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Clinical Practice: Editorial

Free Access

Changing Paradigms in Acute Kidney Injury: From Mechanisms to Management

Mehta R.L.a · Andringa K.K.b · Sanders P.W.b, c · Agarwal A.b, c

Author affiliations

aDepartment of Medicine, Division of Nephrology, University of California, San Diego, Calif., bDepartment of Medicine, Division of Nephrology, University of Alabama at Birmingham, and cBirmingham Veterans Affairs Medical Center, Birmingham, Ala., USA

Corresponding Author

Dr. Anupam Agarwal

Division of Nephrology, THT 647

University of Alabama at Birmingham

1900 University Blvd., Birmingham, AL 35294 (USA)

E-Mail agarwal@uab.edu

Related Articles for ""

Nephron 2016;134:131-132

Recent advances in the field of acute kidney injury (AKI) have provided key insights into understanding the mechanisms and pathways of AKI and its effects on other organs. Biomarkers have been identified that have provided new tools and techniques to characterize this disorder and facilitate point-of-care testing. Multiple underlying mechanisms contribute to the pathophysiology of AKI including genetic and epigenetic modifications, environmental influences and, more importantly, inherent mechanisms within the kidney offer challenging perspectives for clinical and translational research. This issue summarizes proceedings from the 6th University of Alabama at Birmingham (UAB)-University of California San Diego (UCSD) O'Brien Core Center for AKI Research symposium held during the 21st Annual Continuous Renal Replacement Therapy meeting in San Diego, California, USA, on Tuesday, February 16, 2016.

The overall goal of this symposium was to provide a review of the most recent developments in the field and describe emerging knowledge from basic and translational research. The meeting included 21 experts invited from around the world and over 100 participants were in attendance. Symposia sessions focused on defining key molecules and mechanisms involved in the pathogenesis and repair from AKI. The role of the non-selective, calcium (Ca2+)-permeable cation channel of the transient receptor potential melastatin 2, and iron in mediating oxidative stress in AKI were discussed. New targets for intervention were described including autophagy, sphingolipid signaling, macrophage, complement and tubular transport mechanisms [1,2,3,4,5,6]. A major theme was to explore the contributors to progression of AKI to chronic kidney disease, and speakers provided elegant overviews of the experimental evidence and molecular mechanisms that are in play [7,8].

Although it has been difficult to translate findings from experimental models to human interventions, several topics focused on translational research applied to clinical care demonstrating that the field is promising for AKI. Advances in understanding the role of micro-RNA regulation of injury and repair pathways [4], organ cross-talk and lipid pathways were discussed. Knowledge obtained from pre-clinical models is now being applied to evaluating gene delivery approaches, remote ischemic pre-conditioning and novel approaches with lipoic acid [1] and mineralocorticoid receptor antagonism for prevention and management of AKI [5].

Results from ongoing clinical studies were discussed to define the best strategies for effective management of patients. Serum creatinine measurements continue to be the mainstay for detecting and diagnosing AKI, however, are subject to biologic and measurement variations. The patterns of creatinine elevation and alterations in urinary volume continue to evolve as biomarker signals to improve our ability to diagnose AKI [9,10]. Ronco and Chawla [11] provided an overview of the role of kidney damage biomarkers to detect subclinical AKI prior to functional changes, thus providing a rationale for expanding our current definitions for AKI. Functional stress testing with diuretics was discussed as techniques to establish the integrity of the tubules and capacity of the kidney to provide a novel technique to evaluate patients with AKI. Protocol management and follow-up for AKI patients has been a controversial area given the heterogeneity of the disease; however, the experience from the UK described by Selby et al. [12,13] to improve the basic care of AKI appears to be promising in improving outcomes.

The UAB-UCSD O'Brien Center has taken a major role in providing biomedical resources for investigators pursuing AKI-related research by identifying emerging trends and technologies and pursuing these opportunities through enhancement of core resources and educational outreach to investigators through workshops and seminars. This symposium highlighted the exciting developments in the field and provided a forum for exchange of ideas among basic scientists and clinicians. The proceedings from this conference provide a unique collection that we hope will stimulate further thought and continued investigations in the field.

Acknowledgments

We gratefully acknowledge support from the NIH/NIDDK funded UAB-UCSD O'Brien Center for AKI Research (P30 DK079337) for this symposium.


