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).
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Chapter 046. Sodium and Water (Part 18) 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 200mmol 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 + concentrationgradient (TTKG). A TTKG (Na+ intake dose is 10 mL of a 10% solution infused over 2–3 min. The effect begins withinminutes but is short-lived (30–60 min), and the dose can be repeated if no changein the electrocardiogram is seen after 5–10 min. Insulin causes K+ to shift intocells by mechanisms described previously and will temporarily lower the plasmaK+ concentration. Although glucose alone will stimulate insulin release fromnormal pancreatic βcells, a more rapid response generally occurs when exogenousinsulin is administered (with glucose to prevent hypoglycemia). A commonlyrecommended combination is 10–20 units of regular insulin and 25–50 g ofglucose. Obviously, hyperglycemic patients should not be given glucose. Ifeffective, the plasma K+ concentration will fall by 0.5–1.5 mmol/L in 15–30 min,and the effect will last for several hours. Alkali therapy with intravenous NaHCO 3can also shift K+ into cells. This is safest when administered as an isotonic solutionof 3 ampules per liter (134 mmol/L NaHCO3) and ideally should be reserved forsevere hyperkalemia associated with metabolic acidosis. Patients with end-stagerenal disease seldom respond to this intervention and may not tolerate the Na+ loadand resultant volume expansion. When administered parenterally or in nebulizedform, β2-adrenergic agonists promote cellular uptake of K+ (see above). The onsetof action is 30 min, lowering the plasma K+ concentration by 0.5 to 1.5 mmol/L,and the effect lasts 2–4 h. Removal of K+ can be achieved using diuretics, cation-exchange resin, ordialysis. Loop and thiazide diuretics, often in combination, may enhance K +excretion if renal function is adequate. Sodium polystyrene sulfonate is a cation-exchange resin that promotes the exchange of Na+ for K+ in the gastrointestinaltract. Each gram binds 1 mmol of K+ and releases 2–3 mmol of Na+. When givenby mouth, the usual dose is 25–50 g mixed with 100 mL of 20% sorbitol toprevent constipation. This will generally lower the plasma K+ concentration by0.5–1.0 mmol/L within 1–2 h and last for 4–6 h. Sodium polystyrene sulfonate canalso be administered as a retention enema consisting of 50 g of resin and 50 mL of70% sorbitol mixed in 150 mL of tap water. The sorbitol should be omitted fromthe enema in postoperative patients due to the increased incidence of sorbitol-induced colonic necrosis, especially following renal transplantation. The mostrapid and effective way of lowering the plasma K+ concentration is hemodialysis.This should be reserved for patients with renal failure and those with severe life-threatening hyperkalemia unresponsive to more conservative measures. Peritonealdialysis also removes K+ but is only 15–20% as effective as hemodialysis. Finally,the underlying cause of the hyperkalemia should be treated. This may involvedietary modification, correction of metabolic acidosis, cautious volume expansion,and administration of exogenous mineralocorticoid. Further Readings Adrogue HJ, Madias NE: Hypernatremia. N Engl J Med 342:1493, 2000[PMID: 10816188] ———: Hyponatremia. N Engl J Med 342:1581, 2000 Berl T, Verbalis J: Pathophysiology of water metabolism, in Brenner &Rectors The Kidney, 7th ed, BM Brenner (ed). Philadelphia, Saunders, 2004 Cohn JN et al: New guidelines for potassium replacement in clinicalpractice: A contemporary review by the National Council on Potassium in ClinicalPractice. Arch Intern Med 160:2429, 2000 [PMID: 10979053] Goldszmidt MA, Iliescu EA: DDAVP to prevent rapid correction inhyponatremia. Clin Nephrol 53:226, 2000 [PMID: 10749304] Greenberg A, Verbalis JG: Vasopressin receptor antagonists. Kidney Int69:2124, 2006 [PMID: 16672911] Gross P: Treatment of severe hyponatremia. Kidney Int 60:2417, 2001[PMID: 11737620] Harrigan MR: Cerebral salt wasting syndrome. Crit Care Clin 17:125, 2001[PMID: 11219225] Mount DB: Disorders of potassium balance, in Brenner & Rectors TheKidney, 7th ed, BM Brenner (ed). Philadelphia, Saunders, 2004 Nielsen S et al: Aquaporins in the kidney: From molecules to medicine.Physiol Rev 82:205, 2002 [PMID: 11773613] Warnock DG: Genetic forms of renal potassium and magnesium wasting.Am J Med 112:235, ...