| (i) Anemia and CKD-mineral and bone disorder should be treated, using the existing guidelines |
| for the general CKD population. |
| (ii) Dietary salt restriction, diuretics, and adequate ultrafiltration in dialysis patients are key |
| strategies to control fluid overload and HF symptoms. |
| (iii) Beta-blockers (bisoprolol, metoprolol, and carvedilol) can reduce mortality and |
| should, therefore, be recommended to all patients, unless contraindicated or not |
| tolerated. Treatment must be started at very low doses and carefully uptitrated and |
| Monitored, to avoid worsening HF, bradycardia, and hypotension. |
| (iv) ACEIs can reduce mortality and should be indicated to all patients with HF and CKD |
| stages 1–3, unless contraindicated or not tolerated. In those with CKD stages 4 and 5, |
| caution is required, considering that the benefits of ACEIs on survival have not been |
| proven and that there is a higher risk of adverse events. |
| (v) Alternatively, ARBs can be used, particularly in patients who develop cough or |
| angioedema from ACEIs. Dual therapy with ACEIs and ARBs can be considered in |
| resistant cases. |
| (vi) When using RAAS inhibitors (particularly dual therapy), careful dose titration and |
| clinical monitoring are required to prevent serious side effects, such as hypotension, |
| hyperkalemia, and acute kidney injury. |
| (vii) In stage 3 CKD patients, aldosterone antagonists may be tried but should be used |
| with great caution and at very low doses, while closely monitoring potassium levels. |
| They should be avoided in patients with CKD stages 4 and 5. |
| (viii) The addition of digoxin may be considered in selected cases with poorly controlled |
| symptoms of HF or with high-ventricular rate atrial fibrillation, in the presence of |
| optimal-dose therapy with diuretics, RAAS inhibitors, and beta-blockers. Using very |
| low doses and monitoring of serum digoxin concentration are required. |