References

  1. Zhang J, McCullough PA: Lipoic acid in the prevention of acute kidney injury. Nephron 2016;134:133-140. DOI: 10.1159/000448666.
  2. Doi K: Kidney-heart interactions in acute kidney injury. Nephron 2016;134:141-144. DOI: 10.1159/000447021.
  3. Harris RC, Cheng H: Telomerase, autophagy and acute kidney injury. Nephron 2016;134:145-148. DOI: 10.1159/000446665.
  4. Liu Z, Wang S, Mi QS, Dong Z: MicroRNAs in pathogenesis of acute kidney injury. Nephron 2016;134:149-153. DOI: 10.1159/000446551.
  5. Chandrashekar KB, Lopez-Ruiz A, Juncos LA: The promise of mineralocorticoid antagonism in acute kidney injury. Nephron 2016;134:154-159. DOI: 10.1159/000448224.
  6. Vallon V: Tubular transport in acute kidney injury: relevance for diagnosis, prognosis and intervention. Nephron 2016;134:160-166. DOI: 10.1159/000446448.
  7. Perry HM, Okusa MD: Endothelial dysfunction in renal interstitial fibrosis. Nephron 2016;134:167-171. DOI: 10.1159/000447607.
  8. Takaori K, Yanagita M: Insights into the mechanisms of the acute kidney injury-to-chronic kidney disease continuum. Nephron 2016;134:172-176. DOI: 10.1159/000448081.
  9. Warnock DG, Powell TC, Siew ED, Donnelly JP, Wang HE, Mehta RL: Serum creatinine trajectories for community - versus hospital-acquired acute kidney injury. Nephron 2016;134:177-182. DOI: 10.1159/000447757.
  10. Lehner GF, Forni LG, Joannidis M: Oliguria and biomarkers of acute kidney injury: Star struck lovers or strangers in the night? Nephron 2016;134:183-190. DOI: 10.1159/000447979.
  11. Ronco C, Chawla LS: Glomerular and tubular kidney stress test: new tools for a deeper evaluation of kidney function. Nephron 2016;134:191-194. DOI: 10.1159/000449235.
  12. Selby NM, Kolhe NV: Care bundles for acute kidney injury: do they work? Nephron 2016;​134:195-199. DOI: 10.1159/000447758.
  13. Selby NM, Casula A, Lamming L, Mohammed M, Caskey F: Design and rationale of ‘tackling acute kidney injury', a multicentre quality improvement study. Nephron 2016;​134:200-204. DOI: 10.1159/000447675.

Author Contacts

Dr. Anupam Agarwal

Division of Nephrology, THT 647

University of Alabama at Birmingham

1900 University Blvd., Birmingham, AL 35294 (USA)

E-Mail agarwal@uab.edu


Article / Publication Details

Received: May 27, 2016
Accepted: June 15, 2016
Published online: September 07, 2016
Issue release date: November 2016

Number of Print Pages: 2
Number of Figures: 0
Number of Tables: 0

ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)

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References

  1. Zhang J, McCullough PA: Lipoic acid in the prevention of acute kidney injury. Nephron 2016;134:133-140. DOI: 10.1159/000448666.
  2. Doi K: Kidney-heart interactions in acute kidney injury. Nephron 2016;134:141-144. DOI: 10.1159/000447021.
  3. Harris RC, Cheng H: Telomerase, autophagy and acute kidney injury. Nephron 2016;134:145-148. DOI: 10.1159/000446665.
  4. Liu Z, Wang S, Mi QS, Dong Z: MicroRNAs in pathogenesis of acute kidney injury. Nephron 2016;134:149-153. DOI: 10.1159/000446551.
  5. Chandrashekar KB, Lopez-Ruiz A, Juncos LA: The promise of mineralocorticoid antagonism in acute kidney injury. Nephron 2016;134:154-159. DOI: 10.1159/000448224.
  6. Vallon V: Tubular transport in acute kidney injury: relevance for diagnosis, prognosis and intervention. Nephron 2016;134:160-166. DOI: 10.1159/000446448.
  7. Perry HM, Okusa MD: Endothelial dysfunction in renal interstitial fibrosis. Nephron 2016;134:167-171. DOI: 10.1159/000447607.
  8. Takaori K, Yanagita M: Insights into the mechanisms of the acute kidney injury-to-chronic kidney disease continuum. Nephron 2016;134:172-176. DOI: 10.1159/000448081.
  9. Warnock DG, Powell TC, Siew ED, Donnelly JP, Wang HE, Mehta RL: Serum creatinine trajectories for community - versus hospital-acquired acute kidney injury. Nephron 2016;134:177-182. DOI: 10.1159/000447757.
  10. Lehner GF, Forni LG, Joannidis M: Oliguria and biomarkers of acute kidney injury: Star struck lovers or strangers in the night? Nephron 2016;134:183-190. DOI: 10.1159/000447979.
  11. Ronco C, Chawla LS: Glomerular and tubular kidney stress test: new tools for a deeper evaluation of kidney function. Nephron 2016;134:191-194. DOI: 10.1159/000449235.
  12. Selby NM, Kolhe NV: Care bundles for acute kidney injury: do they work? Nephron 2016;​134:195-199. DOI: 10.1159/000447758.
  13. Selby NM, Casula A, Lamming L, Mohammed M, Caskey F: Design and rationale of ‘tackling acute kidney injury', a multicentre quality improvement study. Nephron 2016;​134:200-204. DOI: 10.1159/000447675.
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