DOI: 10.6084/m9.figshare.26992819.v1
title: Additional file 1 of The intervention of cannabinoid receptor in chronic and acute kidney disease animal models: a systematic review and meta-analysis

description: Additional file 1: Figure S1. Quality assessment graph of the included studies: reviewers’ judgments about each risk of bias item for eligible studies based on SYRCLE’s RoB tool for animal studies. Figure S2. Forest plot for sensitivity analysis on CB1 antagonist and knockout primary outcomes including blood urea nitrogen (A), serum creatinine (B) and albuminuria (C). Figure S3. Forest plot for sensitivity analysis on CB2 agonist primary outcomes including blood urea nitrogen (A) and serum creatinine (B); CB2 antagonist and knockout primary outcomes including blood urea nitrogen (C); and serum creatinine (D). Figure S4. Forest plots for subgroup analyses of the CB1 antagonist and knockout on blood urea nitrogen. Subgroup analyses were conducted stratified by the specie is rat or mouse (A); the intervention is antagonist or genetic (B); year of study published (C), (published = 1 means published in 2011 and earlier, published = 2 means published in 2012 and later); disease model is CKD or AKI (D); and method of model establishment is diabetes, cisplatin-induce AKI, DIO, or nephrectomy uremia (E). Figure S5. Forest plots for subgroup analyses of the CB1 antagonist and knockout on serum creatinine. Subgroup analyses were conducted stratified by the specie is rat or mouse (A); the intervention is antagonist or genetic (B); year of study published (C), (published = 1 means published in 2011 and earlier, published = 2 means published in 2012 and later); disease model is CKD or AKI (D); and method of model establishment is diabetes, cisplatin-induce AKI, DIO, or nephrectomy uremia (E). Figure S6. Forest plots for subgroup analyses of the CB1 antagonist and knockout on albuminuria. Subgroup analyses were conducted stratified by the specie is rat or mouse (A); the intervention is antagonist or genetic (B); year of study published (C), (published = 1 means published in 2011 and earlier, published = 2 means published in 2012 and later); disease model is CKD or AKI (D); and method of model establishment is diabetes or genetic obesity (E). Figure S7. Forest plots for subgroup analyses of the CB2 agonist on blood urea nitrogen. Subgroup analyses were conducted stratified by the specie is rat or mouse (A); the intervention is agonist or genetic (B); year of study published (C), (published = 1 means published in 2011 and earlier, published = 2 means published in 2012 and later); disease model is CKD or AKI (D); and method of model establishment is cisplatin-induce AKI, HRS or UUO (E). Figure S8. Forest plots for subgroup analyses of the CB2 agonist on serum creatinine. Subgroup analyses were conducted stratified by the specie is rat or mouse (A); the intervention is agonist or genetic (B); year of study published (C), (published = 1 means published in 2011 and earlier, published = 2 means published in 2012 and later); disease model is CKD or AKI (D); and method of model establishment is cisplatin-induce AKI, DIO, IRI or HRS (E). Figure S9. Forest plots for subgroup analyses of the CB2 antagonist and knockout on blood urea nitrogen. Subgroup analyses were conducted stratified by the specie is rat or mouse (A); the intervention is antagonist or gene knockout (B); year of study published (C), (published = 1 means published in 2011 and earlier, published = 2 means published in 2012 and later); disease model is CKD or AKI (D); and method of model establishment is cisplatin-induce AKI or unilateral nephrectomy and D-gal aged (E). Figure S10. Forest plots for subgroup analyses of the CB2 antagonist and knockout on serum creatinine. Subgroup analyses were conducted stratified by the specie is rat or mouse (A); the intervention is antagonist or gene knockout (B); year of study published (C), (published = 1 means published in 2011 and earlier, published = 2 means published in 2012 and later); disease model is CKD or AKI (D); and method of model establishment is cisplatin-induce AKI, DIO, IRI, or HRS (E).