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When do (or don't) you administer drugs to patients on hemodialysis?

Ryan, E. James BSN, RN, CDN

doi: 10.1097/01.NURSE.0000413613.21436.8c
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If a patient is scheduled for hemodialysis, should you hold antihypertensive medication beforehand? How about antibiotics? This article answers these and other common questions about drug administration for patients on hemodialysis.

E. James Ryan is an acute care hemodialysis nurse at Lakeland Regional Medical Center in Lakeland, Fla.

The author has disclosed that he has no financial relationships related to this article.

HEMODIALYSIS (HD) REPLACES some of the basic functions of healthy kidneys such as removing excess fluid and filtering waste products. Because of this filtering effect, special considerations are needed when patients on HD are taking certain medications, including antihypertensive drugs and antibiotics. This article reviews when you should or shouldn't administer these drugs. Even with multiple comorbidities, patients in renal failure can enjoy a high quality of life, and you play a key role through safe and effective medication administration.

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Renal function problems

One of the kidneys' functions is to maintain a proper balance of calcium and phosphorus (see Functions of the kidney). Complications that can occur when a patient has chronic kidney disease (CKD) include fluid and electrolyte imbalances, acid-base imbalances, bone disease (disorders of mineral metabolism), cardiovascular problems, disorders associated with an accumulation of nitrogenous waste products, anemia and coagulation disorders, and impaired drug elimination (see Complications of CKD).1 A patient with CKD will most likely be taking drugs to treat these complications, such as antihypertensives and phosphate binders.

When a patient has CKD, abnormalities in calcium and phosphorus metabolism occur because of impaired phosphate elimination and vitamin D activation (see Balancing act).1 The most effective treatment for a calcium and phosphorus imbalance related to CKD is the use of phosphate binders (such as calcium carbonate, sevelamer carbonate, or lanthanum carbonate) and dietary modifications such as a low-phosphorus diet.

Phosphate binders reduce the amount of phosphorus that's absorbed from food. This interaction of binder and food occurs in the gastrointestinal tract. So to be effective, binders must be taken with all meals and even snacks.2 For patients on HD, hold phosphate binders only if they're not eating or are hypercalcemic.

Although coordinating a patient's phosphate binder with meals can be difficult, it's critically important. To make this easier:

  • Be aware of the phosphate binders your patient is taking and increase your knowledge of proper binder use.
  • Teach your patients to ask for their binders when their meals are served.
  • Coordinate with the pharmacy and nutritional services to ensure the availability of binders with meals.
  • Monitor serum calcium and phosphate levels.
  • Monitor for signs and symptoms of hypo/hypercalcemia and hypo/hyperphospatemia (for more information, see “Balancing act: Calcium & phosphorus” in the January issue of Nursing2012).
  • Report any abnormalities to the healthcare provider.3
Figure. C

Figure. C

One of the primary ways the body eliminates medications and their metabolites is via renal excretion. Patients with end-stage renal disease (ESRD) who are on HD have altered pharmacokinetics, including absorption, distribution, and elimination of drugs.

The use of large amounts of phosphate-binding antacids interferes with the absorption of some drugs. Many drugs are bound to plasma proteins, including albumin, for distribution through the body. The portion of the drug that's unbound is available to act at various receptor sites, and it's free to be metabolized. Because many CKD patients have fewer plasma proteins, particularly albumin, the body ultimately has less protein-bound drug and greater amounts of free drug. During metabolism, some drugs form intermediate metabolites that are toxic if not eliminated. Due to the decreased filtering of the kidneys, drug dosages may need adjustment for people with CKD.1

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Maintain BP

Many mechanisms can produce hypertension in people with CKD. Increased vascular volume, increased peripheral vascular resistance, increased activity of the renin-angiotensin-aldosterone system, and decreased renal vasodilator prostaglandins are all complications of CKD resulting in hypertension.1

Effective management of BP can be challenging in patients with ESRD. HD removes excess fluid and reduces circulating volume, but symptomatic hypotension may require early discontinuation of HD prior to reaching optimal treatment goals. So should antihypertensive drugs be withheld to prevent hypotension that may occur due to fluid losses during HD?

Unfortunately, there's no simple answer because a one-size-fits-all approach doesn't work. Some ESRD patients require as many as four different classifications of antihypertensives.4 Others may still make urine and not require fluid removal, yet require HD to clear toxins from the blood.

