A predefined chronic kidney disease risk score using proteomic measurements accurately predicted the development of persistent microalbuminuria, according to data presented at EASD 2013.
“In patients with type 2 diabetes and in a normoalbuminuria at baseline, we see the classifier as an independent predictor of the patients progressing to microalbuminuria,” Morten Lindhardt, MD, of the Steno Diabetes Center in Gentofte, Denmark, said during his presentation. “We also see that urinary proteomics may identify the patients for future development of diabetic nephropathy.”
This post-hoc analysis looked at 740 patients from the DIRECT-Protect 2 study. The mean age of the patients was 57 years, with mean diabetes duration of 8.9 years, mean BMI of 29.5 and mean blood pressure of 134 mm Hg/74 mm Hg, and 497 of the patients were treated for hypertension. The researchers included patients with type 2 diabetes who were normoalbuminuric and normotensive, and they excluded patients in need of renin-angiotensin-aldosterone system (RAAS) blocking agents and those with proliferative retinopathy.
“These patients are very healthy at the time of inclusion,” Lindhardt said.
In a “significant shift,” the researchers used all 273 urinary peptides to determine each patient’s CKD risk score, he said. The patients were followed for a mean of 4.7 years.
Persistent microalbuminuria developed in 92 patients, and the predetermined CKD risk score predicted microalbuminuria development, independent of treatment, age, sex, BP, baseline HbA1c and diabetes duration.
Confirmed microalbuminuria was “hard to hit” because the primary endpoint was persistent microalbuminuria in three of four samples.
The researchers also stratified the patients based upon treatment — placebo vs. candesartan — and showed that patients treated with placebo had a higher risk of progression than those on candesartan (HR=2.1 vs. 1.6, respectively). Currently, Lindhardt said, it is speculation that candesartan affected progression.
The upcoming EU PRIORITY study will use this model to identify patients at high risk and put them on additional RAAS blockers to see whether that prevents the development of diabetic nephropathy.
In a poster presented by a Frederik Persson, MD, similar results were shown in patients with type 1 diabetes.
For more information:
Lindhardt M. Oral presentation #93.
Persson F. Abstract #1186. Both presented at: the 49th Annual Meeting of the European Association for the Study of Diabetes; Sept. 24-27, 2013; Barcelona, Spain.
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