Acute Kidney Injury: From Early Signs to Chronic Risk
Acute kidney injury (AKI) isn't just a short-term problem—it's the start of a longer kidney health journey. AKI was previously called 'acute renal failure' or 'renal failure' but the terminology has evolved to reflect the spectrum of kidney injury. AKI occurs when the kidneys suddenly stop filtering waste products from the blood and the kidney function changes rapidly. This complication is very different from diseases such as Polycystic Kidney Disease, which is a genetic disease and genetic disorder caused by gene mutations passed from biological parents to their children.
Whether it happens in the ICU or outpatient clinic AKI carries a big burden: increased risk of hospitalization, long term dialysis and even premature death. AKI is common in hospitalized patients and patients admitted to hospital and impacts outcomes and length of stay.
Recognizing it early, treating it promptly and understanding the link to chronic kidney disease (CKD) is key to preserving kidney function and better patient outcomes. AKI and CKD are both forms of renal disease and show the continuum between acute and chronic conditions.
Let's look at how AKI is classified, how to detect it early and what modern tools and strategies are helping clinicians change the trajectory from injury to recovery.
AKI is classified by where the problem starts:
The KDIGO clinical practice guideline (Kidney Disease: Improving Global Outcomes) defines AKI using changes in serum creatinine levels and urine output. The urine output criteria are also used in AKI staging, such as less than 0.5 mL/kg/h for specified durations.
The Acute Kidney Injury Network (AKIN) is another classification system that incorporates both serum creatinine and urine output criteria. Early detection and classification are key, with identification of renal dysfunction and monitoring of glomerular filtration rate (GFR) as key measures of kidney health.
But while these have been the clinical mainstays, they aren't always fast or specific enough to catch injury early. Serum creatinine level and blood urea nitrogen are traditional markers for assessing renal function but both have limitations in sensitivity and specificity.
That's where newer biomarkers like neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1) and cystatin C come in. These tools are changing early detection, helping clinicians distinguish between mild, reversible cases and more severe or ongoing damage [2] [3].
A 2021 article highlights the importance of fluid balance, electrolyte monitoring and timely renal replacement therapy (RRT) when AKI is confirmed [3]. In the outpatient space, some reviews suggest early medication adjustment and specialist referrals can reduce complications in patients managed outside the hospital [4].
In the context of pathophysiology blood clots can cause vascular obstruction leading to AKI and red blood cells may be seen in kidney biopsies in certain conditions such as anticoagulant-related nephropathy. [5]
Prevention starts by identifying who's most at risk. People with diabetes, hypertension, chronic heart failure, or advanced age are more likely to develop AKI—especially during acute illnesses or when exposed to nephrotoxic medications like NSAIDs or contrast agents. Both patient-related and treatment-related risk factors such as underlying chronic diseases, recent infections, trauma or major surgeries play a key role in increasing the likelihood of AKI.
According to a 2020 Journal of Clinical Medicine review, risk mitigation means taking a proactive, team-based approach: monitor hydration, avoid nephrotoxins and assess kidney function during high-risk scenarios like surgery or infection [7]. It's especially important to identify high risk patients, such as those undergoing major procedures like cardiac surgery and tailor perioperative management strategies to prevent renal complications.
Hospital-based strategies such as standardized monitoring protocols and early nephrology involvement can also reduce AKI rates as emphasized by the American Journal of Kidney Diseases Core Curriculum [11].
In a more recent 2025 article in Lakartidningen Swedish clinicians advocate for a streamlined system to identify and intervene early in AKI cases, especially in older adults or those with fluctuating blood pressure [10].
Relying solely on serum creatinine to assess kidney health is a bit like using a smoke detector after the fire's already burning. Biomarkers offer a more sensitive way to detect kidney injury before significant function is lost. Blood tests are essential for detecting changes in kidney function and guiding the management of AKI patients.
