Teresa K Chen1,2, Chirag R Parikh3,4. 1. Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. 2. Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA. 3. Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, chirag.parikh@jhmi.edu. 4. Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA, chirag.parikh@jhmi.edu.
Abstract
BACKGROUND: Recent studies have demonstrated that intensive blood pressure control is associated with improved cardiovascular outcomes. Acute kidney injury (AKI), however, was more common in the intensive treatment group prompting concern in the nephrology community. SUMMARY: Clinical trials on hypertension control have traditionally defined AKI by changes in serum creatinine. However, serum creatinine has several inherent limitations as a marker of kidney injury, with various factors influencing its production, secretion, and elimination. Urinary biomarkers of kidney injury and repair have the potential to provide insight on the presence and phenotype of kidney injury. In both the Systolic Blood Pressure Intervention Trial and the Action to Control Cardiovascular Risk in Diabetes study, urinary biomarkers have suggested that the increased risk of AKI associated with intensive treatment was due to hemodynamic changes rather than structural kidney injury. As such, clinicians who encounter rises in serum creatinine during intensification of hypertension therapy should "stay calm and carry on." Alternative explanations for serum creatinine elevation should be considered and addressed if appropriate. When the rise in serum creatinine is limited, particularly if albuminuria is stable or improving, intensive blood pressure control should be continued for its potential long-term benefits. Key Messages: Increases in serum creatinine during intensification of blood pressure control may not necessarily reflect kidney injury. Clinicians should evaluate for other contributing factors before stopping therapy. Urinary biomarkers may address limitations of serum creatinine as a marker of kidney injury.
BACKGROUND: Recent studies have demonstrated that intensive blood pressure control is associated with improved cardiovascular outcomes. Acute kidney injury (AKI), however, was more common in the intensive treatment group prompting concern in the nephrology community. SUMMARY: Clinical trials on hypertension control have traditionally defined AKI by changes in serum creatinine. However, serum creatinine has several inherent limitations as a marker of kidney injury, with various factors influencing its production, secretion, and elimination. Urinary biomarkers of kidney injury and repair have the potential to provide insight on the presence and phenotype of kidney injury. In both the Systolic Blood Pressure Intervention Trial and the Action to Control Cardiovascular Risk in Diabetes study, urinary biomarkers have suggested that the increased risk of AKI associated with intensive treatment was due to hemodynamic changes rather than structural kidney injury. As such, clinicians who encounter rises in serum creatinine during intensification of hypertension therapy should "stay calm and carry on." Alternative explanations for serum creatinine elevation should be considered and addressed if appropriate. When the rise in serum creatinine is limited, particularly if albuminuria is stable or improving, intensive blood pressure control should be continued for its potential long-term benefits. Key Messages: Increases in serum creatinine during intensification of blood pressure control may not necessarily reflect kidney injury. Clinicians should evaluate for other contributing factors before stopping therapy. Urinary biomarkers may address limitations of serum creatinine as a marker of kidney injury.
Authors: Mark J Sarnak; Ronit Katz; Anne Newman; Tamara Harris; Carmen A Peralta; Prasad Devarajan; Michael R Bennett; Linda Fried; Joachim H Ix; Suzanne Satterfield; Eleanor M Simonsick; Chirag R Parikh; Michael G Shlipak Journal: J Am Soc Nephrol Date: 2014-02-07 Impact factor: 10.121
Authors: Pranav S Garimella; Alexandra K Lee; Walter T Ambrosius; Udayan Bhatt; Alfred K Cheung; Michel Chonchol; Timothy Craven; Amret T Hawfield; Vasantha Jotwani; Anthony Killeen; Henry Punzi; Mark J Sarnak; Barry M Wall; Joachim H Ix; Michael G Shlipak Journal: Eur Heart J Date: 2019-11-01 Impact factor: 35.855
Authors: Eve-Irene Lepist; Xuexiang Zhang; Jia Hao; Jane Huang; Alan Kosaka; Gabriel Birkus; Bernard P Murray; Roy Bannister; Tomas Cihlar; Yong Huang; Adrian S Ray Journal: Kidney Int Date: 2014-03-19 Impact factor: 10.612