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Kidney Week

Abstract: SA-PO148

Low Dose Anti-Thromboxane Reduces Urinary Albumin in Patients with Diabetic Kidney Disease

Session Information

Category: Diabetic Kidney Disease

  • 602 Diabetic Kidney Disease: Clinical

Authors

  • Steiness, Eva, Serodus, Oslo, Norway
  • Brun, Nikolai, Serodus, Oslo, Norway
  • Skarsfeldt, Torben, Serodus, Oslo, Norway
  • Derwahl, Karl Michael, Ikfe Berlin, Berlin, Germany
Background

Thromboxane facilitates coagulation but is also a pro-inflammatory endogenous agent.
SER150 is an oral, small molecule with a novel dual mode of action that inhibits thromboxane synthase and simultaneously blocks the thromboxane receptor. SER150 inhibited thrombocytes agglutination both in healthy and diabetic patients. Studies in healthy volunteers and in patients with Type 2 diabetes doses from 0,375 to 2,5 mg/kg body weight, SER150 dose-dependently increased bleeding time from insignificant values and up to 294 seconds after the highest dose investigated. However, a dose of 0,16 mg/kg insignificantly attenuated bleeding time compared to placebo and insignificantly reduced agglutination of ex-vivo stimulated (U16466) thrombocytes for few minutes.

Methods

A double-blind, placebo-controlled, clinical study included 49 diabetic patients with HbA1c of 7,08 mmol/mol, blood pressure of 132/75 mmHg and urine albumin > 30 mg/g creatinine (ACR). The patients were treated with SER150 at doses of either 15 mg BID or 30 mg BID (0,16mg/kg or 0,32mg/kg BID) for 4 weeks.

Results

SER150 treatment caused ACR gradually to decrease during the 4 weeks and was statistically significant reduced from baseline (p<0,02 and p<0.04 respectively). 25% of patients with micro-albuminuria at baseline (ACR >30 £300) became normo-albuminuric during the 4 weeks on SER150 treatment. All patients with macro-albuminuria (ACR >300) experienced a decrease in urinary albumin and 45% shifted from macro-albuminuria to micro-albuminuria.

Conclusion

These findings suggest two different sites of action with different dose-efficacy relation of the anti-thromboxane agent SER150. One at the thrombocytes and one at different, still unknown, site of action in the kidney at sites essential for the damage of renal filtration barrier in patients with diabetic kidney disease.

The aim of the next clinical study is to confirm SER150 induced decrease in ACR in patients with diabetes and macro-albuminuria (ACR >500). Furthermore, to demonstrate that decrease in ACR is maintained over time (6 month) with a dose of 15 mg BID. The primary endpoint will be a composite of ACR and a group of relevant renal surrogate markers.

Funding

  • Commercial Support – Serodus ASA, Norway