A definition of 'disease modification' for kidney disease is long overdue. Here, we propose three key criteria for disease modification in immune-mediated glomerulonephritis and podocytopathies: minimizing disease activity, preventing loss of kidney structure and function, and reducing treatment-related toxicity. To be considered a disease-modifying anti-nephropathic drug (DMAND), a drug must fulfil all three criteria, hence the DMAND status of a drug may not be clear at the time of regulatory approval. Notably, the aspect of chronic kidney disease (CKD) in immune-mediated kidney diseases must be considered and treated separately, e.g. renin-angiotensin system inhibitor is a DMAND for the CKD aspect but not for the immune disease itself. Defining DMANDs is an ambitious goal but one that may help to set the priorities for future treatment strategies in immune-mediated kidney disease. This may mean much more rapid tapering or even avoidance of unselective, non-targeted immunosuppressive agents, which carry considerable short (teratogenicity) and long term risks (malignancies). The criteria proposed here set a high bar for 'disease modification' in immune-mediated kidney disease. Inevitably, this must dictate altered priorities with the focus for new therapeutic agents and strategies shifting from solely reduction of proteinuria to preservation of GFR and attenuation of decline, whilst also eliminating long-term toxicity.