Conectar
Renal disease, including chronic kidney disease (CKD) and end-stage renal disease (ESRD), has a profound impact on wound healing. Multiple studies have demonstrated that renal disease leads to an increased risk of diabetic foot ulcers, the formation of unique wounds like calciphylaxis, slower wound healing and a higher risk of amputation. This review details the interrelated mechanisms by which renal disease impacts wound healing. Motor and sensory neuropathies contribute to wound formation via foot deformities and decreased sensation. Neuropathies also decrease neuropeptide release, impairing angiogenesis and inflammatory regulation. Accumulation of uremic toxins in renal disease leads to vessel wall calcification, impairing blood supply and predisposing patients to calciphylaxis. Vitamin and mineral deficiencies lead to impaired clotting, development of a chronic inflammatory state and decreased collagen production. Renal disease and its comorbidities are also associated with immune dysregulation, increasing the risk of wound infections and promoting the persistence of pro-inflammatory macrophages. While hypoxia-inducible factor-1α (HIF-1α) promotes angiogenesis under hypoxic conditions in normal wound healing, oxidative stress and chronic hypoxia in renal disease generate an environment that compromises the activity of HIF-1α. Inadequate erythropoietin response to hypoxia also leads to anaemia, further impairing oxygen delivery to wound sites. Clinically, these factors result in increased 10-year mortality for patients with DFU and CKD compared to those with DFU alone, both with and without amputation. We must utilise our understanding of the pathophysiology of impaired wound healing in renal disease to target preventative measures, optimise treatment and improve overall outcomes.
Allografts derived from live-birth tissue obtained with donor consent have emerged as an important treatment option for wound and soft tissue repairs. Placental membrane derived from the amniotic sac consists of the amnion and chorion, the latter of which contains the trophoblast layer. For ease of cleaning and processing, these layers are often separated with or without re-lamination and the trophoblast layer is typically discarded, both of which can negatively affect the abundance of native biological factors and make the grafts difficult to handle. Thus, a full-thickness placental membrane that includes a fully-intact decellularized trophoblast layer was developed for homologous clinical use as a protective barrier and scaffold in soft tissue repairs. Here, we demonstrate that this full-thickness placental membrane is effectively decellularized while retaining native extracellular matrix (ECM) scaffold and biological factors, including the full trophoblast layer. Following processing, it is porous, biocompatible, supports cell proliferation in vitro, and retains its biomechanical strength and the ability to pass through a cannula without visible evidence of movement or damage. Finally, it was accepted as a natural scaffold in vivo with evidence of host-cell infiltration, angiogenesis, tissue remodelling, and structural layer retention for up to 10 weeks in a murine subcutaneous implant model.
FreshRSS 