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. Author manuscript; available in PMC: 2021 Nov 1.
Published in final edited form as: Semin Nephrol. 2020 Nov;40(6):574–585. doi: 10.1016/j.semnephrol.2020.12.004

Figure 2. Proposed mechanism of uric acid-induced acute kidney injury.

Figure 2.

Hyperuricemia may increase the risk for AKI via both crystal-independent and crystal-dependent pathways. Hyperuricemia appears to affect renal hemodynamics, causing renal vasoconstriction, impaired autoregulation and increased glomerular pressure, while it can also affect tubular function, leading to inflammatory responses, oxidative stress, epithelial mesenchymal transition, and apoptosis. Crystalluria may also contribute to tubular injury.

Key: RBF: renal blood flow; RAS: renin-angiotensin-aldosterone system; NO: nitric oxide; VSMC: vascular smooth muscle cell; VEC: vascular endothelial cell; GFR: glomerular filtration rate; MCP-1: monocyte chemoattractant protein-1; ICAM: intercellular adhesion molecule; PTC: proximal tubular cell; TLR: Toll-like receptor.