Table A1.
Consensus statements
| No. | Statement |
|---|---|
| A) Risk factors and risk stratification for managing hyperkalaemia in cardiorenal patients | |
| 1 | Optimizing RAASi therapy provides better outcomes for patients |
| 2 | Patients with chronic kidney disease, heart failure, or diabetes are at increased risk of hyperkalaemia |
| 3 | RAASi use is a risk factor for hyperkalaemia |
| 4 | Hyperkalaemia can be effectively managed to optimize disease‐modifying therapies, which improve morbidity, mortality, and outcomes |
| 5 | New risk prediction tools are needed if clinicians are to fully individualize risk assessment for their cardiorenal patients |
| 6 | Managing risk of hyperkalaemia should be part of the individualized care plan already in place or planned |
| 7 | There is a need for consistent thresholds for defining and treating hyperkalaemia among sub‐specialties |
| 8 | Hyperkalaemia is associated with down‐titration or discontinuation of RAASi therapy |
| 9 | When managing mild‐to‐moderate hyperkalaemia in cardiorenal patients, RAASis should be maintained due to the inherent benefit in this patient type |
| 10 | Mild‐to‐moderate hyperkalaemia should be managed without de‐escalating or discontinuing disease‐modifying drugs, such as RAASis |
| 11 | Hyperkalaemia is a known and manageable side effect of RAASi treatment |
| 12 | Hyperkalaemia should be recognized as a predictable, treatable, and manageable side effect of optimal heart failure/chronic kidney disease therapy in patients with a history or at high‐risk of hyperkalaemia |
| B) Prevention of hyperkalaemia for at‐risk cardiorenal patients | |
| 13 | For high‐risk patients currently not hyperkalaemic, preventative measures should be considered (e.g. removal of salt substitutes from diet; and considering diuretics for people with hypertension or some volume expansion) |
| 14 | For those patients who have a known history of hyperkalaemia preventing optimization of RAASi therapy, a novel K+ binder can be used to enable a trial of RAASi optimization |
| 15 | For high‐risk patients currently not hyperkalaemic, the use of a novel K+ binder can be considered when starting/up‐titrating RAASi |
| 16 | Non‐disease‐modifying therapies that cause hyperkalaemia should be avoided in patients at high‐risk of hyperkalaemia, e.g. NSAIDs, amiloride, and herbal supplements |
| 17 | A low K+ diet is often advised to help manage K+ levels, with no/little evidence to support, and is counter to a healthy diet that is beneficial to cardiorenal patients |
| 18 | In people for whom dietary restrictions may not be appropriate or desired, the use of novel K+ binders may enable a balanced diet |
| 19 | People at risk should be monitored closely with a strategy in place to manage K+ levels effectively |
| C) Correction of hyperkalaemia for at‐risk cardiorenal patients with K+ lowering therapy | |
| 20 | A reduction in emergency department visits and unplanned hospitalizations due to complications associated with hyperkalaemia should be a goal of good management |
| 21 | A goal for the management of high‐risk cardiorenal patients should be to utilize the maximum recommended dose of RAASi therapy |
| 22 | RAASi‐induced hyperkalaemia should not be considered intolerance until other strategies to reduce K+ have been exhausted |
| 23 | De‐escalation or discontinuation of RAASi therapy is associated with worse cardiovascular and renal outcomes in cardiorenal patients |
| 24 | Permanent discontinuation of RAASi therapy should only be considered as a last resort strategy for chronic hyperkalaemia |
| 25 | Hyperkalaemia should no longer be seen as a barrier to optimization of guideline‐directed therapy |
| 26 | Novel K+ binders enable guideline‐recommended RAASi dosing and the proven benefits that this brings to patients |
| 27 | Use of novel K+ binders in patients with mild hyperkalaemia can enable guideline‐recommended doses of RAASi therapy |
| 28 | RAASi use should not be de‐escalated or discontinued due to hyperkalaemia unless alternative measures of hyperkalaemia management have been optimized, including initiation of K+ binder therapy |
| 29 | Novel K+ binders can enable optimization of RAASi therapy in a similar way that antiemetics can enable optimization of chemotherapy |
| 30 | Novel K+ binders should not need to show mortality benefit; they enable RAASi therapy, which have an already proven mortality benefit |
| 31 | The use of SPS should be avoided due to concerns with GI toxicity, low compliance due to poor palatability, and is only indicated in severely oliguric or anuric patients |
| 32 | SPS should not be used in the medium‐ or long‐term as it may cause severe GI side effects, including bowel necrosis |
| D) Cross‐specialty alignment (cardiology and nephrology) | |
| 33 | Patients with cardiorenal comorbidities should be managed by a multidisciplinary team with an agreed management plan |
| 34 | Cross‐specialty alignment can enable optimal doses of disease‐modifying drugs (RAASi) to be maintained |
| 35 | Cross‐specialty management improves patient satisfaction, patient outcomes, and quality of life |
| 36 | Cross‐specialty management is a good use of resources and should improve patient outcomes |
| 37 | Enhanced communication between interdisciplinary teams could improve patient outcomes |
| 38 | Cardiology and nephrology guidelines should contain consistent recommendations for the management of hyperkalaemia |
| 39 | Collaborative care and evidence‐based decision making (based on guidelines and expert consensus) is an example of best practice and patient centered care |
GI, gastrointestinal; K+, potassium; NSAID, non‐steroidal anti‐inflammatory drug; RAASi, renin–angiotensin–aldosterone system inhibitor; SPS, sodium polystyrene sulfonate.