Prediction and Management of Hyperkalemia across the Spectrum of Chronic Kidney Disease

Department of Medicine, ASH Comprehensive Hypertension Center, The University of Chicago Medicine, Chicago, IL 60637
Seminars in Nephrology (Impact Factor: 2.94). 05/2014; DOI: 10.1016/j.semnephrol.2014.04.008

ABSTRACT Hyperkalemia commonly limits optimizing treatment to slow Stage 3 or higher CKD progression. The risk of hyperkalemia is linked to dietary potassium intake, level of kidney function, concomitant diseases that may affect potassium balance such as diabetes and use of medications that influence potassium excretion. The risk predictor for developing hyperkalemia are an estimated glomerular filtration rate of <45 ml/min/1.73m2 and a serum potassium level >4.5 mEq/L in the absence of blockers of the renin angiotensin aldosterone system (RAAS). Generally, monotherapy with RAAS blockers does not increase risk substantially unless hypotension or volume depletion occur. Dual RAAS blockade involving any combination of an ACEI, ARB, renin inhibition or aldosterone receptor blocker markedly increases risk of hyperkalemia in those with Stage 3 or higher CKD. Moreover, dual RAAS blockade further reduces albuminuria by 25-30% over monotherapy, it has failed to demonstrate a benefit on CKD progression or cardiovascular outcome, thus, not indicated in such patients due its marked increase in hyperkalemia potential. While sodium polystyrene resins exist to manage hyperkalemia in those requiring therapy that increase serum potassium, they are not well tolerated. Newer more predictable, better tolerated polymers to bind potassium are on the horizon and may be approved within the next one to two years.

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    ABSTRACT: Apparent treatment-resistant hypertension (aTRH) is defined as blood pressure (BP) >140/90 mmHg despite three different antihypertensive drugs including a diuretic. aTRH is associated with an increased risk of cardiovascular events, including stroke, chronic renal failure, myocardial infarction, congestive heart failure, aortic aneurysm, atrial fibrillation, and sudden death. Preliminary studies of renal nerve ablation as a therapy to control aTRH were encouraging. However, these results were not confirmed by the Symplicity 3 trial. Therefore, attention has refocused on drug therapy. Secondary forms of hypertension and associated conditions such as obesity, sleep apnea, and primary aldosteronism are common in patients with aTRH. The pivotal role of aldosterone in the pathogenesis of aTRH in many cases is well recognized. For patients with aTRH, the Joint National Committee-8, the European Society of Hypertension, and a recent consensus conference recommend that a diuretic, ACE inhibitor, or angiotensin receptor blocker and calcium channel blocker combination be used to maximally tolerated doses before starting a 'fourth-line' drug such as a mineralocorticoid receptor (MR) antagonist. Although the best fourth-line drug for aTRH has not been extensively investigated, a number of studies summarized here show that an MR antagonist is effective in reducing BP when added to the standard multi-drug regimen.
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