Angioedema and urticaria often constitute a challenge in daily clinical practice. They may either co‑occur or present as independent conditions. They are characterized by a complex pathomechanism, and their symptoms may be triggered by diverse factors. These differences are crucial for developing a successful treatment regimen. Both conditions may have an allergic origin (immunoglobulin [Ig] E and non‑IgE‑related), usually induced by histamine, or a nonallergic one, such as bradykinin‑mediated angioedema in patients with C1 inhibitor (C1‑INH) deficiency or angioedema induced by certain drugs (eg, angiotensin‑converting enzyme inhibitors). Currently, we distinguish 5 types of nonallergic angioedema: hereditary angioedema (HAE) due to C1‑INH deficiency, acquired angioedema (AAE), and angioedema induced by the renin–angiotensin–aldosterone system, all of which are mediated by bradykinin, as well as pseudoallergic angioedema and idiopathic angioedema. Bradykinin‑mediated angioedema (eg, laryngeal angioedema) may be life‑threatening because of resistance to corticosteroids and antihistamine drugs. C1‑INH concentrates are the drugs of choice in the treatment of HAE and AAE. In recent years, some new drugs have been introduced in the treatment of bradykinin‑mediated angioedema, such as bradykinin B2‑receptor antagonist, icatibant, and kallikrein inhibitor, ecallantide, which allow to improve treatment outcomes.