A 2022 review in Medicina presents compelling evidence that biomarkers can guide both diagnosis and risk stratification, helping clinicians decide when to intensify care or when to hold off on aggressive treatments [6].
These biomarkers also help distinguish between transient AKI (due to things like dehydration) and persistent AKI, which is more likely to result in long-term damage. This distinction is critical when managing critically ill patients or adjusting medications like ACE inhibitors and diuretics.
One of the biggest changes in kidney medicine over the past decade is that AKI doesn't always resolve cleanly. Many patients recover creatinine levels but their kidneys never return to full health. This transitional phase, called acute kidney disease (AKD), spans from 7 to 90 days after AKI onset. Renal recovery after AKI depends on factors such as the severity of injury, underlying comorbidities and the presence of biomarkers indicating renal repair mechanisms.
A 2022 Nephron review calls AKD the 'missing link' between AKI and CKD, emphasizing the need for follow-up labs and patient education [8]. If kidney function hasn't bounced back within that 90-day window CKD is usually diagnosed.
New research in the Yonsei Medical Journal shows how early post-discharge care—such as nephrology visits, medication reviews and blood pressure control—can slow progression to irreversible kidney damage [9]. Kidney disease progression after AKI increases the risk of developing chronic renal failure, chronic kidney failure, end stage kidney disease and end stage renal disease.
Meanwhile a 2024 American Journal of Physiology review looks into the biological mechanisms behind this progression. It points to inflammation, fibrosis (scarring) and microvascular injury as key drivers—and possible therapeutic targets—of the AKI-to-CKD transition [12]. Cardiovascular disease is also a major cause of morbidity and mortality in patients with a history of AKI.
When it comes to managing AKI a few core principles apply across both hospital and outpatient settings:
The Acute Dialysis Quality Initiative (ADQI) has developed consensus guidelines and classification systems for AKI management.
The sooner these are implemented the better the chances of preventing permanent kidney damage and the slide to CKD.
Acute kidney injury is more than a short term health crisis—it's a long term disease. As we learn more about AKI we have more opportunity to intervene early, personalize care and protect long term kidney health. By using advanced biomarkers, prevention focused strategies and recognizing AKD as a key phase clinicians can change the story for thousands of patients with kidney injury every year.
[1] Rahman, M., Shad, F., & Smith, M. C. (2012). Acute kidney injury: a guide to diagnosis and management. American family physician, 86(7), 631–639. https://pubmed.ncbi.nlm.nih.gov/23062091/
[2] Mercado, M. G., Smith, D. K., & Guard, E. L. (2019). Acute Kidney Injury: Diagnosis and Management. American family physician, 100(11), 687–694. https://pubmed.ncbi.nlm.nih.gov/31790176/
[3] Kellum, J. A., Romagnani, P., Ashuntantang, G., Ronco, C., Zarbock, A., & Anders, H. J. (2021). Acute kidney injury. Nature reviews. Disease primers, 7(1), 52. https://doi.org/10.1038/s41572-021-00284-z
[4] Jacob, J., Dannenhoffer, J., & Rutter, A. (2020). Acute Kidney Injury. Primary care, 47(4), 571–584. https://doi.org/10.1016/j.pop.2020.08.008
[5] Neyra, J. A., & Chawla, L. S. (2021). Acute Kidney Disease to Chronic Kidney Disease. Critical care clinics, 37(2), 453–474. https://doi.org/10.1016/j.ccc.2020.11.013
[6] Yoon, S. Y., Kim, J. S., Jeong, K. H., & Kim, S. K. (2022). Acute Kidney Injury: Biomarker-Guided Diagnosis and Management. Medicina (Kaunas, Lithuania), 58(3), 340. https://doi.org/10.3390/medicina58030340
[7] Gameiro, J., Fonseca, J. A., Outerelo, C., & Lopes, J. A. (2020). Acute Kidney Injury: From Diagnosis to Prevention and Treatment Strategies. Journal of clinical medicine, 9(6), 1704. https://doi.org/10.3390/jcm9061704
[8] Levey A. S. (2022). Defining AKD: The Spectrum of AKI, AKD, and CKD. Nephron, 146(3), 302–305. https://doi.org/10.1159/000516647
