Orv Hetil. 2026 Aug 2;167(31):1231-1237. doi: 10.1556/650.2026.33622. Print 2026 Aug 2.
ABSTRACT
Albuminuria is one of the most important biomarkers of chronic kidney disease and also a target that can be influenced by treatment. The amount of albumin excreted in the urine is an independent predictor of declining kidney function, cardiovascular events, and all-cause mortality. It is most easily determined based on the albumin-to-creatinine ratio (ACR) measured in the first morning urine sample; in the vast majority of cases, 24-hour urine collection is not required. The pathophysiology of albuminuria centers on damage to the glomerular filtration barrier - particularly podocytes - hemodynamic hyperfiltration, inflammation associated with tubular protein reabsorption, and activation of the renin-angiotensin-aldosterone system (RAAS). Modern four-pillar pharmacotherapy - RAS inhibitors (ACE inhibitors/ARBs), SGLT2 inhibitors, non-steroidal mineralocorticoid receptor antagonists (finerenone), and GLP1 receptor agonists in type 2 diabetes - acts on these processes through complementary mechanisms. When tailored to the degree of albuminuria and eGFR, this treatment significantly slows the progression of chronic kidney disease and reduces cardiovascular risk. Measuring and monitoring albuminuria must therefore be an essential part of daily clinical practice. Orv Hetil. 2026; 167(31): 1231-1237.
PMID:42543015 | DOI:10.1556/650.2026.33622