Glomerular hyperfiltration represents a defining feature of renal dysfunction in the context of obesity and diabetes mellitus. The term ‘hyperfiltration nephropathy’ has been used to describe obesity-related glomerulopathy and other adaptive nephropathies, emphasizing the central role of hyperfiltration in the pathogenesis of these conditions. Recent clinical trials have demonstrated that sodium-glucose cotransporter-2 inhibitors or glucagon-like peptide-1 agonists are effective in reducing glomerular hyperfiltration and provide additional renal protection when used in conjunction with renin-angiotensin blockade in diabetic nephropathy. This review assesses the current evidence for a cause-and-effect relationship between physical forces related to hyperfiltration and the development of chronic kidney disease beyond diabetes. It also considers potential therapeutic interventions that could be offered to patients.