Effects of sodium-glucose cotransporter 2 inhibitors, mineralocorticoid receptor antagonists, and their combination on albuminuria in diabetic patients.

AIMS: Diabetes mellitus (DM) is the leading cause of chronic kidney disease. Albuminuria is associated with an increased risk of cardiovascular mortality. Sodium-glucose cotransporter 2 inhibitors (SGLT2-Is) and mineralocorticoid receptor antagonists (MRAs) protect against albuminuria; however, their combined effects on albuminuria are unclear. We performed a network meta-analysis to investigate the effects of SGLT2-Is, MRAs and their combination on albuminuria in type 2 DM. METHODS: We systematically searched PubMed, Medline, EMBASE and the Cochrane Library from inception up to 20 November 2022. We selected randomized control and crossover trials that compared MRAs, SGLT2-Is, MRAs + SGLT2-Is, or a placebo in patients with type 2 DM with a urinary albumin-creatinine ratio (UACR) ≥30 mg/g creatinine. The primary outcome was the change in the UACR. RESULTS: This meta-analysis analysed 17 studies with 34 412 patients. The use of combination treatment with SGLT2-Is and MRAs was associated with lower albuminuria compared with the use of SGLT2-Is, MRAs, or the placebo alone [mean difference (95% CI): -34.19 (-27.30; -41.08), -32.25 (-24.53; -39.97) and -65.22 (-57.97; -72.47), respectively]. Treatment with SGLT2-Is or MRAs alone caused a significant reduction in UACR compared with the placebo [mean difference (95% CI): -31.03 (-28.35; -33.72) and -32.97 (-29.68; -36.27), respectively]. The effects of MRAs on the UACR are comparable with those of SGLT2-Is. Sensitivity analyses showed similar results. CONCLUSION: Combination therapy with SGLT2-Is and MRAs was associated with lower albuminuria in patients with type 2 DM compared with monotherapy with SGLT2-Is or MRAs alone.

Flecainide-induced myalgias and weakness: a rare adverse reaction.

Flecainide is a class 1C antiarrhythmic, which is known to cause several cardiac and non-cardiac adverse reactions. We report a case of a 62-year-old woman with atrial fibrillation who presented with generalised myalgias and intermittent chest heaviness after being started on flecainide. She had undergone her third cardiac ablation 1 week prior to presentation and was subsequently started on flecainide 150 mg two times per day. On physical examination, she had diminished reflexes and diffuse calf tenderness. Her blood tests demonstrated an increased erythrocyte sedimentation rate and C reactive protein, but otherwise normal infectious and autoimmune labs. Her ECG showed normal sinus rhythm. A Naranjo score of 7 suggested flecainide as a probable cause of her myalgias. The patient's symptoms started to normalise within 24 hours of discontinuation of flecainide. Our case highlights that myalgias are a potential rare adverse effect that should be considered in patients prescribed flecainide.