Approach to hyperkalemia: hyperkalemia without total body potassium excess. Spurious hyperkalemia is suggested by the absence of electrocardiographic (ECG) findings in patients with elevated serum potassium. The most common cause of spurious hyperkalemia is hemolysis, which may be apparent on visual inspection of serum. For patients with extreme leukocytosis or thrombocytosis, potassium levels should be measured in plasma samples that have been promptly separated from the cellular components since extreme elevations in either leukocytes or platelets results in leakage of potassium from these cells. Familial pseudohyperkalemia is a rare condition of increased potassium efflux from red blood cells in vitro. Ischemia due to tight or prolonged tourniquet application or fist clenching increases serum potassium concentrations by as much as 1.0 to 1.6 mEq/L. Hyperkalemia can also result from decreases in K movement into cells or increases in potassium movement from cells. Hyper-chloremic metabolic acidosis (in contrast to organic acid, anion-gap metabolic acidosis) causes potassium ions to flow out of cells. Hypertonic states induced by mannitol, hypertonic saline, or poor blood sugar control promote movement of water and potassium out of cells. Depolarizing muscle relaxants such as succinylcholine increase permeability of muscle cells and should be avoided by hyperkalemic patients. The mechanism of hyperkalemia with ^-adrenergic blockade is illustrated in Figure 3-3. Digitalis impairs function of the Na+-K+-ATPase pumps and blocks entry of potassium into cells. Acute fluoride intoxication can be treated with cation-exchange resins or dialysis, as attempts at shifting potassium back into cells may not be successful.
Approach to hyperkalemia: hyperkalemia with reduced glomerular filtration rate (GFR). Normokalemia can be maintained in patients who consume normal quantities of potassium until GFR decreases to less than 10 mL/min; however, diminished GFR predisposes patients to hyperkalemia from excessive exogenous or endogenous potassium loads. Hidden sources of endogenous and exogenous potassium—and drugs that predispose to hyperkalemia—are listed.
Approach to hyperkalemia: hyporeninemic hypoaldosteronism. Hyporeninemic hypoal-dosteronism accounts for the majority of cases of unexplained hyperkalemia in patients with reduced glomerular filtration rate (GFR) whose level of renal insufficiency is not what would be expected to cause hyperkalemia. Interstitial renal disease is a feature of most of the diseases listed. The transtubular potassium gradient (see Fig. 3-26) can be used to distinguish between primary tubule defects and hyporeninemic hypoaldostero-nism. Although the transtubular potassium gradient should be low in both disorders, exogenous mineralocorticoid would normalize transtubular potassium gradient in hyporeninemic hypoaldosteronism.
Physiologic basis of the transtubular potassium concentration gradient (TTKG). Secretion of potassium in the cortical collecting duct and outer medullary collecting duct accounts for the vast majority of potassium excreted in the urine. Potassium secretion in these segments is influenced mainly by aldosterone, plasma potassium concentrations, and the anion composition of the fluid in the lumen. Use of the TTKG assumes that negligible amounts of potassium are secreted or reabsorbed distal to these sites. The final urinary potassium concentration then depends on water reabsorption in the medullary collecting ducts, which results in a rise in the final urinary potassium concentration without addition of significant amounts of potassium to the urine. The TTKG is calculated as follows:
The ratio of (U/P)osm allows for "correction" of the final urinary potassium concentration for the amount of water reabsorbed in the medullary collecting duct. In effect, the TTKG is an index of the gradient of potassium achieved at potassium secretory sites, independent of urine flow rate. The urine must at least be iso-osmolal with respect to serum if the TTKG is to be meaningful .
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