Q: I know that I have to tell my patients to be careful with dietary potassium when they are taking spironolactone and ACE inhibitors or angiotensin II receptor blockers (ARBs). However, what foods are bad? What is an acceptable K+ level for patients with chronic kidney disease (CKD)?
Potassium (K) is a mineral that aids in the regulation of osmotic pressure and acid–base balance. It is essential for normal excitability of muscle tissue, in particular the cardiac muscle, and it plays a role in the conduction of nerve impulses. A safe serum potassium level for a patient with CKD is 4.0 to 5.0 mmol/L. A serum level between 5.0 and 5.5 mmol/L is considered a caution zone, requiring potassium restriction and laboratory monitoring1 (note: values and ranges vary according to lab). Prescription and OTC medications, herbs, herbals, and dietary intake affect serum potassium.
Medications such as ACE inhibitors and ARBs can cause hyperkalemia by blocking aldosterone production. The Kidney Disease Outcomes Quality Initiative (K/DOQI)2 defines hyperkalemia resulting from ACE inhibitor/ARB use as an increase of serum potassium exceeding 5.0 mmol/L. Therapeutic options to reduce serum potassium include:
Lowering the dose of the ACE inhibitor or ARB by 50%
Stopping or reducing other medications that can cause hyperkalemia
Starting or increasing the dosage of a loop diuretic; or
Reinforcing dietary restriction.2
Alkali replacement or the use of Kayexalate® (sodium polystyrene sulfonate) may also be used to treat persistent or significant increases in serum potassium.
Diets high in potassium may lead to hyperkalemia in patients with CKD, particularly in patients with a glomerular filtration rate (GFR) below 60 mL/min/1.73 m2. K/DOQI2 recommends 4 g/d of potassium for patients with CKD Stage 1 or Stage 2 and 2 to 4 g/d for patients with CKD Stage 3 or Stage 4. In the latter group, daily recommendations for potassium intake should be based on the individual patient’s serum potassium level.3
Foods containing more than 200 mg of potassium per serving are considered high-potassium foods. Fruits in this designation include avocado, bananas, cantaloupe, honeydew, kiwi, orange, mango, nectarines, bananas, and prunes. High-potassium vegetables include artichokes, dried beans (including baked beans, refried beans, and black beans), broccoli, carrots, canned mushrooms, potatoes (white or sweet), pumpkin, spinach, and tomatoes. Other foods that are high in potassium include bran products, chocolate, milk, molasses, nuts, seeds, peanut butter, salt substitutes, and yogurt.1
Leaching is a helpful way to “pull out” some of the potassium in high-potassium vegetables.4,5 For potatoes, sweet potatoes, or carrots, cut the peeled vegetable into 1/8-inch-thick slices, rinse in warm water, and soak in water 10 times the volume of the vegetables’ volume for a minimum of two hours. Rinse under warm water again, then cook the vegetable in water five times the volume of the vegetables’.
Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA
Q: How much of a bump in serum creatinine (SCr) can I expect after I start a patient on an ACE inhibitor or an angiotensin II receptor blocker (ARB)? How often should I check the patient’s SCr?
ACE inhibitors and ARBs inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the glomerular microcirculation. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by these medications reduces both intraglomerular filtration pressure and proteinuria, delaying the progression of kidney disease.6 In response to RAAS inhibition, the GFR is slightly decreased and SCr is increased, reflecting the beneficial effects of the ACE inhibitor or the ARB on renal hemodynamics.7,8 SCr may rise 10% to 30% from baseline within the first two weeks and generally stabilizes within two to four weeks.8
Patients with normal renal function initiated on an ACE inhibitor or an ARB experience a rise in SCr of about 0.2 mg/dL over a two- to three-week period, returning to baseline during week 4. Patients with abnormal renal function will have an increase in SCr of approximately 0.5 mg/dL over a four-week period.9 A progressive increase in SCr as great as 2.0 mg/dL may be seen in patients with bilateral renal artery stenosis, extensive atherosclerotic cardiovascular disease, or dehydration. In these instances, treatment with the ACE inhibitor or the ARB should be discontinued.9
Close monitoring is recommended in patients with chronic kidney disease Stage 3 through Stage 5 who are started on an ACE inhibitor or an ARB. SCr and K should be evaluated before and four weeks after initiating or titrating therapy.9 If SCr has increased by less than 0.5 mg/dL from a baseline measurement of 2.5 mg/dL or less; or if the rise in SCr is 1.0 mg/dL or less when the baseline SCr exceeds 2.5 mg/dL and K is 5.5 mEq/L or less, continue to titrate the agents, rechecking blood pressure (BP) and levels of SCr and K every four weeks until BP is at goal.8 Once SCr, K, and BP are stable, they should be rechecked annually.9
The adverse effects of ACE inhibitor/ARB use include angioedema and hyperkalemia, while only ACE inhibitors cause patients to cough.
