ALBUMINURIA is a major risk factor for kidney damage and is one of the first signs of chronic kidney disease (CKD). Patients with CKD have abnormally elevated levels of albumin in their urine. Therefore, reducing albumin is a desirable therapeutic target. In the recent DAPA-CKD clinical trial, scientists aimed to evaluate the effects of the sodium-glucose co-transporter-2 inhibitor dapagliflozin on albuminuria in patients with CKD, with and without diabetes.
The study involved 4,304 participants from over 20 countries receiving either 10 mg of dapagliflozin or placebo once daily. The individuals had a follow-up at a median of 2.4 years. The trial defined CKD as a urinary albumin-to-creatinine ratio (UACR) between 200 and 5,000. From these participants, the median UACR was 949. Due to the positive, efficacious results, the trial was stopped early. The prespecified analysis showed that dapagliflozin decreased the UACR by 29.3% in comparison to the placebo. Additionally, there was a reduction of UACR by 35.1% in patients with Type 2 diabetes compared with 14.8% reduction in patients without diabetes.
Further analysis demonstrated that dapagliflozin increased the likelihood of regression in patients with a UACR of 300 or more in 3,860 patients. Moreover, dapagliflozin decreased the risk of progression in UACR stage. At Day 14 of treatment with dapagliflozin, greater reductions in UACR were significantly linked with a reduction in estimated glomerular filtration rate.
Hiddo Heerspink, University Medical Centre Groningen, the Netherlands, expressed his concluding thoughts on the study: “The similar efficacy in patients with and without Type 2 diabetes on clinical outcomes suggests that part of dapagliflozin’s protective effect is mediated through pathways unrelated to albuminuria reduction.”
Finally, Katherine Tuttle, University of Washington, School of Medicine, Seattle, USA, shared the direction future work should take: “More education, co-ordination, and multidisciplinary/multispecialty care models are needed.”