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Chapter 046. Sodium and Water (Part 18)

Algorithm depicting clinical approach to hyperkalemia. NSAID, nonsteroidal anti-inflammatory drug; ACE, angiotensin-converting enzyme; RTA, renal tubular acidosis; TTKG, transtubular K+ concentration gradient. The appropriate renal response to hyperkalemia is to excrete at least 200 mmol of K+ daily. In most cases, diminished renal K+ loss is due to impaired K+ secretion, which can be assessed by measuring the transtubular K + concentration gradient (TTKG). | Chapter 046. Sodium and Water Part 18 Algorithm depicting clinical approach to hyperkalemia. NSAID nonsteroidal anti-inflammatory drug ACE angiotensin-converting enzyme RTA renal tubular acidosis TTKG transtubular K concentration gradient. The appropriate renal response to hyperkalemia is to excrete at least 200 mmol of K daily. In most cases diminished renal K loss is due to impaired K secretion which can be assessed by measuring the transtubular K concentration gradient TTKG . A TTKG 10 implies a decreased driving force for K secretion due to either hypoaldosteronism or resistance to the renal effects of mineralocorticoid. This can be determined by evaluating the kaliuretic response to administration of mineralocorticoid e.g. 9a-fludrocortisone . Primary adrenal insufficiency can be differentiated from hyporeninemic hypoaldosteronism by examining the renin-aldosterone axis. Renin and aldosterone levels should be measured in the supine and upright positions following 3 days of Na restriction Na intake 10 mmol d in combination with a loop diuretic to induce mild volume contraction. Aldosterone-resistant hyperkalemia can result from the various causes of impaired distal Na reabsorption or from a Cl- shunt. The former leads to salt wasting ECF volume contraction and high renin and aldosterone levels. In contrast enhanced distal Cl- reabsorption is associated with volume expansion and suppressed renin and aldosterone secretion. As mentioned above hypoaldosteronism seldom causes severe hyperkalemia in the absence of increased dietary K intake renal insufficiency transcellular K shifts or antikaliuretic drugs. Hyperkalemia Treatment The approach to therapy depends on the degree of hyperkalemia as determined by the plasma K concentration associated muscular weakness and changes on the electrocardiogram. Potentially fatal hyperkalemia rarely occurs unless the plasma K concentration exceeds 7.5 mmol L and is usually associated with profound weakness and absent P waves QRS