Afix Kehinde, PharmD, College of Pharmacy, University of Illinois at Chicago; Cheryl L. Gilmartin, PharmD, Clinical Assistant Professor, Department of Pharmacy Practice, College of Pharmacy,
University of Illinois at Chicago; Clinical Pharmacist, Ambulatory Pharmacy Services, University of Illinois Hospital & Health Sciences System, Chicago
Q: Is there any science behind the use of acetylcysteine/fluid prep for cardiac catheterizations, or is that just “voodoo” medicine?
Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute kidney injury. In recent years, the use of iodinated radiocontrast medium has increased significantly, due to increased use of both percutaneous coronary interventions and CT scanning. The radiocontrast medium causes vasoconstriction, which leads to a reduction in renal blood flow, with a resulting decrease in GFR. Preexisting impaired kidney function results in increased risk due to slower clearance of the contrast materials, and the resulting prolonged exposure increases the risk for further renal injury.10
A GFR below 60 mL/min/1.73m2, volume depletion, and diabetes all increase the risk for CIN. Among patients who experience an acute kidney injury due to contrast medium, the risk for adverse outcomes increases, including early or late cardiovascular events, prolonged hospitalizations, and death. As no FDA-approved treatment yet exists for CIN, the best medicine is to try to prevent it.11
Several interventions can reduce the patient’s risk for CIN. These include IV hydration, acetylcysteine/fluid prep, selection of the safest possible type and volume of radiocontrast medium, and avoidance of nephrotoxic medications immediately before the patient’s exposure to contrast medium.
In multiple randomized clinical trials, the efficacy of IV hydration in reducing the risk for CIN has been examined. Most notably, the REMEDIAL trial12 demonstrated that IV hydration with sodium bicarbonate was superior to 0.9% hydration with normal saline. However, the largest trial to date did not show any benefit in using sodium bicarbonate, compared with normal saline.13 There is no consensus regarding the optimal hydration solution or timing, rate, or total volume of fluid administered, although the current literature does show that IV hydration in some form appears to decrease the risk for CIN.11
The recently released Kidney Disease Improving Global Outcomes (K/DIGO) Clinical Practice Guidelines for Acute Kidney Injury14 recommend IV volume expansion with normal saline or sodium bicarbonate solution. No particular regimen is recommended.
Acetylcysteine is an antioxidant with vasodilatory properties. A number of clinical trials and meta-analyses have been conducted to examine its efficacy. For instance, Kelly et al15 have suggested the benefit of acetylcysteine in the prevention of CIN, but several studies included in their meta-analysis were criticized for being of low quality. While the findings among these studies vary, none of the research teams reported any negative outcomes from the use of acetylcysteine. Although there is no definitive proof of its benefit, acetylcysteine is well tolerated, economical, and easily accessible; the general consensus is to use it.11 The K/DIGO Clinical Practice Guidelines for Acute Kidney Injury14 recommend using acetylcysteine in conjunction with isotonic solution in patients at increased risk for acute kidney injury.15
Other interventions include careful consideration of the type of radiocontrast agent to be used. Use of a low-osmolality agent such as iohexol (Omnipaque™ 350) or an iso-osmolar agent such as iodixanol (Visipaque™ 320) incurs much lower risk than do older, higher-osmolarity agents.16 In addition, although there are no scientific data to support this, withholding all potentially nephrotoxic medications (eg, ACE inhibitors, ARBs, NSAIDs, aminoglycosides, high-dose loop diuretics) prior to exposure to contrast medium is a prudent measure to reduce a patient’s risk profile.10
In summary, there are considerable conflicting data from multiple clinical studies regarding the use of acetylcysteine or IV hydration to minimize the risk for CIN. In fact, new guidelines are due to be published soon that may take a more definitive stand. Nevertheless, categorization as “voodoo” medicine seems inappropriate when an intervention appears to offer positive impact on patient care.
Kimberley Brinkman, MS, CNN, GNP-BC, Nephrology, Hypertension, and
Internal Medicine, Lawrence, MA
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.
2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.
3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.
4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.
5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.
6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy
.com/content.aspx?aid=9130075. Accessed November 21, 2012.
7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.
8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.
9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.
10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.
11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-
contrast-induced-nephropathy. Accessed November 21, 2012.
12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.
13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.
14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline
.pdf. Accessed November 21, 2012.
15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.
16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.