Prolonged Renal Hypoperfusion and GFR Recovery Despite Early MAP Normalization After Ischemia–Reperfusion Injury
Abstract
Ischemia-reperfusion (IR) injury is a major cause of acute kidney injury (AKI) and can lead to prolonged renal dysfunction and chronic kidney disease (CKD). Studies differ on the time course of renal blood flow (RBF) and glomerular filtration rate (GFR) recovery after IR, ranging from near-normalization within 3-5 days to deficits beyond one week. Characterizing these dynamics in the conscious state is critical for understanding progression from AKI to CKD. We hypothesized that bilateral IR injury in conscious, chronically instrumented rats would result in a prolonged period of renal hypoperfusion and dysfunction. To determine this, male Sprague–Dawley rats (n=9; 8-9-weeks-old) were implanted with a blood pressure radiotelemeter, RBF transit-time ultrasonic probe, and FITC-inulin pump. After a 1-week recovery, baseline measurements of mean arterial pressure (MAP), RBF, and GFR (FITC-inulin clearance) were obtained. Rats then underwent 35 min bilateral IR (n=5) or sham (n=4) under anesthesia. For 2 weeks post-surgery, MAP and RBF were measured daily and GFR assessed every 3 days starting day 2 in conscious rats. Group comparisons used 2-way repeated measures ANOVA with Tukey post hoc tests. Data are mean±SE; P<0.05 was considered significant. The results showed that MAP was higher in IR vs. sham rats on postoperative day 1 (P<0.05) but not thereafter. In IR rats, RBF fell to 70±6% and GFR to 40±14% of baseline by day 2, then both gradually increased to ~88% by day 14. From days 1-13, both measures remained at 67-75% of baseline, with RBF significantly lower in IR vs. sham rats (P<0.05). GFR differences did not reach statistical significance due to variability. Overall, bilateral IR injury produces parallel, sustained reductions in RBF and GFR for nearly two weeks, revealing a previously underappreciated period of renal vulnerability that may inform strategies to mitigate the development of CKD after AKI.
Start Time
15-4-2026 10:00 AM
End Time
15-4-2026 11:00 AM
Room Number
303
Presentation Type
Oral Presentation
Presentation Subtype
Grad/Comp Orals
Presentation Category
Health
Student Type
Graduate
Faculty Mentor
Aaron Polichnowski
Prolonged Renal Hypoperfusion and GFR Recovery Despite Early MAP Normalization After Ischemia–Reperfusion Injury
303
Ischemia-reperfusion (IR) injury is a major cause of acute kidney injury (AKI) and can lead to prolonged renal dysfunction and chronic kidney disease (CKD). Studies differ on the time course of renal blood flow (RBF) and glomerular filtration rate (GFR) recovery after IR, ranging from near-normalization within 3-5 days to deficits beyond one week. Characterizing these dynamics in the conscious state is critical for understanding progression from AKI to CKD. We hypothesized that bilateral IR injury in conscious, chronically instrumented rats would result in a prolonged period of renal hypoperfusion and dysfunction. To determine this, male Sprague–Dawley rats (n=9; 8-9-weeks-old) were implanted with a blood pressure radiotelemeter, RBF transit-time ultrasonic probe, and FITC-inulin pump. After a 1-week recovery, baseline measurements of mean arterial pressure (MAP), RBF, and GFR (FITC-inulin clearance) were obtained. Rats then underwent 35 min bilateral IR (n=5) or sham (n=4) under anesthesia. For 2 weeks post-surgery, MAP and RBF were measured daily and GFR assessed every 3 days starting day 2 in conscious rats. Group comparisons used 2-way repeated measures ANOVA with Tukey post hoc tests. Data are mean±SE; P<0.05 was considered significant. The results showed that MAP was higher in IR vs. sham rats on postoperative day 1 (P<0.05) but not thereafter. In IR rats, RBF fell to 70±6% and GFR to 40±14% of baseline by day 2, then both gradually increased to ~88% by day 14. From days 1-13, both measures remained at 67-75% of baseline, with RBF significantly lower in IR vs. sham rats (P<0.05). GFR differences did not reach statistical significance due to variability. Overall, bilateral IR injury produces parallel, sustained reductions in RBF and GFR for nearly two weeks, revealing a previously underappreciated period of renal vulnerability that may inform strategies to mitigate the development of CKD after AKI.