When forming your patient's care plan, ask the dialysis nurse about any hypotensive episodes or persistent hypertension during or after treatment. Provide this information to the patient's healthcare provider and ask for recommendations about holding any or all of the patient's antihypertensive drugs before HD. A thorough assessment and care coordination will produce better results for the patient than a generalized, nonspecific approach.

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Prevent infection

Patients with ESRD have a heightened risk for infection and require prompt treatment with antibiotics for bacterial infections.5 According to the 2009 report of the United States Renal Data Systems, infections were the cause for 37.5% of hospitalizations for patients on HD.6 Early recognition and treatment of bacterial infections with antibiotics can preserve HD access.7

Infection is commonly seen in patients with CKD. High levels of urea and metabolic waste decrease the efficiency of the immune response to infection. This alteration includes decreased granulocyte count, impaired humoral and cell-mediated immunity, defective phagocyte function, dysfunctional acute inflammatory response, and delayed-type hypersensitivity responses. Also, the skin and mucosal barriers, the body's first line of defense, may be impaired.1

Because maintaining therapeutic serum levels of antibiotics is critical, an adjustment in therapy may be indicated depending on the type of dialyzer and the specific drug. Some antibiotics won't be dialyzed out and should be routinely given. Other antibiotics are easily removed by HD and should be held before HD; a supplemental replacement dose may be prescribed to be given after HD.8 Information on drug dializability isn't found in many nursing drug books, but can be found online.9 The hospital pharmacist is also an excellent source of information.

If your patient is scheduled for HD and is prescribed antibiotics before treatment, consult with the healthcare provider regarding the best times to administer these drugs. Make a note in the patient's care plan or electronic medical record and pass along the information in the shift report.

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Avoid complications

Deciding when to administer a patient's drugs on days HD is scheduled is an important part of treatment. Knowing when to give—and when to hold—drugs will help avoid complications.

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Functions of the kidney1

The kidney regulates many functions necessary for homeostasis. It controls the composition and pH of body fluids by way of reabsorption and elimination of sodium, potassium, hydrogen, chloride, and bicarbonate ions. In addition, it eliminates metabolic wastes such as urea, uric acid, and creatinine.

Renal excretion is one of the main ways that drugs and their metabolites are removed from the body. The kidney regulates the osmolarity of the extracellular fluid through the effect of antidiuretic hormone, and BP through the renin-angiotensin-aldosterone mechanism. The skeletal system's metabolic functions rely on the kidney to activate vitamin D and to regulate calcium and phosphate. New red blood cell formation occurs, in part, through the release of erythropoietin from the kidney.

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Balancing act1

Dysfunction of calcium and phosphorus metabolism results from altered phosphate elimination and vitamin D activation. As renal function decreases, phosphate isn't removed adequately from the blood, resulting in higher levels of serum phosphate. Because calcium and phosphate are inversely regulated, higher phosphate levels result in a decrease in serum calcium levels. When this happens, parathyroid hormone is released in an effort to boost serum calcium levels. Calcium is then reabsorbed from bone. Over time, as renal function continues to decline, this pathway is destructive to the skeletal system and body organs.

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REFERENCES

1. Porth CM. Essentials of Pathosphysiology. Philadelphia, PA: Lippincott Williams & Wilkins; 2011.
2. Burrows-Hudson S, Prowant B. Nephrology Nursing Standards of Practice and Guidelines for Care. Pitman, NJ: American Nephrology Nurses' Association; 2005.
3. National Kidney Foundation. Elements of Excellence: A Team Approach to Chronic Kidney Disease Care. New York, NY: National Kidney Foundation; 2008.
4. Eskridge MS. Hypertension and chronic kidney disease: the role of lifestyle modification and medication management. Nephrol Nurs J. 2010;37(1):55–60, 99.
5. Molzahn A, Butera E. Contemporary Nephrology Nursing: Principles and Practice. 2nd ed. Pitman, NJ: American Nephrology Nurses' Association; 2007.
6. U.S. Renal Data System (USRDS). USRDS 2009 Annual Data Report: Atlas of Chronic Kidney Disease and End-stage Renal Disease in the United States. Bethseda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Disorders; 2009.
7. Deaver K. Preventing infections in hemodialysis fistula and graft vascular access. Nephrol Nurs J. 2010;37(5):503–506.
8. Fine R, Nissenson A. Handbook of Dialysis Therapy. 4th ed. Philadelphia, PA: Elsevier Saunders; 2008.
© 2012 Lippincott Williams & Wilkins, Inc.