Moderate stepwise restriction of potassium intake to reduce risk of hyperkalemia in chronic kidney disease: A literature review

Table 3 Strategies to reduce the risk of hyperkalemia in chronic kidney disease before employing potassium dietary restriction

Strategy
Calculate the eGFR to assess the patient’s risk of hyperkalemia
Avoid hidden sources, especially potassium-based additives in processed food and salt substitutes in low-sodium processed food
Increase stool frequency to increase the proportion of potassium excreted by the gut
Identify and correct non-dietary factors that influence serum potassium levels to keep potassium within normal range: (1) Drugs that may elevate serum potassium that can and should be discontinued/avoided (NSAIDs, COX-2 inhibitors, PPIs, potassium supplements, herbal remedies); (2) Inorganic metabolic acidosis associated with advanced CKD when serum bicarbonate level < 22 mmol/L; (3) Uncontrolled DM. Insulin deficit and/or hyperglycemic hyperosmolality lower acute potassium load movement into cells; and (4) Other causes that may directly or indirectly increase potassium level include volume depletion, adrenal insufficiency, catabolic state (major cell damage, hemolysis) and GI problems (diarrhea, constipation, bleeding)
Reduce the dose of medications known to elevate serum potassium level if in use or switch to an alternative if possible: RAASi (DRA, ACEI, ARB, MRA, ARNI, ASI), β-Blockers, potassium-sparing diuretics (Amiloride, Triamterene), calcineurin inhibitors (cyclosporine, tacrolimus), digoxin, heparin, trimethoprim/co-trimoxazole
Use diuretics. The effect depends on eGFR. Dialysis patients with reasonable residual kidney function may respond to loop diuretics. Diuretics work best when diuresis is desired, or an additional antihypertensive agent is considered
Implement sick-day rules by advising patients on the risk of AKI and hyperkalemia during acute illness and on measures to avoid them. However, it can be difficult and counterproductive
Improve potassium removal in hemodialysis (thrice weekly, 4-h sessions), which is mainly by diffusion: (1) Increase session duration and frequency, increase blood and dialysate flow, increase filter surface area, correct vascular access status recirculation, and use lower dialysate potassium; (2) Higher dialysate glucose concentration triggers insulin release, which enhances cellular uptake of potassium; (3) Higher bicarbonate bath concentration increases blood pH, which enhances cellular uptake of potassium; (4) Minimize pre-dialysis exposure to drugs that increase cellular uptake of potassium such as insulin and β2-agonist inhalers because they reduce pre-dialysis potassium, which reduces dialytic removal and exacerbates potassium rebound post-dialysis
Use one of the newer generation potassium binders (patiromer or sodium zirconium cyclosilicate). However, they primarily target chronic hyperkalemia not acute postprandial hyperkalemia and may increase pill burden

Information compiled from references[1,3,5,13,15-17,45-51]. ACEI: Angiotensin converting enzyme inhibitor; AKI: Acute kidney injury ARB: Angiotensin receptor blocker; ARNI: Angiotensin receptor/neprilysin inhibitor; ASI: Aldosterone synthase inhibitor; CKD: Chronic kidney disease; COX-2: Cyclooxygenase 2; DM: Diabetes mellitus; DRA: Direct renin antagonist; eGFR: Estimated glomerular filtration rate; GI: Gastrointestinal; MRA: Mineralocorticoid receptor antagonist; NSAID: Nonsteroidal anti-inflammatory drugs; PPI: Proton pump inhibitor; RAASi: Renin angiotensin aldosterone system inhibitors.