{"id":643,"date":"2025-01-20T10:28:44","date_gmt":"2025-01-20T10:28:44","guid":{"rendered":"https:\/\/www.nordicbioscience.com\/?post_type=biomarker-solutions&p=643"},"modified":"2025-11-10T08:12:59","modified_gmt":"2025-11-10T08:12:59","slug":"diabetic-kidney-disease","status":"publish","type":"biomarker-solution","link":"https:\/\/www.nordicbioscience.com\/biomarker-solution\/renal\/diabetic-kidney-disease\/","title":{"rendered":"Diabetic Kidney Disease"},"content":{"rendered":"
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Biomarkers for diabetic kidney disease (DKD)<\/h2>\n \n\n <\/div>\n
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Diabetic kidney disease (DKD) is a major complication of diabetes and can progress to kidney failure. Despite advances in treatment, many patients continue to progress due to ongoing, often subclinical, fibrotic injury in the kidney. Conventional clinical markers such as albuminuria and eGFR are limited in detecting early fibrotic changes or reflecting treatment effects.<\/p>\n

Kidney fibrosis, a hallmark of DKD, is driven by extracellular matrix (ECM)<\/a> accumulation and remodeling, which contributes to declining kidney function. ECM-derived biomarkers offer direct insight into active fibrogenesis and fibrolysis, enabling earlier detection of disease progression.<\/p>\n <\/div>\n <\/div>\n

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Nordic ProteinFingerPrint\u2122 biomarkers advance drug development in DKD<\/h2>\n \n\n <\/div>\n
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Our biomarker assays quantify ECM fragments released into the blood or urine during active fibrogenesis and fibrolysis. These biomarkers provide mechanistic insights into kidney tissue remodeling and fibrotic activity.<\/p>\n

This enables earlier detection of disease progression and support MoA and pharmacodynamic evaluation of novel drugs. Integrating ECM biomarkers into DKD clinical trials enhances the ability to identify responders early, reduce trial duration, and increase the likelihood of demonstrating efficacy.<\/p>\n

This results in more efficient and targeted drug development, supporting faster and better-informed decision-making across all trial phases.<\/p>\n <\/div>\n <\/div>\n

\n \n Browse our DKD biomarkers \n \n <\/svg>\n \n <\/a>\n <\/div>\n <\/article>\n
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NordicPRO-C6\u2122 – Evidence as a risk marker for development and progression of kidney disease in diabetes<\/h2>\n

The risk marker potential of nordicPRO-C6\u2122 for the development and\/or progression of kidney disease has been demonstrated in multiple large, well-characterized cohorts, including people with diabetes and varying degrees of kidney disease, with or without a history of CVD.<\/p>\n

In all studies, higher levels of nordicPRO-C6\u2122 were independently associated with the risk of developing the kidney endpoint after adjustment for conventional risk factors. These results highlight the role of fibrotic processes in early kidney function decline and support the potential of nordicPRO-C6\u2122 to guide risk stratification and targeted intervention.<\/p>\n

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Markers of tissue turnover are modulated by GLP1 receptor agonist treatment in patients with type 2 diabetes<\/h2>\n

During fibrosis, elevated circulating levels of PRO-C6 and reduced urinary levels of C3M<\/a>, reflecting type III collagen degradation, are observed.<\/p>\n

Patients with DKD treated with dulaglutide in the AWARD-7 trial showed a reversal of this process, by reducing PRO-C6 and increasing C3M (Figure 2A-B).<\/p>\n

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Figure 2.<\/strong> NordicPRO-C6\u2122 and C3M biomarkers show GLP1 receptor agonist treatment in patients with type 2 diabetes in AWARD-7<\/em><\/figcaption><\/figure>\n <\/div>\n <\/div>\n<\/section>\n\n\n\n\n
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NordicPRO-C3\u2122 in patients with type 2 diabetes<\/h2>\n \n\n <\/div>\n
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During fibrosis, elevated type III collagen formation, as measured by nordicPRO-C3\u2122\/PRO-C3<\/a>, is observed. The data demonstrate that patients in the placebo group experience the greatest increase in PRO-C3 over time, reflecting sustained collagen synthesis and ongoing fibrotic activity.<\/p>\n

In contrast, both doses of the SGLT2 inhibitor result in a reduced rise in PRO-C3, with the 300 mg dose showing the strongest suppression. This indicates that collagen turnover is modulated by SGLT2 inhibitor therapy in patients with type 2 diabetes.<\/p>\n

The dose-dependent reduction in PRO-C3 suggests a pharmacological effect on pathways linked to tissue remodeling and fibrosis, supporting the concept that SGLT2 inhibitors may slow fibrotic progression in this population.<\/p>\n

Figure 3a. <\/em><\/strong>Elevated <\/em>nordicPRO-C3\u2122 modulated by SGLT2 inhibitor in patients with type 2 diabetes in the CANVAS trial<\/em><\/p>\n <\/div>\n <\/div>\n <\/article>\n

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NordicCTX-III\u2122 in patients with type 2 diabetes<\/h2>\n \n\n <\/div>\n
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During the same fibrotic process we observed with PRO-C3, we have also seen a reduction in type III collagen degradation, as indicated by lower nordicCTX-III\u2122\/CTX-III<\/a> concentrations. This reduced collagen degradation is further highlighted in the placebo group, which exhibits a smaller increase in CTX-III over time. SGLT2 inhibition with canagliflozin (both 100 mg and 300 mg) modulates this process as well, as demonstrated by a dose-dependent increase in CTX-III levels at follow-up.<\/p>\n

These results, in the context of the CANVAS trial, indicate that patients treated with canagliflozin show reversal of fibrotic remodeling\u2014not only by reducing type III collagen formation (as seen in Figure 3a) but also by enhancing its degradation (increasing CTX-III, Figure 3b). This dual modulation of collagen turnover provides mechanistic evidence that both of these biomarkers are modulated by SGLT2 inhibitors, targeting key fibrotic pathways in type 2 diabetes.<\/p>\n

Figure 3b.<\/strong> Reduced nordicCTX-III\u2122 modulated by SGLT2 inhibitor in patients with type 2 diabetes in the CANVAS trial<\/em><\/p>\n <\/div>\n <\/div>\n <\/article>\n

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About diabetic kidney disease (DKD)<\/h2>\n \n <\/div>\n
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