ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: PO0588

Effects of the SGLT2 Inhibitor Dapagliflozin on Proteinuria in Non-Diabetic Patients with CKD (DIAMOND): A Randomized Double-Blind Cross-Over Trial

Session Information

Category: CKD (Non-Dialysis)

  • 2102 CKD (Non-Dialysis): Clinical, Outcomes, and Trials


  • L Heerspink, Hiddo Jan, Department of Clinical Pharmacy and Pharmacology, University Medical Centre Groningen, Groningen, Netherlands
  • Dekkers, Claire, Department of Clinical Pharmacy and Pharmacology, University Medical Centre Groningen, Groningen, Netherlands
  • Cherney, David, Department of Medicine, Division of Nephrology, University Health Network and University of Toronto, Toronto, Ontario, Canada

Sodium glucose co-transporter 2 (SGLT2) inhibition decreases albuminuria and reduces the risk of kidney disease progression in patients with type 2 diabetes. These benefits are unlikely mediated by improvements in glycemic control alone. We therefore examined the renal effects of the SGLT2 inhibitor dapagliflozin in patients with proteinuric kidney disease without diabetes.


A multicenter double-blind placebo controlled 6-week crossover study was performed in six hospitals in the Netherlands, Canada, and Malaysia. Patients (18-75 years old), without diagnosis of diabetes, 24-h urinary protein excretion >500 and ≤3500 mg/24h and estimated glomerular filtration rate (eGFR) ≥25 ml/min/1.73m2 on stable renin angiotensin system blockade were included. Participants were randomly assigned to one of the two consecutive treatment periods of first placebo and then dapagliflozin 10 mg/day or vice versa. The primary outcome was percentage change from baseline in 24-h proteinuria. The main secondary outcome was change in iohexol measured GFR (mGFR).


Fifty-eight patients were screened of whom 53 patients were randomized. Median baseline proteinuria was 1110 mg/24h (IQR 730, 1560) mg/24h; mean mGFR was 58.3 ml/min/1.73m2 (SD 23). The difference in mean proteinuria change from baseline between dapagliflozin and placebo was 0.9% (95% CI: -16.6, 22.1; p=0.93). Compared to placebo, mGFR changed with dapagliflozin treatment by -6.6 ml/min/1.73m2 (95% CI: -9.0, -4.2; p<0.0001) at week 6, which was completely reversible within 6 weeks after dapagliflozin discontinuation. Differences between dapagliflozin and placebo in body weight, systolic blood pressure and hematocrit were -1.5 kg (95% CI: -3.0, -0.03; p=0.0455), -3.6 mmHg (95% CI: -7.6, 0.4; p=0.0775) and 0.02 L/L (95% CI: 0.01, 0.03; p<0.0001). HbA1c did not change. The number of patients with adverse events during dapagliflozin treatment (n=17; 32.1%) and during placebo treatment (n=13; 25.0%) was similar. No hypoglycemic events were reported.


Six week treatment with dapagliflozin does not affect proteinuria in patients with chronic kidney disease without diabetes, but did induce acute and reversible decline in mGFR, body weight reduction, and increased hemoconcentration.


  • Commercial Support