A patient with chronic kidney disease has a serum potassium of 6.8 mEq/L. Nerve conduction studies early in the rise show increased excitability, but further elevation leads to weakness and eventually conduction block. The final conduction failure is best explained by:

• A Hyperpolarization of the resting membrane potential beyond the threshold for sodium channel activation
• B Persistent depolarization causing inactivation of voltage-gated sodium channels ✓
• C Increased activity of the sodium-potassium pump raising the threshold potential
• D Widening of the absolute refractory period due to delayed potassium channel closure

Explanation

Elevated extracellular potassium shifts the resting membrane potential toward zero, initially bringing it closer to threshold and increasing excitability. As depolarization progresses, the inactivation gates of voltage-gated sodium channels close and fail to reset, leaving the membrane inexcitable despite being closer to threshold. Option A describes the opposite direction of resting potential change. Sodium pump activity would actually help restore gradients, and potassium channel kinetics are not the limiting factor here.

Reference: Guyton and Hall Textbook of Medical Physiology, 14th ed.

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