion in the pons, consistent with central pontine myelinolysis. She was treated with 0.45% saline and 5% dextrose water and intravenous corticosteroids. Serum sodium normalized and her clinical course gradually improved. Brain lesion of myelinolysis also improved in a follow-up imaging study. This is the first report of a successful treatment of hypernatremia caused by iatrogenic salt intake, and it confirms the importance of adequate fluid supplementation in severe hypernatremia.

Role of IL-1α in cisplatin-induced acute renal failure in mice.

BACKGROUND/AIMS: For unknown reasons, caspase-1 -/- mice, protected against cisplatin-induced acute renal failure (ARF), are deficient in interleukin (IL)-1α. We thus asked whether IL-1α deficiency underlies the mechanism of protection against cisplatin-induced ARF in these mice. METHODS: Cisplatin (30 mg/kg) was injected intraperitoneally into wild-type C57BL/6 mice to produce a cisplatin-induced model of ARF. IL-1α was measured in control vehicle- and cisplatin-treated wild-type animals. We also examined whether IL-1α -/- mice were similarly protected against cisplatin-induced ARF. Additionally, infiltration of CD11b- and CD49b-positive cells, as markers of macrophages, natural killer, and natural killer T cells (pan-NK cells), was investigated in wild-type and IL-1α -/- mice. RESULTS: Compared with vehicle-treated mice, renal IL-1α increased in cisplatin-treated wild-type mice beginning on day 1. IL-1α -/- mice were shown to be protected against cisplatin-induced ARF. No significant difference in the infiltration of neutrophils or CD11b- and CD49b-positive cells were observed between wild-type and IL-1α -/- mice. CONCLUSIONS: Mice deficient in IL-1α are protected against cisplatin-induced ARF. The lack of IL-1α may explain, at least in part, the protection against cisplatin-induced ARF observed in caspase-1 -/- mice. Investigation of the protective mechanism (s) in IL-1α -/- mice in cisplatin-induced ARF merits further study.