In this paper titled “The Kidney Knows the Answers to the hidden Messages in body water”, the memorial lecture on retirement of Sung-Kyew Kang who laid the groundwork for establishment in the Korean Society of Electrolyte and Blood Pressure Research is summarized.
Mannitol is an osmotic diuretic agent useful in a variety of clinical conditions. This study is based on acid-base and electrolyte changes seen after the intravenous infusion of hypertonic mannitol for the prevention of cerebral edema. The study subjects were divided into 3 groups: for group A, an amount of 300-900 mL 15% mannitol was intravenously infused over the period of 60 to 90 minutes; for group B, 1,200-2,600 mL over 12 to 24 hours; and for group C, 3,200-4,900 mL over more than 24 hours. In group A, blood pH is increased from 7.43±0.07 to 7.46±0.04, and plasma HCO3- from 25.3±2.1 to 28.9±2.9 mEq/L, but plasma K＋ is decreased from 4.3±0.6 to 3.7±0.8 mEq/L. In group B, blood pH is increased from 7.42±0.02 to 7.47±0.06, and plasma HCO3- from 25.2±1.8 to 29.1±2.9 mEq/L, but plasma K＋ is decreased from 4.2±0.3 to 3.8±0.5 mEq/L. In group C, blood pH is increased from 7.41±0.01 to 7.52±0.04, and plasma HCO3- from 24.9±1.2 to 27.7±2.5 mEq/L, but plasma K＋ is decreased from 4.2±0.1 to 3.9±0.2 mEq/L. These results showed that intravenous infusion of mannitol could induce metabolic alkalosis and hypokalemia, regardless of its dose. The mannitol induced metabolic alkalosis may be due to increased renal HCO3- production.
Hypernatremia reflects a net water loss or a hypertonic sodium gain, with inevitable hyperosmolality. Severe symptoms are usually evident only with acute and large increases in plasma sodium concentrations to above 158-160 mmol/l. Importantly, the sensation of intense thirst that protects against severe hypernatremia in health may be absent or reduced in patients with altered mental status or with hypothalamic lesions affecting their sense of thirst and in infants and elderly people. Non-specific symptoms such as anorexia, muscle weakness, restlessness, nausea, and vomiting tend to occur early. More serious signs follow, with altered mental status, lethargy, irritability, stupor, and coma. Acute brain shrinkage can induce vascular rupture, with cerebral bleeding and subarachnoid hemorrhage. However, in the vast majority of cases, the onset of hypertonicity is low enough to allow the brain to adapt and thereby to minimize cerebral dehydration. Organic osmolytes accumulated during the adaptation to hypernatremia are slow to leave the cell during rehydration. Therefore, if the hypernatremia is corrected too rapidly, cerebral edema results as the relatively more hypertonic ICF accumulates water. To be safe, the rate of correction should not exceed 12 mEq/liter/day.
Rapid correction of hyponatremia is frequently associated with increased morbidity and mortality. Therefore, it is important to estimate the proper volume and type of infusate required to increase the serum sodium concentration predictably. The major common management errors during the treatment of hyponatremia are inadequate investigation, treatment with fluid restriction for diuretic-induced hyponatremia and treatment with fluid restriction plus intravenous isotonic saline simultaneously. We present two cases of management errors. One is about the problem of rapid correction of hyponatremia in a patient with sepsis and acute renal failure during continuous renal replacement therapy in the intensive care unit. The other is the case of hypothyroidism in which hyponatremia was aggravated by intravenous infusion of dextrose water and isotonic saline infusion was erroneously used to increase serum sodium concentration.
Serum consists of water (93% of serum volume) and nonaqueous components, mainly lipids and proteins (7% of serum volume). Sodium is restricted to serum water. In states of hyperproteinemia or hyperlipidemia, there is an increased mass of the nonaqueous components of serum and a concomitant decrease in the proportion of serum composed of water. Thus, pseudohyponatremia results because the flame photometry method measures sodium concentration in whole plasma. A sodium-selective electrode gives the true, physiologically pertinent sodium concentration because it measures sodium activity in serum water. Whereas the serum sample is diluted in indirect potentiometry, the sample is not diluted in direct potentiometry. Because only direct reading gives an accurate concentration, we suspect that indirect potentiometry which many hospital laboratories are now using may mislead us to confusion in interpreting the serum sodium data. However, it seems that indirect potentiometry very rarely gives us discernibly low serum sodium levels in cases with hyperproteinemia and hyperlipidemia. As long as small margins of errors are kept in mind of clinicians when serum sodium is measured from the patients with hyperproteinemia or hyperlipidemia, the present methods for measuring sodium concentration in serum by indirect sodium-selective electrode potentiometry could be maintained in the clinical practice.
A 52-year-old woman was referred to our hospital due to chronic renal failure with a 10-year history of hypertension. We found polycystic kidney disease, pulmonary tuberculosis and an aldo-sterone-producing adrenocortical mass. At this time, her serum potassium level and blood pressure were within the normal range. She refused hemodialysis and then was hospitalized because of uremic encephalopathy. On admission, her serum potassium level was normal without treatment and plasma aldosterone concentration highly elevated. She received hemodialysis, and thereafter hypokalemia developed. We then administered spironolactone, whereupon serum potassium level returned to the normal range. In this case, we thought that normokalemia was balanced hypokalemia of primary aldosteronism with hyperkalemia of chronic renal failure, and that hypokalemia developed after hemodialysis was due to an imbalanced primary aldosteronism with end stage renal disease.