{"id":6644,"date":"2025-05-23T11:00:20","date_gmt":"2025-05-23T11:00:20","guid":{"rendered":"https:\/\/www.nordicbioscience.com\/?post_type=biomarker-solution&p=6644"},"modified":"2025-06-01T09:48:28","modified_gmt":"2025-06-01T09:48:28","slug":"iga-nephropathy-bergers-disease","status":"publish","type":"biomarker-solution","link":"https:\/\/www.nordicbioscience.com\/biomarker-solution\/kidney-diseases\/iga-nephropathy-bergers-disease\/","title":{"rendered":"IgA Nephropathy (Berger\u2019s Disease)"},"content":{"rendered":"
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Biomarkers for IgA nephropathy <\/h2>\n \n\n <\/div>\n
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IgA nephropathy (IgAN) is the most common form of glomerulonephritis worldwide and a leading cause of end-stage kidney disease (ESKD). IgAN is characterized by the deposition of IgA in the glomerular basement membrane. While the clinical trajectory of IgAN varies among individuals, its progression is frequently driven by subclinical and persistent kidney fibrosis. Excessive accumulation of extracellular matrix (ECM)<\/a> proteins occurs during fibrosis, which disrupts cellular organization and function within the kidney.<\/p>\n

Current clinical markers are limited in their ability to detect early fibrotic changes or to monitor dynamic treatment responses. Biomarkers offer a powerful tool to uncover dynamic disease processes and enable earlier, more informed decision-making. Biomarkers of the ECM can provide direct insight into active fibrogenesis\u2014the key mechanism underlying irreversible kidney damage.<\/p>\n <\/div>\n <\/div>\n

\n \n Biomarkers for kidney diseases \n \n <\/svg>\n \n <\/a>\n <\/div>\n <\/article>\n
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Advancing drug development in IgA nephropathy with Nordic ProteinFingerPrint\u2122 Biomarkers<\/h2>\n \n\n <\/div>\n
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Our biomarker assays quantify ECM fragments released into the blood<\/a> or urine during active fibrogenesis and fibrolysis \u2014processes central to IgAN progression. These markers provide disease-relevant insights into kidney tissue remodeling, including matrix formation, degradation, and fibrosis resolution. Unlike broad omics approaches, our biomarkers are highly specific to ECM dynamics, offering precise detection of fibrotic activity that directly reflects pathological changes in the kidney.<\/p>\n

In IgAN, progressive fibrosis is a key driver of long-term kidney function decline and a critical determinant of patient prognosis. By measuring ECM-derived biomarker<\/a>s, we can non-invasively assess the extent and activity of fibrosis, even before conventional markers show decline. This enables earlier identification of high-risk patients and more accurate tracking of pharmacodynamic effects. Integrating ECM biomarkers into IgAN clinical trials accelerates development timelines and enhances decision-making across all trial phases.<\/p>\n <\/div>\n <\/div>\n

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Increased type VI collagen deposition and nordicPRO-C6\u2122 in fibrotic kidneys<\/h2>\n \n\n <\/div>\n
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Type VI collagen is located near the basement membrane and has several bindings sites for basement membrane proteins. Upon maturation of new type VI collagen molecules produced by highly activated fibroblasts, a bioactive fragment called Endotrophin<\/a> is released. Endotrophin has pro-fibrotic, pro-tumorigenic and pro-inflammatory signalling roles. We measure nordicEndotrophin\u2122<\/a> and formation of type VI collagen with our biomarker nordicPRO-C6\u2122 (PRO-C6)<\/a>.<\/p>\n

Type VI collagen is highly upregulated in fibrotic kidney sections (Fig. 1B & 1D) compared to the non-fibrotic (Fig 1A &1C). The fragment measured by PRO-C6 is virtually absent in the non-fibrotic kidneys (Fig. 1E), while it shows a significant presence in fibrotic kidneys (Fig. 1F).<\/p>\n <\/div>\n <\/div>\n

\n \n Our publications on IgAN \n \n <\/svg>\n \n <\/a>\n <\/div>\n <\/article>\n
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Markers of tissue turnover are modulated by anti-inflammatory treatment<\/h2>\n \n\n <\/div>\n
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During fibrosis, elevated circulating levels of nordicPRO-C6\u2122<\/a> and reduced urinary levels of C3M<\/a>, reflecting type III collagen degradation, are observed.<\/p>\n

Patients with IgAN treated with budenoside in the NEFIGAN trial showed a reversal of this process, by reducing nordicPRO-C6\u2122 and increasing C3M (Figure 2).<\/p>\n

Figure 2.<\/strong> Anti-inflammatory treatment modulates tissue turnover in IgAN<\/em><\/p>\n <\/div>\n <\/div>\n <\/article>\n

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About IgA nephropathy (Berger\u2019s Disease)<\/h2>\n \n <\/div>\n
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