Chronic kidney disease (CKD) is one of the main chronic diseases affecting the world population due to its high prevalence and increasing morbidity. Similarly, obesity gained the interest of the scientific community as it directly or indirectly increases mortality from cardiovascular causes, and its prevalence characterizes a pandemic. The objective of this study was to investigate obesity measured by body mass index as a predictor for end-stage renal disease in the general adult population. A systematic review and meta-analysis was carried out by searching 10 databases for prospective or retrospective cohort studies, with no restrictions on the language of publication, including adults with obesity without previous renal disease and who evolved to CKD (diagnosed by estimated glomerular filtration rate below 60 mL&mac_middot;min-1&mac_middot;(1.73 m2)-1 over the follow-up period. The R software and Meta package were used for data analysis. After removing duplicates, 5431 studies were submitted to the steps of the systematic review, and 21 articles were included in the data analysis. In total, 3,504,303 patients, 521,216 with obesity, and an average follow-up time of 9.86 years were included. The relative risk of obese people for developing CKD in the random effects model was 1.81 (95%CI: 1.52-2.16). The evidence found in this meta-analysis confirmed that obese people are at higher risk of developing CKD that the non-obese population (1.81 times higher), with obesity being a priority risk factor in preventive actions.

Kidney stone disease is a major cause of chronic renal insufficiency. The role of long non-coding RNAs (lncRNAs) in calcium oxalate-induced kidney damage is unclear. Therefore, we aimed to explore the roles of lncRNAs in glyoxylate-exposed and healthy mouse kidneys using microarray technology and bioinformatics analyses. A total 376 mouse lncRNAs were differentially expressed between the two groups. Using BLAST, 15 lncRNA homologs, including AU015836 and CHCHD4P4, were identified in mice and humans. The AU015836 expression in mice exposed to glyoxylate and the CHCHD4P4 expression in human proximal tubular epithelial (HK-2) cells exposed to calcium oxalate monohydrate were analyzed, and both lncRNAs were found to be upregulated in response to calcium oxalate. To further evaluate the effects of CHCHD4P4 on the cell behavior, we constructed stable CHCHD4P4-overexpressing and CHCHD4P4-knockdown HK-2 cells. The results showed that CHCHD4P4 inhibited cell proliferation and promoted the epithelial-mesenchymal transition in kidney damage and fibrosis caused by calcium oxalate crystallization and deposition. The silencing of CHCHD4P4 reduced the kidney damage and fibrosis and may thus be a potential molecular target for the treatment of kidney stones.