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<p>The PromarkerD test accurately predicts diabetic kidney disease. We aimed to determine whether PromarkerD and/or its constituent biomarkers would also identify an increased risk of distal sensory polyneuropathy (DSPN) complicating type 2 diabetes (T2D). We selected 160 community-based adults without baseline DSPN (mean age 69 years, 56% males), 80 of whom were free of DSPN after four years and 80 who developed DSN based on the vibration perception threshold. Baseline plasma apolipoprotein A-IV (ApoA4), CD5 antigen-like protein (CD5L) and insulin-like growth factor binding protein 3 (IBP3) concentrations were measured and PromarkerD risk scores were generated. Logistic regression modelling assessed associations between PromarkerD risk and its component proteins and incident DSPN. At Year 4, 77 of 151 with valid data (51%) had developed DSPN. The PromarkerD area under the receiver operating characteristic curve was 0.53 (95% CI 0.43–0.62). The odds ratio for the PromarkerD score for identifying incident DSPN was 0.97 (95% CI 0.82–1.16, <i>P</i> = 0.76), with similar non-significant results for plasma ApoA4, CD5L, and IBP3. PromarkerD and its constituent protein concentrations, each with some preclinical or epidemiological evidence of an association with DSPN, did not predict incident DSPN over 4 years of follow-up. These data support microangiopathy-specific pathophysiological mechanisms in T2D.</p>

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Assessment of biomarkers associated with renal decline for prediction of incident distal sensory polyneuropathy in type 2 diabetes

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月17日

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  • Kirsten Peters,
  • Timothy M. E. Davis,
  • Isabella A. Joubert,
  • Martin K. Mead,
  • Angelo Bautista,
  • Wendy A. Davis

摘要

The PromarkerD test accurately predicts diabetic kidney disease. We aimed to determine whether PromarkerD and/or its constituent biomarkers would also identify an increased risk of distal sensory polyneuropathy (DSPN) complicating type 2 diabetes (T2D). We selected 160 community-based adults without baseline DSPN (mean age 69 years, 56% males), 80 of whom were free of DSPN after four years and 80 who developed DSN based on the vibration perception threshold. Baseline plasma apolipoprotein A-IV (ApoA4), CD5 antigen-like protein (CD5L) and insulin-like growth factor binding protein 3 (IBP3) concentrations were measured and PromarkerD risk scores were generated. Logistic regression modelling assessed associations between PromarkerD risk and its component proteins and incident DSPN. At Year 4, 77 of 151 with valid data (51%) had developed DSPN. The PromarkerD area under the receiver operating characteristic curve was 0.53 (95% CI 0.43–0.62). The odds ratio for the PromarkerD score for identifying incident DSPN was 0.97 (95% CI 0.82–1.16, P = 0.76), with similar non-significant results for plasma ApoA4, CD5L, and IBP3. PromarkerD and its constituent protein concentrations, each with some preclinical or epidemiological evidence of an association with DSPN, did not predict incident DSPN over 4 years of follow-up. These data support microangiopathy-specific pathophysiological mechanisms in T2D.