[9] Koh, E. S., & Chung, S. (2024). Recent Update on Acute Kidney Injury-to-Chronic Kidney Disease Transition. Yonsei medical journal, 65(5), 247–256. https://doi.org/10.3349/ymj.2023.0306
[10] Bell, M., M Öberg, C., & Ewert Broman, M. (2025). Akut njurskada – prevention och behandling [Acute kidney injury - prevention and treatment]. Lakartidningen, 122, 23182. https://pubmed.ncbi.nlm.nih.gov/40421748/
[11] Moore, P. K., Hsu, R. K., & Liu, K. D. (2018). Management of Acute Kidney Injury: Core Curriculum 2018. American journal of kidney diseases : the official journal of the National Kidney Foundation, 72(1), 136–148. https://doi.org/10.1053/j.ajkd.2017.11.021
[12] Zhang, T., Widdop, R. E., & Ricardo, S. D. (2024). Transition from acute kidney injury to chronic kidney disease: mechanisms, models, and biomarkers. American journal of physiology. Renal physiology, 327(5), F788–F805. https://doi.org/10.1152/ajprenal.00184.2024
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Los Angeles Times
2 days ago
- Los Angeles Times
Acute Kidney Injury: From Early Signs to Chronic Risk
Acute kidney injury (AKI) isn't just a short-term problem—it's the start of a longer kidney health journey. AKI was previously called 'acute renal failure' or 'renal failure' but the terminology has evolved to reflect the spectrum of kidney injury. AKI occurs when the kidneys suddenly stop filtering waste products from the blood and the kidney function changes rapidly. This complication is very different from diseases such as Polycystic Kidney Disease, which is a genetic disease and genetic disorder caused by gene mutations passed from biological parents to their children. Whether it happens in the ICU or outpatient clinic AKI carries a big burden: increased risk of hospitalization, long term dialysis and even premature death. AKI is common in hospitalized patients and patients admitted to hospital and impacts outcomes and length of stay. Recognizing it early, treating it promptly and understanding the link to chronic kidney disease (CKD) is key to preserving kidney function and better patient outcomes. AKI and CKD are both forms of renal disease and show the continuum between acute and chronic conditions. Let's look at how AKI is classified, how to detect it early and what modern tools and strategies are helping clinicians change the trajectory from injury to recovery. AKI is classified by where the problem starts: The KDIGO clinical practice guideline (Kidney Disease: Improving Global Outcomes) defines AKI using changes in serum creatinine levels and urine output. The urine output criteria are also used in AKI staging, such as less than 0.5 mL/kg/h for specified durations. The Acute Kidney Injury Network (AKIN) is another classification system that incorporates both serum creatinine and urine output criteria. Early detection and classification are key, with identification of renal dysfunction and monitoring of glomerular filtration rate (GFR) as key measures of kidney health. But while these have been the clinical mainstays, they aren't always fast or specific enough to catch injury early. Serum creatinine level and blood urea nitrogen are traditional markers for assessing renal function but both have limitations in sensitivity and specificity. That's where newer biomarkers like neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1) and cystatin C come in. These tools are changing early detection, helping clinicians distinguish between mild, reversible cases and more severe or ongoing damage [2] [3]. A 2021 article highlights the importance of fluid balance, electrolyte monitoring and timely renal replacement therapy (RRT) when AKI is confirmed [3]. In the outpatient space, some reviews suggest early medication adjustment and specialist referrals can reduce complications in patients managed outside the hospital [4]. In the context of pathophysiology blood clots can cause vascular obstruction leading to AKI and red blood cells may be seen in kidney biopsies in certain conditions such as anticoagulant-related nephropathy. [5] Prevention starts by identifying who's most at risk. People with diabetes, hypertension, chronic heart failure, or advanced age are more likely to develop