Month: July 2022

The future of the kidney with a simple urine test

Autosomal dominant polycystic kidney disease (ADPKD) is a hereditary condition that causes the development of cysts in the kidneys. This condition affects millions of people worldwide and can lead to kidney failure if left untreated. One of the biggest challenges in treating ADPKD is identifying biomarkers that can predict disease progression and response to treatment.

Our Renal and Cardiovascular Research team showed that biomarkers of collagen remodeling measured in urine and circulation at baseline are associated with the rate of decline in kidney function in patients with ADPKD. In the study (DIPAK-1), we measured the effect of lanreotide on patients with stage 3 chronic kidney disease. The following demographics were involved:

To assess the effect of lanreotide, the team selected a number of biomarkers that were best suited to assess the effect of the drug on interstitial matrix turnover and basement membrane turnover. We have selected a number of biomarkers:

• PRO-C3, measuring collagen type III formation in serum and urine (interstitial matrix turnover)
• C3M, measuring collagen type III degradation in serum and urine (interstitial matrix turnover)
• PRO-C6, measuring collagen type VI formation in serum and urine. Also measures the release of the bioactive fragment endotrophin, associated with pro-fibrotic and pro-inflammatory processes (interstitial matrix turnover)
• LG1M, measuring Laminin gamma 1 degradation in serum and urine (basement membrane turnover)

The data we found implies that fibrogenesis may be an important pathophysiological process driving ADPKD disease progression. In addition, the use and development of drugs that interfere with fibrogenesis may be promising to halt disease progression in ADPKD. However, we still need to validate in an independent cohort, preferably in early-stage disease.

The findings of the study are significant because they offer new insights into the potential for biomarkers to predict disease progression in ADPKD. This information may help clinicians to identify patients who are at risk of developing kidney failure and to develop more effective treatments to slow or halt disease progression.

We have shown that biomarkers of collagen remodeling are associated with the rate of decline in kidney function in patients with ADPKD. These findings suggest that fibrogenesis may be an important pathophysiological process driving ADPKD disease progression and that the use of drugs that interfere with fibrogenesis may be promising to halt disease progression. Further research is needed to validate these findings in an independent cohort, but the results of this study offer new hope for patients with ADPKD.

We believe it is time to put kidney fibrosis more in the center – even in diseases where other aspects (such as kidney volume) are the focus of attention. At Nordic Bioscience, we have the tools to do so. 

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How much load can the cartilage in the joints absorb?

Mechanical loading is an essential part of the function and maintenance of the joint. Despite the importance of intermittent mechanical loading, this factor is rarely considered in preclinical models of cartilage, limiting their translatability.

The cartilage of the joints of patients with osteoarthritis is negatively affected in their capacity to absorb the load. Despite this pivotal role, mechanical load is rarely a component of translational drug screening assays when testing novel OA treatments.

We showcased our novel translational cartilage loading model in a publication in Applied Sciences.

In a culture plate format well suited for lead candidate screening we investigated the effect of growth factors on ex-vivo cartilage remodeling and the interaction with dynamic intermittent loading. Cartilage remodeling was investigated in the presence of IGF-1 or TGF-β1, as well as a TGF-β receptor 1 (ALK5) kinase inhibitor and assessed with biomarkers for type II collagen formation and fibronectin degradation (FBN-C).

Amongst others, PRO-C2 has shown that not only does mechanical loading preserve cartilage, but it also positively modulates the effect of known growth factors, such as IGF-1.

Screening potential drug candidates in physiological loading conditions could provide a more accurate translation to push forward the urgent medical need for better treatments of osteoarthritis.

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Which organ decompensates first?

The race to organ death is not a show you want to be a part of. The main cause of death in patients with metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD) is liver and cardiovascular complications, while disease activity remains a major feature of liver fibrosis progression.

Metabolic associated steatohepatitis (MASH, formerly NASH) is a consequence of metabolic problems including obesity and is often characterized by multiple organ failure, with hepatic cirrhosis driving organ decompensation. But what is the true event and death rate of MASH patients? What do they suffer from and why do they die? And how do we know which organ decompensates first? 

The answer is simple.

It is essential to measure the functions of different organs and their activity/progression rates, including the liver, heart, and kidney.

Can we thus assume that for MASH patients, the smallest problem is the liver-related event? Yes and no. The liver is important, but we need to consider the patient as a normal human – with not just a liver, but a heart, kidney, and other organs. These patients are also in the highest risk group for osteoarthritis (OA) and inflammatory bowel diseases (IBD), albeit that is not the focus of this blog article.

We can conclude that it is central to measure several organ functions and their activity/progression rates – which has been the exact focus for Nordic in the recent period. Our technologies, biomarkers, and drug development projects are perfectly aligned for this.

For example, PRO-C3 (also available on the high-precision Roche Cobas platform), a biomarker of type III collagen formation, is an excellent marker of MASH progression of fibrogenic activity in the liver. PRO-C3 is FDA approved and utilizes Nordic Bioscience’s protein fingerprint technology.

In relation to the organ death race, Nordic Bioscience received a Letter of Support (LoS) from the FDA for the first serological biomarker for enrichment in clinical studies and trials in heart failure (HFpEF).

Our protein fingerprint biomarkers can be measured in serum and they specifically target the neo-epitopes that are released during protein formation of degradation and signaling the extent of fibrogenesis or fibrolysis.

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Your scientific area Select areaCardiologyDermatologyGastroenterologyHepatologyNephrologyNeurologyObesityPulmonologyRheumatologyMulti-organ/Other Your request Select requestGeneral inquiryBiomarkersLaboratorySomething else

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Email Phone (optional) Your message (optional) Nordic Bioscience ApS and its non-profit partner, The Extracellular Matrix Pharmacology Congress, can contact me by email with news on research, events, products, and similar. I can always withdraw my consent at any time. This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.