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Journal Article
Research Support, Non-U.S. Gov't
Renal Perfusion during Hemodialysis: Intradialytic Blood Flow Decline and Effects of Dialysate Cooling.
BACKGROUND: Residual renal function (RRF) confers survival in patients with ESRD but declines after initiating hemodialysis. Previous research shows that dialysate cooling reduces hemodialysis-induced circulatory stress and protects the brain and heart from ischemic injury. Whether hemodialysis-induced circulatory stress affects renal perfusion, and if it can be ameliorated with dialysate cooling to potentially reduce RRF loss, is unknown.
METHODS: We used renal computed tomography perfusion imaging to scan 29 patients undergoing continuous dialysis under standard (36.5°C dialysate temperature) conditions; we also scanned another 15 patients under both standard and cooled (35.0°C) conditions. Imaging was performed immediately before, 3 hours into, and 15 minutes after hemodialysis sessions. We used perfusion maps to quantify renal perfusion. To provide a reference to another organ vulnerable to hemodialysis-induced ischemic injury, we also used echocardiography to assess intradialytic myocardial stunning.
RESULTS: During standard hemodialysis, renal perfusion decreased 18.4% ( P <0.005) and correlated with myocardial injury ( r =-0.33; P <0.05). During sessions with dialysis cooling, patients experienced a 10.6% decrease in perfusion (not significantly different from the decline with standard hemodialysis), and ten of the 15 patients showed improved or no effect on myocardial stunning.
CONCLUSIONS: This study shows an acute decrease in renal perfusion during hemodialysis, a first step toward pathophysiologic characterization of hemodialysis-mediated RRF decline. Dialysate cooling ameliorated this decline but this effect did not reach statistical significance. Further study is needed to explore the potential of dialysate cooling as a therapeutic approach to slow RRF decline.
METHODS: We used renal computed tomography perfusion imaging to scan 29 patients undergoing continuous dialysis under standard (36.5°C dialysate temperature) conditions; we also scanned another 15 patients under both standard and cooled (35.0°C) conditions. Imaging was performed immediately before, 3 hours into, and 15 minutes after hemodialysis sessions. We used perfusion maps to quantify renal perfusion. To provide a reference to another organ vulnerable to hemodialysis-induced ischemic injury, we also used echocardiography to assess intradialytic myocardial stunning.
RESULTS: During standard hemodialysis, renal perfusion decreased 18.4% ( P <0.005) and correlated with myocardial injury ( r =-0.33; P <0.05). During sessions with dialysis cooling, patients experienced a 10.6% decrease in perfusion (not significantly different from the decline with standard hemodialysis), and ten of the 15 patients showed improved or no effect on myocardial stunning.
CONCLUSIONS: This study shows an acute decrease in renal perfusion during hemodialysis, a first step toward pathophysiologic characterization of hemodialysis-mediated RRF decline. Dialysate cooling ameliorated this decline but this effect did not reach statistical significance. Further study is needed to explore the potential of dialysate cooling as a therapeutic approach to slow RRF decline.
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