AKI—especially during acute illnesses or when exposed to nephrotoxic medications like NSAIDs or contrast agents. Both patient-related and treatment-related risk factors such as underlying chronic diseases, recent infections, trauma or major surgeries play a key role in increasing the likelihood of AKI. According to a 2020 Journal of Clinical Medicine review, risk mitigation means taking a proactive, team-based approach: monitor hydration, avoid nephrotoxins and assess kidney function during high-risk scenarios like surgery or infection [7]. It's especially important to identify high risk patients, such as those undergoing major procedures like cardiac surgery and tailor perioperative management strategies to prevent renal complications. Hospital-based strategies such as standardized monitoring protocols and early nephrology involvement can also reduce AKI rates as emphasized by the American Journal of Kidney Diseases Core Curriculum [11]. In a more recent 2025 article in Lakartidningen Swedish clinicians advocate for a streamlined system to identify and intervene early in AKI cases, especially in older adults or those with fluctuating blood pressure [10]. Relying solely on serum creatinine to assess kidney health is a bit like using a smoke detector after the fire's already burning. Biomarkers offer a more sensitive way to detect kidney injury before significant function is lost. Blood tests are essential for detecting changes in kidney function and guiding the management of AKI patients. A 2022 review in Medicina presents compelling evidence that biomarkers can guide both diagnosis and risk stratification, helping clinicians decide when to intensify care or when to hold off on aggressive treatments [6]. These biomarkers also help distinguish between transient AKI (due to things like dehydration) and persistent AKI, which is more likely to result in long-term damage. This distinction is critical when managing critically ill patients or adjusting medications like ACE inhibitors and diuretics. One of the biggest changes in kidney medicine over the past decade is that AKI doesn't always resolve cleanly. Many patients recover creatinine levels but their kidneys never return to full health. This transitional phase, called acute kidney disease (AKD), spans from 7 to 90 days after AKI onset. Renal recovery after AKI depends on factors such as the severity of injury, underlying comorbidities and the presence of biomarkers indicating renal repair mechanisms. A 2022 Nephron review calls AKD the 'missing link' between AKI and CKD, emphasizing the need for follow-up labs and patient education [8]. If kidney function hasn't bounced back within that 90-day window CKD is usually diagnosed. New research in the Yonsei Medical Journal shows how early post-discharge care—such as nephrology visits, medication reviews and blood pressure control—can slow progression to irreversible kidney damage [9]. Kidney disease progression after AKI increases the risk of developing chronic renal failure, chronic kidney failure, end stage kidney disease and end stage renal disease. Meanwhile a 2024 American Journal of Physiology review looks into the biological mechanisms behind this progression. It points to inflammation, fibrosis (scarring) and microvascular injury as key drivers—and possible therapeutic targets—of the AKI-to-CKD transition [12]. Cardiovascular disease is also a major cause of morbidity and mortality in patients with a history of AKI. When it comes to managing AKI a few core principles apply across both hospital and outpatient settings: The Acute Dialysis Quality Initiative (ADQI) has developed consensus guidelines and classification systems for AKI management. The sooner these are implemented the better the chances of preventing permanent kidney damage and the slide to CKD. Acute kidney injury is more than a short term health crisis—it's a long term disease. As we learn more about AKI we have more opportunity to intervene early, personalize care and protect long term kidney health. By using advanced biomarkers, prevention focused strategies and recognizing AKD as a key phase clinicians can change the story for thousands of patients with kidney