Briefly describe the renal tubular handling of potassium and list the physiological consequences of hypokalemia and hyperkalemia.

Outline:

·        Distribution of potassium in body

·        Secretion and reabsorption by renal tubules

·        Cellular mechanism of potassium transport

·        Physiological consequences of hypokalemia and hyperkalemia

Essay:

            Potassium is one of the most abundant cations in the body and is critical for many cell functions. The body contains between 3000-4000 mEq of K⁺. 99% (150 mEq/L) resides within the intracellular fluid and only 2% (3.5-5.0 mEq/L) within the extracellular fluid (ECF). Despite wide fluctuations in dietary K⁺ intake, its concentration in cells and (ECF) remains constant. The kidneys maintain the amount of potassium in the body by adjusting renal K⁺ excretion to match dietary K⁺ intake.

            The kidneys play the major role in maintaining potassium balance. The kidneys excrete 90% to 95% of the K⁺ ingested in the diet. Because K⁺ is not bound to plasma proteins, it is freely filtered by the glomerulus. The proximal tubule reabsorbs 67% of the filtered K⁺ and the Henle’s loop absorb 20%. The distal tubule and the collecting duct are able to either absorb or secrete K⁺. When K⁺ intake is normal, K⁺ is secreted. A rise in dietary K⁺ intake increases K⁺ secretion. A low-potassium diet activates K⁺ reabsorption along the distal tubule and collecting duct.

            Reabsorption of K⁺ in the proximal tubule is a passive process. The reabsorption of sodium, bicarbonate and organic anions establishes a transtubular osmotic gradient that provides the driving force for passive reabsorption of water by osmosis. Potassium is carried along in the reabsorbed fluid by the solvent drag.

            Secretion from blood into tubular fluid is a two-step process involving K⁺ uptake across the basolateral membrane by Na⁺- K⁺-ATPase and diffusion of K⁺ from the cell into the tubular fluid. The operation of the Na⁺- K⁺-ATPase creates a high intracellular [K⁺], which provides the driving force for K⁺ exit across the apical membrane through K⁺ channels. The three major factors that control the rate of K⁺ secretion by the distal tubule and the collecting duct are the activity of the Na⁺- K⁺-ATPase, the driving force for K⁺ movement across the apical membrane and the permeability of the apical membrane to K⁺. Regulation of K⁺ excretion is achieved mainly by alterations in K⁺ secretion by principal cells of the distal tubule and collecting duct.

            The precise balance of K⁺ between the ECF and ICF establishes a cell’s resting membrane potential. K⁺ is critical for the excitability of nerve and muscle cells. Cardiac arrhythmias are produced by both hypokalemia and hyperkalemia. Hypokalemia hyperpolarizes the membrane potential, thereby reducing excitability, leading to muscular weakness and eventual cardiac failure.

            Hyperkalemia is a very dangerous and potentially lethal condition because of its effects on the heart. As the plasma K⁺ levels rises, the first change in the ECG is the presence of tall peaked T waves, a manifestation of altered repolarization. Hyperkalemia causes the membrane potential to become less negative, which decreases the excitability by inactivating fast Na channels. At higher K⁺ levels, paralysis of the atria and prolongation of the QRS complexes occur. Ventricular arrhythmias may develop. The fibers eventually become unexcitable, and the heart stops in diastole.