{'fraction_non_alphanumeric': 0.02359550561797753, 'fraction_numerical': 0.0, 'mean_word_length': 6.185483870967742, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 2, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Mechanisms in remodeling of the kidney].

Representative remodeling of the kidney in CKD includes development of glomerulosclerosis and tubulointerstitial fibrosis. Injury to glomerular endothelium, mesangium, or podocyte can induce glomerulosclerosis, although recent studies have focused on a role of podocytes due to its lack of proliferation. Development of tubulointerstitial fibrosis is multi-factorial, and includes proteinuria, chronic hypoxia, activation of the intra-renal renin-angiotensin system, imbalance of matrix production and protease activity, and epithelial-mesenchymal transdifferentiation. Optimal remodeling may induce restoration of normal kidney structure, and some potential candidates of resident renal stem cells have been proposed. Development of therapeutic approaches targeting final common pathways will open a new avenue in management of patients with CKD.