injury every year. [1] Rahman, M., Shad, F., & Smith, M. C. (2012). Acute kidney injury: a guide to diagnosis and management. American family physician, 86(7), 631–639. [2] Mercado, M. G., Smith, D. K., & Guard, E. L. (2019). Acute Kidney Injury: Diagnosis and Management. American family physician, 100(11), 687–694. [3] Kellum, J. A., Romagnani, P., Ashuntantang, G., Ronco, C., Zarbock, A., & Anders, H. J. (2021). Acute kidney injury. Nature reviews. Disease primers, 7(1), 52. [4] Jacob, J., Dannenhoffer, J., & Rutter, A. (2020). Acute Kidney Injury. Primary care, 47(4), 571–584. [5] Neyra, J. A., & Chawla, L. S. (2021). Acute Kidney Disease to Chronic Kidney Disease. Critical care clinics, 37(2), 453–474. [6] Yoon, S. Y., Kim, J. S., Jeong, K. H., & Kim, S. K. (2022). Acute Kidney Injury: Biomarker-Guided Diagnosis and Management. Medicina (Kaunas, Lithuania), 58(3), 340. [7] Gameiro, J., Fonseca, J. A., Outerelo, C., & Lopes, J. A. (2020). Acute Kidney Injury: From Diagnosis to Prevention and Treatment Strategies. Journal of clinical medicine, 9(6), 1704. [8] Levey A. S. (2022). Defining AKD: The Spectrum of AKI, AKD, and CKD. Nephron, 146(3), 302–305. [9] Koh, E. S., & Chung, S. (2024). Recent Update on Acute Kidney Injury-to-Chronic Kidney Disease Transition. Yonsei medical journal, 65(5), 247–256. [10] Bell, M., M Öberg, C., & Ewert Broman, M. (2025). Akut njurskada – prevention och behandling [Acute kidney injury - prevention and treatment]. Lakartidningen, 122, 23182. [11] Moore, P. K., Hsu, R. K., & Liu, K. D. (2018). Management of Acute Kidney Injury: Core Curriculum 2018. American journal of kidney diseases : the official journal of the National Kidney Foundation, 72(1), 136–148. [12] Zhang, T., Widdop, R. E., & Ricardo, S. D. (2024). Transition from acute kidney injury to chronic kidney disease: mechanisms, models, and biomarkers. American journal of physiology. Renal physiology, 327(5), F788–F805.
Los Angeles Times
3 days ago
- Los Angeles Times
Polycystic Kidney Disease: Causes, Treatments, and What's Ahead
Polycystic Kidney Disease (PKD) is a progressive inherited disorder that causes many cysts, not just fluid filled cysts, to form in the kidneys and ultimately impair their function. PKD is a genetic disease and genetic disorder caused by gene mutations passed from biological parents to their children. There are two main types of PKD: autosomal dominant PKD (ADPKD) which is the most common and autosomal recessive PKD. The disorder affects men and women equally. Over time these cysts can grow, replace normal kidney tissue and lead to end stage kidney disease (ESKD). Risk factors for PKD include having an affected parent as the condition is inherited and other genetic variables. PKD can also lead to serious complications beyond kidney failure such as pre-eclampsia and aneurysms. As we learn more about the genetic and molecular basis of PKD – particularly ADPKD – research is starting to shape more targeted treatments and patient centered care models. PKD is driven by mutations in two genes: PKD1 and PKD2 which encode the proteins polycystin-1 and polycystin-2. These proteins are crucial for the structure and function of kidney tubules. When they malfunction kidney cells start to divide abnormally and secrete fluid leading to cyst formation and kidney enlargement. Autosomal recessive PKD (also known as autosomal recessive polycystic kidney disease) is a rarer form of PKD caused by a genetic fault that occurs when both parents carry the abnormal gene and pass it on to their child. According to a 2014 review in Wiley Interdisciplinary Reviews: Developmental Biology [1] polycystin-1 is a mechanoreceptor – essentially a sensor that helps kidney cells respond to fluid flow. A 2004 study deepens this understanding by showing polycystin-1's role in complex cellular signaling [2]. More recent research in Physiological Reviews (2025) looks at the primary cilium – a tiny antenna-like structure on kidney cells. This cilium helps sense mechanical changes in fluid flow and interacts with polycystins and another protein fibrocystin all of which are essential in preventing cyst development [4]. Disruption of normal development of