1. Figure 7 Overview of crystal deposition in the
different compartments of the kidney and segments of the nephron
Figure 7 | Overview of crystal deposition in the different compartments of the kidney and segments of the nephron. a | Particles such as free immunoglobulin light chains enter the proximal tubule in the ultrafiltrate. They are taken up by proximal tubular cells and can lead to proximal tubule injury. b | Cystal or plug formation in the distal collecting tubule also cause tubular injury. c | Interstitial hydroxyapatite deposits at the inner medulla around the tips of the loops of Henle can form Randall plaques, which serve as a papillary nidus for the formation of calcium oxalate (CaOx), urate, apatite or cystine stones inside the renal pelvis (panel d). e | The thick ascending limb of the loop of Henle is the site of Tamm–Horsfall protein (uromodulin) secretion, which promotes the formation of casts and crystal plugs at this site. Such plugs and casts can lead to tubule obstruction further downstream in the nephron. f | Urine concentration and acidification in the collecting ducts promotes crystallization of many minerals as well as uric acid. g | The duct of Bellini — the terminal part of the collecting duct — is a preferred site of hydroxyapatite plug formation, which obstructs the outflow of numerous of nephrons that feed into this collecting duct. h | Diffuse crystallization with formation of microcrystals can occur in the interstitial compartment and can also affect the cortex. This process activates interstitial dendritic cells to produce inflammatory mediators.
Mulay, S. R. & Anders, H.-J. (2017) Crystal nephropathies: mechanisms of crystal-induced kidney injury
Nat. Rev. Nephrol. doi: /nrneph