There were over 12,500 delegates participating in the American Society of Nephrology Kidney Week 2023 that took place last week in Philadelphia, PA from November 2 – 5. As expected, there was plenty of exciting science presented and discussed, with regards to both clinical care and scientific research.
While there were many interesting sessions, presentations and abstracts, we have chosen some of our own personal highlights from the congress to discuss here.
Highlight 1: Vascular aging: pulsatile hemodynamics, arterial stiffness, and cardiorenal target organ damage
The ‘Vascular Aging: pulsatile hemodynamics, arterial stiffness, and cardiorenal target organ damage’, was a highlight for us. The session, moderated by Wendy I. McCallum and Mahboob Rahman, and including presentations by Julio Alonso Chirinos, Elaine M. Urbina, Raymond R. Townsend, and Timothy M. Hughes, covered the mechanisms involved in arterial stiffness, how it can be measured, and why it is important to measure with regards to organ damage and other health consequences.
Cardiovascular disease is the leading cause of death worldwide, and many cardiovascular diseases are characterised by atherosclerosis, or hardening of the arteries. Arterial stiffness is very much an age-related process, whereby the pulsatile nature of the circulatory system passively subjects the arteries to repetitive strain throughout the lifetime.
The process can be influenced by various genetic and lifestyle factors and can also be accelerated via various risk factors such as obesity, hypertension, and diabetes. Importantly, arterial stiffness leads to structural and often irreversible consequences that can cause damage across multiple organs. It is thought that arterial stiffness might play a causal role in the development of chronic kidney disease (CKD), and in driving cardiovascular disease in patients with CKD. Hardening of the arteries increases the velocity of the pulse wave of moving blood from the heart. We have learnt that the kidney and the brain are especially susceptible to damage from the pulse wave, as these are soft organs with high rates of perfusion.
Pulse wave velocity (PWV), the estimated time taken for the pulse wave to travel between two arteries (most commonly between the carotid and femoral arteries), can be used as a surrogate for arterial stiffness, assuming that the relative wall thickness is constant. This is done by measuring the elapsed time and the distance between the two points.
There are several different ways to measure PWV, including a probe or tonometer, ultrasound, doppler, or phase contrast magnetic resonance imaging (PC-MRI). We found it very promising that PC-MRI was presented as the technique with the best agreement in measuring the distance between the carotid and femoral arteries. As we are currently using this method in studies, including the HEROIC study, it was extremely beneficial for us to hear all about these techniques especially in the context of the various mechanisms involved in arterial stiffness.
Highlight 2: Human kidney organoids for disease modelling and regeneration
The Donald W. Seldin Young Investigator Award and Address from Benjamin S. Freedman during the Friday Plenary both stood out amongst the research presented at the congress and illustrated some very promising and exciting paths for the future of treating kidney disease.
His talk, titled ‘Human kidney organoids for disease modelling and regeneration’, described several different exciting advances. For example, how we are now able to generate and characterise stem cells from patients with polycystic kidney disease, and then grown them in vitro to track how cysts develop. Another advance described was the identification of the first pluripotent stem cell phenotype relevant to kidney disease. It is also possible to grow cells in multi-well plates, making it suitable to test several therapeutic approaches simultaneously or to test therapies under different conditions at the same time.
He also explained how protocols have been developed that direct differentiation of stem cells into kidney progenitor cells and human kidney organoids that can be used to functionally model morphogenesis, physiology, and injury, as well as how kidney organoid models of several genetic and acquired kidney diseases have been established.
Most existing therapies and those in development are aiming to halt disease progression. The kidney cannot normally replace nephrons that have been lost. However, what excited us most about the advancements described in this talk were that they illustrate a different approach, one that may, in the future, be able to give patients new nephrons and reverse disease progression. This represents a very exciting path for the future or kidney disease treatment, and we are looking forward to seeing how the research advances in the coming years.
Highlight 3: Novel therapies: on the mechanisms of action
Another highlight was the Robert W. Schrier, MD, Endowed Lectureship, given by Thomas M. Coffman. The lecture formed part of the ‘Changing landscape of diabetic kidney disease treatment’ and provided an updated clinical perspective on treating diabetic kidney disease (DKD).
This included an overview of recent insights into underlying biology, mechanisms of action, and challenges related to therapies such as glucagon-like peptide 1 (GLP-1) receptor agonists and sodium-glucose cotransporter-2 (SGLT-2) inhibitors within the context of DKD.
Several mechanisms for the observed kidney protective effects of these treatments have been proposed: glycaemic control, renal hemodynamic alterations, anti-pronteinuric actions, impact on mediators of inflammation, a systematic effect of the immune system, reduction in blood pressure, as well as changes in proximal tubule metabolism and restoring metabolic homeostasis with SGLT-2 inhibitors.
Despite several studies confirming the nephroprotective effects of both GLP-1 receptor agonists and SGLT-2 inhibitors, and that SGLT-2 inhibitors are now recommended treatment for individuals with type 2 diabetes (T2D) and CKD, treating kidney disease is not without its challenges.
What we found particularly interesting about this sessions was the notion that despite having these new drugs available, they are being under prescribed in kidney disease. One of our takeaways from this was that perhaps more still needs to be understood about the various mechanisms of these drugs in the kidney, as well as how they slow disease progression, for them to be available for all the patients who might benefit from them.
In summary, while there was plenty of interesting research at Kidney Week 2023, we chose three of our personal highlights to reflect on in this post:
- Vascular aging: pulsatile hemodynamics, arterial stiffness, and cardiorenal target organ damage, Julio Alonso Chirinos, Elaine M. Urbina, Raymond R. Townsend, and Timothy M. Hughes, moderated by Wendy I. McCallum and Mahboob Rahman
- Human kidney organoids for disease modelling and regeneration, Benjamin S. Freedman
- Novel therapies: on the mechanisms of action, Thomas M. Coffman
We are already looking forward to attending Kidney Week 2024 next year in San Diego, CA.
The views and opinions expressed in this article are solely those of the contributing author/s. These views and opinions do not necessarily represent those of Antaros Medical.
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