Background

An internal evaluation of the inpatient pharmacy order entry database (WORx) at a university hospital revealed that the nature of the reaction was documented for only 47% of patients with reported drug allergies/intolerance. Insufficient documentation of drug allergy/intolerance may result in administration of drugs that should not be prescribed. Similarly, valuable agents that should be used may not be prescribed due to an unnecessary fear of adverse drug reaction. More complete description of drug allergy/intolerance may result in more correct prescribing of medications.

Objective

Evaluate the impact of a pharmacist-driven protocol on the quality of drug allergy/intolerance documentation.

Methods

Four pre-intervention evaluations were conducted every 2 weeks documenting the completeness of drug allergy/intolerance information in the pharmacy order entry database. One week following the implementation of a pharmacist-driven protocol intended to improve the completeness of drug allergy/intolerance information, a series of 4 postintervention evaluations was repeated. Proportional analysis of pre- and postinterventional data was performed to evaluate the effectiveness of the intervention.

Results

A total of 1,686 allergies from 2,174 patients were reviewed pre and post intervention. The frequency of complete drug allergy/intolerance documentation pre intervention was 52% to 62%. Following implementation of the hospitalwide, pharmacist-driven protocol, this rate increased to 60% to 76%. Pediatric services demonstrated the most substantial improvement, increasing from 53% to 79% to 67% to 93%. Blank reaction fields decreased by 10% in both age groups.

Conclusion

A pharmacy-driven initiative intended to improve the completeness of drug allergy/intolerance documentation was associated with modest success. Other mechanisms, including electronic health record systems with computerized physician order entry and decision support, are needed to improve the completeness of drug allergy/intolerance information.

Purpose of review

Medications used frequently after kidney transplantation, including calcineurin inhibitors, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta blockers and antimicrobials, are considered the leading culprit for posttransplant hyperkalaemia in recipients with a well functioning allograft. Other risk factors include comorbidities such as diabetes, hypertension and heart failure; and consumption of a potassium-enriched diet. We review the mechanisms for hyperkalaemia following kidney transplantation that are addressed using nonpharmacological and pharmacological interventions. We also discuss emerging therapeutic approaches for the management of recurrent hyperkalaemia in solid organ transplantation, including newer potassium binding therapies.

Recent findings

Patiromer and sodium zirconium cyclosilicate are emerging potassium binders approved for the treatment of hyperkalaemia. Patiromer is a polymer that exchanges potassium for calcium ions. In contrast, sodium zirconium cyclosilicate is a nonpolymer compound that exchanges potassium for sodium and hydrogen ions. Both agents are efficacious in the treatment of chronic or recurrent hyperkalaemia and may result in fewer gastrointestinal side effects than older potassium binders such as sodium polystyrene sulfonate and calcium polystyrene sulfonate. Large-scale clinical studies have not been performed in kidney transplant patients. Patiromer may increase serum concentrations of tacrolimus, but not cyclosporine. Sodium zirconium cyclosilicate does not appear to compromise tacrolimus pharmacokinetics, although it may have a higher sodium burden.

Summary

Patiromer and sodium zirconium cyclosilicate may be well tolerated options to treat asymptomatic hyperkalaemia and have the potential to ease potassium dietary restrictions in kidney transplant patients by maintaining a plant-dominant, heart-healthy diet. Their efficacy, better tolerability and comparable cost with respect to previously available potassium binders make them an attractive therapeutic option in chronic hyperkalaemia following kidney transplantation.

Hyperkalemia is a common and potentially life-threatening complication following kidney transplantation that can be caused by a composite of factors such as medications, delayed graft function, and possibly potassium intake. Managing hyperkalemia after kidney transplantation is associated with increased morbidity and healthcare costs, and can be a cause of multiple hospital admissions and barriers to patient discharge. Medications used routinely after kidney transplantation are considered the most frequent culprit for post-transplant hyperkalemia in recipients with a well-functioning graft. These include calcineurin inhibitors (CNIs), pneumocystis pneumonia (PCP) prophylactic agents, and antihypertensives (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta blockers). CNIs can cause hyperkalemic renal tubular acidosis. When hyperkalemia develops following transplantation, the potential offending medication may be discontinued, switched to another agent, or dose-reduced. Belatacept and mTOR inhibitors offer an alternative to calcineurin inhibitors in the event of hyperkalemia, however should be prescribed in the appropriate patient. While trimethoprim/sulfamethoxazole (TMP/SMX) remains the gold standard for prevention of PCP, alternative agents (e.g. dapsone, atovaquone) have been studied and can be recommend in place of TMP/SMX. Antihypertensives that act on the Renin-Angiotensin-Aldosterone System are generally avoided early after transplant but may be indicated later in the transplant course for patients with comorbidities. In cases of mild to moderate hyperkalemia, medical management can be used to normalize serum potassium levels and allow the transplant team additional time to evaluate the function of the graft. In the immediate post-operative setting following kidney transplantation, a rapidly rising potassium refractory to medical therapy can be an indication for dialysis. Patiromer and sodium zirconium cyclosilicate (ZS-9) may play an important role in the management of chronic hyperkalemia in kidney transplant patients, although additional long-term studies are necessary to confirm these effects.