Water and Electrolyte Disturbances in Acute Renal Failure

Hyperkalemia

Hyperkalemia is arguably the most dramatic, and certainly most life-threatening, of the metabolic consequences of acute renal failure in the intensive care unit (ICU) setting. Estimates for mortality associated with hyperkalemia are difficult to determine for the ICU population. The 1996 US Renal Data System survey, however, estimated a mortality rate of 1.9% for 1993. The incidence of hyperkalemia among all hospitalized patients has been reported to range between 1.1 and 10 patients per 100 hospitalized. The severity of hyperkalemia most often is determined by the concomitant severity of the pathophysiologic derangements leading to acute renal failure, and certainly, because acute renal failure typically is a multifactorial process, the distinct pathophysiology of hyperkalemia in association with this disorder often is also multifactorial.

In general, factors mediating potassium balance may be separated into external factors and internal factors. External factors refer to the renal and extrarenal factors controlling potassium balance in the serum. Internal factors are those that mediate the transcellular distribution of potassium. The body loses minimal potassium in sweat. The main extrarenal site of potassium elimination is in the colon, where mineralocorticoids may affect potassium secretion. This source of potassium loss is negligible during acute renal failure but may account for up to 10% of dietary potassium elimination among patients with chronic renal failure under the direct stimulation of increased aldosterone. By contrast, the kidneys are extremely efficient at excreting potassium loads. It is difficult to induce hyperkalemia among patients with normal renal function strictly by increasing ingestion of potassium. In patients who have persistent hyperkalemia, particularly those who are critically ill with associated acute renal failure, hyperkalemia nearly always is associated with a decreased glomerular filtration rate (GFR), a defect in tubular flow, or inadequate aldosterone activity.

Acidosis, also a prominent feature of acute renal failure, promotes potassium exit from the cells. Maintaining normal serum potassium concentration between 3.5 and 5 mEq/L depends on the balance of potassium ingestion and potassium excretion, as well as the distribution of potassium into its usual intracellular location. Because 98% of total body potassium is located intracellularly, small shifts of even as little as 1% to 2% can cause increases in serum potassium that indeed can be life threatening. These disorders are exacerbated dramatically in acute renal failure, in which ability to excrete this potassium load is decreased.

In acute renal failure, hyperkalemia results from either exogenous or endogenous sources. Medications including potassium and penicillin VK and some multivitamins, and potassium chloride administration, are common sources of exogenous intake among patients in the ICU ( Box 105.1 ). Endogenous sources are more common, however. Pathomechanisms of endogenous potassium accumulation such as tissue hypoxemia, specifically from skeletal muscle necrosis or red cell lysis, resorption of hematoma, or tumor lysis, often result in a dramatic shift of potassium from the intracellular to the extracellular space, with resultant life-threatening hyperkalemia.