the kidneys and liver is a hallmark of autosomal recessive PKD as the genetic fault interferes with the organs' typical growth and function. While the exact mechanics are still being studied it's clear that disturbances in this cellular machinery is at the heart of PKD pathology. Genetic testing can identify mutations in PKD related genes such as PKD1, PKD2 or PKHD1 and help with diagnosis and family planning. A genetic counselor can help families understand inheritance patterns, the risks associated with autosomal recessive PKD and guide them through genetic testing and family planning decisions. Beneath the genetic mutations are a set of signaling pathways that drive cyst growth. One key player is cyclic AMP (cAMP) which increases fluid secretion and cell proliferation; increased cAMP levels cause cysts to grow in the kidneys. Other important pathways include epidermal growth factor (EGF) and AMP-activated protein kinase (AMPK) as noted in a 2021 review from Biochemical Society Transactions [5]. These molecules act like traffic signals for cell activity – when their function goes awry cysts can grow unchecked. Another major breakthrough is on vasopressin receptors, especially V2. The drug called tolvaptan, currently the only FDA approved disease modifying therapy for ADPKD works by blocking these V2 receptors to reduce cAMP production and slow cyst expansion. For ADPKD patients the drug tolvaptan can slow the rate at which cysts grow and delay disease progression. A 2025 study in the American Journal of Physiology confirms that blocking other receptors (V1a, V1b) doesn't provide added benefit refining our understanding of this treatment's specificity [11]. Modern PKD care is about early diagnosis, genetic counseling and personalized treatment. To diagnose PKD imaging tests such as ultrasound, computed tomography scan and MRI scans are used to detect and monitor cyst development. The 2020 Chinese clinical practice guidelines are a comprehensive resource for clinicians covering everything from risk stratification to long term monitoring and intervention strategies [3]. These guidelines build on earlier frameworks such as the 2018 Nature Reviews: Disease Primers article which bridges cellular biology with real world clinical application [6]. Meanwhile a 2017 review in Comprehensive Physiology helps contextualize both hereditary and sporadic forms of PKD and offers a deeper dive into how and why cysts form [9]. As treatment advances patient voices are becoming more central to shaping research priorities. A 2025 study in Kidney360 gathered insights from patients, caregivers and healthcare professionals and found that preserving kidney function, improving quality of life and managing related health conditions are top concerns [10]. PKD can have a big impact on mental health. Many patients experience emotional challenges such as depression and anxiety. Addressing these mental health concerns is essential for overall well being. Healthcare providers play a crucial role in supporting patients by offering resources, guidance and referrals to mental health professionals when needed. Adopting a healthy lifestyle – staying active, reducing stress, quitting smoking and maintaining a healthy weight – can help manage PKD and related health conditions. This shift towards value based, participatory care is a trend across nephrology – where patients are not just recipients of care but active collaborators in defining meaningful outcomes. Even with these advances there are still many questions: Research is ongoing to prevent kidney damage and to avoid factors that can make kidney damage worse in PKD. PKD is one of many kidney diseases; for example acquired cystic kidney disease can develop in people with chronic kidney disease especially those on long term dialysis. Prevention of kidney failure is key for PKD patients. Historical perspectives from the 2009 Annual Review of Medicine and 2013 Minerva Urologica e Nefrologica show just how far we have come and how far we have to go [7] [8]. These reviews highlight the need for therapies that not only slow cyst growth but also reverse or repair the cellular defects that underlie PKD. Polycystic Kidney