Hypertension is a major public health concern due to its high prevalence and increased risk of cardiovascular disease and mortality. Complex traits resulting from both genetic and environmental factors affect the development of hypertension. Among environmental factors, a high salt diet is an important cause for hypertension. Humans show a heterogeneous blood pressure (BP) response to sodium intake. Although the precise mechanisms for the association between salt sensitivity and hypertension have not been fully elucidated, renal sodium handling has been considered to play a pivotal role. However, this conventional view has recently been challenged in that a third compartment, namely, skin may have a role in the regulation of sodium homeostasis. Skin is comprised of a significant portion of interstitium, which is a major extracellular fluid compartment, and its complex capillary network regulates body temperature and skin perfusion. Growing evidence indicates that local regulatory action of cutaneous blood flow as well as salt and water metabolism is associated with systemic BP control. Previous experimental studies have shown that dietary salt loading resulted in nonosmotic sodium accumulation via glycosaminoglycans and lymphatics embedded in the skin that were mediated by several endogenous factors and attenuated an increase in BP. Studies in humans have also suggested that the skin serves as a buffer system for sodium storage and that skin sodium contributes to salt sensitivity and hypertension. Thus, skin sodium storage provides the possibility of being an additional buffering system in response to salt loading and concomitant BP changes in humans.

• Skin
• Sodium
• Blood pressure
• Salt sensitivity

Autosomal dominant polycystic kidney disease is the most common hereditary renal disease affecting more than 13 million people worldwide. Renal function deteriorates as the cysts in both kidneys increase in number and size, which eventually results in end-stage kidney failure. Until recently, conservative management for chronic kidney disease such as blood pressure control, low sodium diet, adequate water intake, and weight control were known for the only treatment of polycystic kidney disease. However, the introduction of disease-modifying drug has led to the new paradigm shift in the management of polycystic kidney disease. Tolvaptan, the vasopressin V2 receptor antagonist, has been introduced to the patients with large kidneys since it can inhibit cyclic adenosine monophosphate, attenuates cyst growth, and delays renal failure. This article reviews the two important practical issues in the management of polycystic kidney disease: blood pressure and water balance. Firstly, the article will review the pathogenesis of high blood pressure in polycystic kidney disease and will demonstrate the current up-to-date management plan for blood pressure control. Secondly, this article will explain the mechanism of Tolvaptan on the treatment of polycystic kidney disease and its possible adverse effect on water and sodium balance.

• Autosomal dominant polycystic kidney disease
• Blood pressure
• Vasopressin V2 receptor antagonist
• Water balance

Nicorandil is an anti-anginal drug that is commonly used in the treatment of ischemic heart disease. Nicorandil acts as a nitrate donor and ATP-sensitive potassium channel agonist, inducing coronary artery vasodilation. Potassium efflux through ATP-sensi- tive potassium channels activated by nicorandil can cause refractory hyperkale- mia, particularly in patients with chronic kidney disease (CKD). Here, we report the case of an 85-year-old man who presented with severe refractory hyperkalemia, despite proper medical management. His serum potassium level increased from 4.96 to 7.21 mEq/L 7 days after restarting nicorandil. Hyperkalemia resolved shortly after discontinuation of nicorandil, which was presumed to be the offending drug. Previously, a few cases reported nicorandil-induced hyperkalemia called potassium channel syndrome in patients with CKD, and hyperkalemia can be reversed by ceasing nicorandil or using sulfonyl urea drugs. Given that CKD patients may have several contributing factors to this adverse event, clinicians should be aware of the risk of nicorandil-induced hyperkalemia, and medication review and drug discontinuation should be considered.

• Nicorandil
• Hyperkalemia
• Chronic kidney disease
• Potassium channel syndrome

The Korean Society for Electrolyte and Blood Pressure Research, in collaboration with the Korean Society of Nephrology, has published a clinical practice guideline (CPG) document for hyponatremia treatment. The document is based on an extensive evidence- based review of the diagnosis, evaluation, and treatment of hyponatremia with the multidisciplinary participation of representative experts in hyponatremia with methodo- logist support for guideline development. This CPG consists of 12 recommendations (two for diagnosis, eight for treatment, and two for special situations) based on eight detailed topics and nine key questions. Each recommendation begins with statements graded by the strength of the recommendations and the quality of the evidence. Each statement is followed by rationale supporting the recommendations. The committee issued condi- tional recommendations in favor of rapid intermittent bolus administration of hypertonic saline in severe hyponatremia, the use of vasopressin receptor antagonists in heart failure with hypervolemic hyponatremia, and syndrome of inappropriate antidiuresis with moderate to severe hyponatremia, the individualization of desmopressin use, and strong recommendation on the administration of isotonic fluids as maintenance fluid therapy in hospitalized pediatric patients. We hope that this CPG will provide useful recommendations in practice, with the aim of providing clinical support for shared decision-making to improve patient outcomes.

• Special Article: Hyponatremia