Potassium plays various important roles in water balance, neuronal maintenance, blood vessel extension, arrhythmia prevention, and blood pressure maintenance. Its deficiency leads to arrhythmia, loss of appetite, convulsions, constipation, fatigue, asthenia, and hypoglycemia etc. Although foods are primary prevention for diseases, there are few literatures on dietary potassium in both Korea and U.S. Also, its acceptable level is not determined yet and is only recommended 2,000-3,000 mg and 1,500-5,000 mg for adult in Korea and US, respectively. The main source of potassium is vegetables such as calabash, fruit, sea tangle, yeast, bean, and banana etc. Therefore, this is to provide information on dietary potassium in order to prevent the risk of cardiovascular disease and guide for patients who suffer from kidney related disease etc.

• Potassium
• Dietary intake

The maintenance of potassium balance depends primarily on excretion by the kidney. The regulated secretion of potassium normally accounts for most of urinary potassium excretion. Potassium transport along the nephron has two main features : the ubiquitous Na,K-ATPase defines basolateral membranes, whereas site-specific potassium transporters are responsible for the apical transport. Two different cell types mediate secretion and reabsorption of potassium. Principal cells secrete potassium, whereas intercalated cells, especially those belonging to the subfamily of β-intercalated cells, reabsorb potassium. The factors that stimulate potassium secretion by the principal cells include (1) increased extracellular fluid potassium concentration (2) increased aldosterone and (3) increased tubular flow rate. One factor that decreases potassium secretion is increased hydrogen concentration (acidosis). In situations associated with severe potassium depletion, there is a cessation of potassium secretion and net reabsorption of potassium. It is believed that H,K-ATPase transport mechanism located in the luminal membrane of the cortical and outer medullary collecting duct cells reabsorb potassium in exchange for hydrogen secreted into the tubular lumen.

• Potassium balance
• Principal cells
• Intercalated cells
• Aldosterone
• Acidosis
• Na
• K-ATPase
• H

Plasma potassium level is maintained within a narrow normal range through a transcellular shift between intracellular and extracellular space, and through renal excretion. Internal potassium balance via transcellular shift is affected by several hormones and physiologic conditions. Catecholamine through β2-adrenergic receptor stimulates cellular uptake of potassium and defends against increments in plasma potassium concentration. Insulin promotes cellular potassium uptake in muscle, liver and adipose tissues. Changes of acid-base status affects internal potassium balance as well as renal potassium excretion. Other physiologic and pathophysiologic conditions such as exercise or tissue damage also have acute effects on the distribution of potassium. Although a lot of medications are the causes of hyperkalemia, drugs that alter internal potassium balance would appear to be uncommon. Understanding the physiology of potassium distribution is important to evaluate and manage the patients with potassium disturbances including hypokalemia or hyperkalemia.

• Internal potassium balance
• Catecholamine
• β2-adrenergic receptor
• Insulin
• Na
• K-ATPase
• Acid-base
• Organic acid
• Hypertonicity

Potassium balance and serum potassium level are maintained until very late in chronic kidney disease (CKD), mainly because of an increase in renal and colonic excretion. Hyperkalemia may develop earlier in the course of CKD in patients with hyporeninemic hypoaldosteronism. Hyperkalemia in CKD patients may occur in association with excess dietary potassium intake, constipation or prolonged fasting. It may also be seen with the use of potassium-sparing diuretics, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and non-steroidal anti-inflammatory drugs. If suspected, pseudohyperkalemia should be excluded to avoid unnessary treatments. Acute treament of hyperkalemia in marked or symptomatic hyperkalemia, particularly in the presence of electrocardiographic changes includes combinations of intravenous calcium gluconate and infusions of glucose and insulin with or without bicarbonate. In patients with kidney failure, dialysis may be required. Either asymptomatic and mild hyperkalemia or chronic hyperkalemia in CKD patients can be treated by potassium restriction, a loop diuretic at high doses, and cation exchange resin.

• Potassium
• Hyperkalemia
• Chronic kidney disease

All urate transport occurs across the renal epithelial cells of the proximal tubule. Most of the filtered urate is reabsorbed in the S1 segment of the early proximal tubule. This is followed by tubular secretion in the S2 segment of the proximal tubule and approximately 50% of the filtered urate flows back into the tubular lumen. Most of the secreted urate undergoes postsecretory reabsorption that occurs predominantly in the last S3 segment of the proximal tubule. Recently, four proteins that transport urate have been identified at the molecular level. These proteins are an electrogenic urate uniporter, urate transporter/channel (UAT), two members of the organic anion transporter (OAT) family, OAT1 and OAT3, and a protein with some homology to OAT4, designated URAT1.