Disease is a complex condition rooted in genetic and cellular abnormalities that are slowly being uncovered by modern science. Advances in molecular biology, imaging and drug development have improved how the disease is diagnosed and managed. But long term success depends on closing the gaps in knowledge, refining the therapies and keeping patients at the centre of both clinical and research efforts. [1] Paul, B. M., & Vanden Heuvel, G. B. (2014). Kidney: polycystic kidney disease. Wiley interdisciplinary reviews. Developmental biology, 3(6), 465–487. [2] Wilson P. D. (2004). Polycystic kidney disease: new understanding in the pathogenesis. The international journal of biochemistry & cell biology, 36(10), 1868–1873. [3] Writing Group For Practice Guidelines For Diagnosis And Treatment Of Genetic Diseases Medical Genetics Branch Of Chinese Medical Association, Xu, D., & Mei, C. (2020). Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics, 37(3), 277–283. [4] Boletta, A., & Caplan, M. J. (2025). Physiologic mechanisms underlying polycystic kidney disease. Physiological reviews, 105(3), 1553–1607. [5] Richards, T., Modarage, K., Malik, S. A., & Goggolidou, P. (2021). The cellular pathways and potential therapeutics of Polycystic Kidney Disease. Biochemical Society transactions, 49(3), 1171–1188. 6] Bergmann, C., Guay-Woodford, L. M., Harris, P. C., Horie, S., Peters, D. J. M., & Torres, V. E. (2018). Polycystic kidney disease. Nature reviews. Disease primers, 4(1), 50. [7] Harris, P. C., & Torres, V. E. (2009). Polycystic kidney disease. Annual review of medicine, 60, 321–337. [8] Czarnecki, P. G., & Steinman, T. I. (2013). Polycystic kidney disease: new horizons and therapeutic frontiers. Minerva urologica e nefrologica = The Italian journal of urology and nephrology, 65(1), 61–68. [9] Ghata, J., & Cowley, B. D., Jr (2017). Polycystic Kidney Disease. Comprehensive Physiology, 7(3), 945–975. [10] Mustafa, R. A., Kawtharany, H., Kalot, M. A., Lumpkins, C. Y., Kimminau, K. S., Creed, C., Fowler, K., Perrone, R. D., Jaure, A., Cho, Y., Baron, D., & Yu, A. S. L. (2025). Establishing Meaningful Patient-Centered Outcomes with Relevance for Patients with Polycystic Kidney Disease: Patient, Caregiver, and Researcher Priorities for Research in Polycystic Kidney Disease. Kidney360, 6(4), 573–582. [11] Wang, X., Jiang, L., Nanayakkara, K., Hu, J., & Torres, V. E. (2025). Vasopressin V1a and V1b receptor antagonism does not affect the efficacy of tolvaptan in Polycystic Kidney Disease. American journal of physiology. Renal physiology, 10.1152/ajprenal.00350.2024. Advance online publication.
Associated Press
3 days ago
- Associated Press
Asahi Kasei Receives Imperial Invention Prize in Japan for Nickel-Coated Absorption Layer - Mitigating the Deterioration of Electrodes and Contributing to a Stable, Long-Term Electrolyzer Operation
TOKYO & NOVI, Mich. & DÜSSELDORF, Germany--(BUSINESS WIRE)--Jun 3, 2025-- Asahi Kasei has received the 2025 Imperial Invention Prize from the Japan Institute of Invention and Innovation, the highest award presented at the 2025 National Commendation for Invention. The formal award ceremony is scheduled to be held on July 1, 2025. The company was honored for its invention of a nickel-coated absorption layer, which extends the service life of electrodes for chlor-alkali electrolysis (patent no. 6120804). This honor underscores Asahi Kasei's commitment to continuous innovation in materials science and electrochemical processes. This press release features multimedia. View the full release here: Ion-exchange membrane process for chlor-alkali electrolysis Chlor-alkali electrolysis uses ion-exchange membranes to produce chlorine, caustic soda, and hydrogen through the electrolysis of brine. Since its commercialization by Asahi Kasei in 1975, this process has been adopted at over 160 plants in more than 30 countries worldwide (as of December 2024). In a commitment to its global support, the division held a Grand Opening Ceremony of its Houston, Texas office in late 2024. During this event, Asahi Kasei unveiled its ' DENKAI AS ONE ' model, making it a one-stop solution provider, offering electrolyzers, membranes, design, and