Hyperkalemia is frequently complicated in patients with advanced chronic kidney disease (CKD) because kidney is the major route of potassium excretion. Urinary potassium excretion is reduced according to the decline in glomerular filtration rate, and the risk of hyperkalemia is increased in patients with high potassium intake, advanced age, diabetes mellitus, congestive heart failure, and medications such as renin-angiotensin-aldosterone system(RAAS) blockades. On the other hand, the benefits of RAAS blockades and a high-potassium diet should be considered in CKD patients. To overcome these contradictory treatment strategies, potassium binders have emerged as new options to enhance fecal potassium excretion. In different regions of the world, four types of potassium binders are preferentially used. Whereas sodium polystyrene sulfonate (SPS) exchanges sodium for potassium, calcium polystyrene sulfonate (CPS) has the advantage of avoiding hypervolemia because it exchanges calcium for potassium. SPS was first introduced in the 1950s and used for a long time in western countries, and CPS is currently prescribed in Asia including South Korea. In contrast with the paucity of clinical studies using SPS or CPS, the recent randomized, controlled trials reported that two newer potassium binders, patiromer and sodium zirconium cyclosilicate (ZS-9), effectively and safely reduce serum potassium levels in CKD patients taking RAAS blockades. Our experiences showed that the long-term administration of a small dose of CPS was also effective and safe in treatment of chronic hyperkalemia. Further comparative trials among patiromer, ZS-9, and CPS are required to provide guides to cost-effective management of hyperkalemia in CKD patients.

• Calcium polystyrene sulfonate
• Patiromer
• Potassium
• Sodium polystyrene sulfonate
• Sodium zirconium cyclosilicate

Background: Alcoholic ketoacidosis (AKA) is known as a benign disease, but the related mortality reported in Korea is high. Acidosis and alcohol change the immunity profile, and these changes can be identified early using the delta neutrophil index (DNI). We aimed to evaluate the use of DNI and other standard laboratory parameters as predictors of prognosis in AKA patients. Methods: One hundred eighteen males with AKA were evaluated at the Wonju Severance Christian hospital between 2009 and 2014. We performed a retrospective analysis of demographic, clinical, and laboratory parameters data. Receiver operating characteristic curves (ROC) and multivariate Cox regression was used to identify renal survival and mortality. Results: Survival patients had lower initial DNI levels than non-survival patients (4.8±6.4 vs 11.4±12.5, p<0.001). In multivariate-adjusted Cox regression analysis, higher initial increased DNI (HR 1.044, 95% CI 1.003-1.086, p=0.035), and lower initial pH (HR 0.044, 95% CI 0.004-0.452, p=0.008) were risk factors for dialysis during hospitalization. Further, higher initial DNI level (HR 1.037; 95% CI 1.006-1.069; p=0.018), lower initial pH (HR 0.049; 95% CI 0.008-0.312; p=0.001) and lower initial glomerular filtration rate (GFR) (HR 0.981; 95% CI 0.964-0.999; p=0.033) were predictors of mortality. A DNI value of 4.5% was selected as the cut-off value for poor prognosis and Kaplan-Meier plots showed that AKA patients with an initial level DNI ≥4.5% had lower cumulative survival rates than AKA patients with an initial DNI <4.5%. Conclusion: Increased initial serum DNI levels may help to predict renal survival and prognosis in male AKA patients.

• Alcoholic ketoacidosis
• Prognosis
• Delta neutrophil index

A 68-year-old man presented at the emergency room with sudden blindness. The day before, he had eaten sashimi and eel and drank alcohol for dinner. He experienced nausea, vomiting, and dizziness afterward. His medical history included hypertension and diabetes, and the latter was treated with metformin. Initial laboratory tests revealed severe metabolic acidosis (lactic acidosis). Massive hydration and intravenous sodium bicarbonate replacement therapies were initiated, but severe metabolic acidosis (lactic acidosis) did not resolve, in turn, leading to hemodialysis, which decreased metabolic acidosis. The patient’s blindness improved, and his vision gradually recovered. As it is not easy to distinguish between blindness related to metformin-associated lactic acidosis (MALA) and blindness related to other causes, rapid correction of metabolic acidosis through hemodialysis might be helpful in differentiating this from of blindness from blindness related to other causes.

• Transient blindness
• Metformin-associated lactic acidosis (MALA)
• Metabolic acidosis
• Hemodialysis