• Uric acid
• Urate transporters
• Proximal tubule

Although the obstruction is potentially reversible with treatment, marked and sometimes prolonged diuresis and natriuresis associated with an impaired ability to concentrate the urine may follow relief of the obstruction. Various factors contributing to the postobstructive Although the obstruction is potentially reversible with treatment, marked and sometimes prolonged diuresis and natriuresis associated with an impaired ability to concentrate the urine may follow relief of the obstruction. Various factors contributing to the postobstructive diuresis and natriuresis have been suggested, including decreases of tubular sodium reabsorption, retention of urea and expansion of extracellular fluid volume. Tubular damage as a consequence of obstruction may occur one or more nephron segments and may result in decreased reabsorption of filtrate. The discovery of aquaporin (AQP) membrane water channels and sodium (co)transporters and channels provided insight, at the molecular level, into the fundamental physiology and pathophysiology of water and sodium balance. In addition, recent studies have shown that the kidney per se is also a site of production and release of atrial natriuretic peptide (ANP). The locally synthesized ANP may act in a paracrine manner to increase the urinary excretion of sodium and water. In this context, an altered regulation of ANP in the kidney may result in an altered urinary excretion. The combined interactions of multiple independent mechanisms are thought to be involved in the pathogenesis of postobstructive diuresis and natriuresis. We examined the changes of AQP water channels, sodium (co)transporters and natriuretic peptide system in obstructed kidneys. The expression of AQP water channels and sodium transporters was decreased in the obstructed kidneys, which may at least in part account for the urinary concentration defect associated with postobstructive diuresis and natriuresis. In addition, the postobstructive natriuresis was associated with an enhanced renal expression of ANP mRNA and an increased urinary excretion of ANP. The plasma dendroaspis natriuretic peptide (DNP) level was increased following an experimental ureteral obstruction. The urinary excretion of DNP was increased along with the postobstructive diuresis. An enhanced activity of DNP system may in part play a role in mediating the postobstructive diuresis

• Aquaporins
• Sodium transporters
• Natriuretic peptides
• Ureteral obstruction

Chronic renal failure, which has an increased single nephron glomerular filtration rate in remnant kidney, is known to cause characteristic structural alterations in renal tubule epithelia in association with impaired urinary concentration and deranged urinary sodium excretion. This mini-review will deal with the changes in the renal expression of aquaporins (AQPs) and sodium transporters for elucidating the underlying cellular and molecular mechanisms for the urinary abnormalities of decreased urinary concentration and increased urinary sodium excretion.

• Kidney Failure
• Chronic
• Aqauporins
• Membrane transport proteins

Hypernatremia in adults is a common problem that has been associated with mortality rates ranging from 40% to 60%. Clinical characteristics of hospital-acquired hypernatremia have not been well defined. To evaluate the difference between hypernatremia on admission and hospital-acquired hypernatremia, we reviewed 50 patients with hypernatremia at Hanyang University Guri Hospital for 51-month period from 1 March 2001 to 31 May 2005. We defined hypernatremia as serum sodium concentration more than or equal to 150 mEq/L. Hospital-acquired hypernatremia was more frequently (62%) observed than hypernatremia on admission (38%). Patients with hypernatremia on admission (73.1±11.7 years) were older than those with hospital-acquired hypernatremia (59.3±13.7 years). Only 30% of patients was alert in mental status. Fifty six percent of all patients (n=50) had neurologic problem such as head injury, cerebral infarction or hemorrhage. Admission hypernatremia was caused by severe dehydration due to no access to water. Seventy seven percent of hospital-acquired hypernatremic patients were associated with diuretics and solute diuresis. Treatments of hospital-acquired hypernatremia were also delayed and inadequate. Rate of correction in 6, 12, 24 hours after peak sodium level was not different between hypernatremia on admission and hospital-acquired hypernatremia. More rapid correction during 6 hours in hypernatremia on admission was associated with higher mortality (survival 2.1±0.7 mEq/L, death 7.1±4.9 mEq/L, p<0.05). Higher mortality was observed in patients with more severe renal insufficiency. In conclusion, hospital-acquired hypernatremia is largely avoidable by clinical attention and appropriate therapy. Patients with cerebrovascular events or renal insufficiency, patients treated with diuretics or hypertonic solute need careful fluid management and the close monitoring of blood sodium level. Particularly, the rate of correction during the first 6 hours should be also managed very cautiously in hypernatermia on admission.

• Hypernatremia
• Hospital-acquired
• Rate of correction