operational support. The awarded nickel-coated absorption layer addresses a long-term key issue of the chlor-alkali electrolysis process: When the electrolysis is stopped due to temporary reductions in demand for chlorine and caustic soda, equipment malfunctions, or power outages, the electrodes—especially the cathode—deteriorate due to reverse current. This leads to problems such as increased power consumption and shortened cathode service life. Conventional measures have used mechanical solutions to suppress such reverse current. However, this approach is susceptible to malfunctions and operator errors, making it challenging to avoid cathode deterioration completely. Installing a reverse current absorption layer with a nickel coating offers an alternative method to eliminate the need for mechanical equipment. When stopping the electrolysis process, the reverse current absorption layer undergoes a chemical reaction with the nickel, preventing cathode degradation and enabling the equipment's stable, long-term operation. The nickel-coated reverse current absorption layer overcomes an additional hurdle for electrolyzer operators. Previously, customers often had to compromise porosity for strength and vice versa. Asahi Kasei's technology remedies this issue with its nickel-coated layer, which is both porous and sturdy while remaining processable over large areas. Commercialization was successfully achieved by applying nickel to a substrate with thermal spraying, which involves heating a material to a molten or near-molten state and applying it onto a surface to form a coating. Akiyasu Funakawa, General Manager of Asahi Kasei's Ion Exchange Membrane Research & Development Dept. said, 'Chlorine and caustic soda are indispensable raw materials that form the basis of various products which support our daily lives. This prize is a great encouragement as I continue to work on developing electrolysis technology that contributes to the world.' Toshinori Hachiya, General Manager of the Microza & Water Processing Quality Assurance Dept. at Asahi Kasei, added, 'In response to customer troubles, we have faced many issues and worked with many members to devise ideas. I am very happy that the results of our persistent efforts have been recognized in this way.' Chlor-alkali electrolysis equipment incorporating this technical breakthrough has already been adopted by chemical manufacturers worldwide, with market expansion continuing. Asahi Kasei is also investigating the technology's applicability to other electrolysis processes, such as alkaline water electrolysis for green hydrogen production. In addition to the Imperial Invention Prize, Koshiro Kudo, President of Asahi Kasei, accepted the Award for Distinguished Contribution to Driving the Invention into Implementation on behalf of the company. For additional information on Asahi Kasei's Ion-Exchange Membrane Business, visit The Imperial Invention Prize Akiyasu Funakawa General Manager Ion Exchange Membrane Research & Development Dept. Ion Exchange Membrane & Electrolysis System Division Asahi Kasei Corp. Toshinori Hachiya General Manager Microza & Water Processing Quality Assurance Dept. Microza & Water Processing Division Asahi Kasei Corp. Award for Distinguished Contribution for Driving the Invention into Implementation Koshiro Kudo President and Representative Director Asahi Kasei Corp. (Affiliations are current as of the date of the award.) Asahi Kasei is also dedicated to sustainability initiatives and is contributing to reaching a carbon neutral society by 2050. To learn more, visit View source version on CONTACT: North America Contact: Asahi Kasei America Inc. Christian OKeefe [email protected] Contact: Asahi Kasei Europe GmbH Sebastian Schmidt [email protected] KEYWORD: MICHIGAN UNITED STATES JAPAN NORTH AMERICA ASIA PACIFIC EUROPE GERMANY INDUSTRY KEYWORD: BUILDING SYSTEMS CHEMICALS/PLASTICS AUTOMOTIVE MANUFACTURING ALTERNATIVE ENERGY CONSTRUCTION & PROPERTY ENERGY MANUFACTURING TECHNOLOGY OTHER NATURAL RESOURCES ENVIRONMENT NATURAL RESOURCES OTHER TECHNOLOGY SCIENCE UTILITIES RESEARCH SOURCE: Asahi Kasei Copyright Business Wire 2025. PUB: 06/03/2025 08:30 AM/DISC: 06/03/2025 08:28 AM
