Diabetic kidney disease is a major cause of morbidity and mortality in both type 1 and 2 diabetes mellitus. It is strongly associated with cardiovascular disease, particularly heart failure, the incidence of which (SGLT-2) is about 15-fold greater with diabetic kidney disease. All-cause mortality in those with diabetic kidney disease is nearly 20–40 times higher than in those without it. Many people with diabetes, particularly type 2, and kidney impairment die from cardiovascular disease well before they progress to end-stage kidney disease. Nevertheless, diabetic kidney disease is the most common single cause of end-stage kidney disease worldwide. Suboptimal glycaemic control and higher blood pressure are particularly important risk factors for developing diabetic kidney disease. Over a lifetime, diabetic kidney disease (any stage) occurs in approximately 30–35% of people with types 1 and 2 diabetes. The disease can usually be detected many years before the development of advanced kidney failure, by identifying raised urinary albumin excretion. Early detection allows time for a multifactorial approach with intensive treatment of glycaemic control, including use of sodium-glucose co-transporter 2 inhibitors, blood pressure reduction (renin–angiotensin system inhibitors as first-line treatment), diet and lifestyle modifications, and lipid-lowering therapy to reduce the associated morbidity and mortality.

Diabetic kidney disease (DKD) is the leading cause of kidney failure and is associated with substantial risk of cardiovascular disease, morbidity, and mortality. Traditionally, DKD prevention and management have focused on addressing hyperglycemia, hypertension, obesity, and renin-angiotensin system activation as important risk factors for disease. Over the last decade, sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists have been shown to meaningfully reduce risk of diabetes-related kidney and cardiovascular complications. Additional agents demonstrating benefit in DKD such as non-steroidal mineralocorticoid receptor antagonists and endothelin A receptor antagonists are further contributing to the growing arsenal of DKD therapies. With the availability of greater therapeutic options comes the opportunity to individually optimize DKD prevention and management. Novel applications of transcriptomic, proteomic, and metabolomic/lipidomic technologies, as well as use of artificial intelligence and reinforced learning methods through consortia such as the Kidney Precision Medicine Project and focused studies in established cohorts hold tremendous promise for advancing our understanding and treatment of DKD. Specifically, enhanced understanding of the molecular mechanisms underlying DKD pathophysiology may allow for the identification of new mechanism-based DKD subtypes and the development and implementation of targeted therapies. Implementation of personalized care approaches has the potential to revolutionize DKD care.

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Mishita
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Journal of Clinical & Experimental Nephrology