Obesity and chronic kidney disease (CKD) are converging global epidemics with a complex, bidirectional relationship. Obesity directly drives de novo CKD and accelerates its progression via hemodynamic, metabolic, inflammatory, and neuroendocrine pathways culminating in obesity-related glomerulopathy. While advanced and dialysis-dependent CKD exhibit an "obesity paradox, " where higher BMI correlates with survival, this is largely driven by reverse causality, survival bias, and BMI's failure to capture true body composition. Emerging metrics like the Body Roundness Index (BRI) demonstrate that central adiposity remains harmful in dialysis populations, with no paradox found in early CKD or kidney transplantation, adding a second, under-recognised dimension to this dual burden. Beyond progression, obesity significantly increases technical risks for core procedures: kidney biopsies, vascular access creation, peritoneal catheter insertion, and kidney transplantation. This review translates these procedural risks into practical optimization strategies, establishes that intentional, structured weight loss in obese CKD individuals is not associated with the excess mortality attributed to unintentional weight loss in CKD. An expanded overview of body composition assessment methods, contemporary and emerging pharmacotherapy including dual incretin agonists, and bariatric and metabolic surgery, including its role and timing relative to kidney transplantation, is presented, alongside a research agenda emphasising precision obesity management and artificial intelligence-assisted risk prediction.
