Glomerular Ultrafiltration Pressure Following Acute Kidney injury in Rats with Pre-existing Chronic Kidney Disease

Background: GFR emerges from physical determinants, but GFR does not imply values for those determinants. It is unknown what happens to individual determinants of GFR in previously healthy, or chronically diseased, kidneys as they recover from acute injury. Objective: To define changes in single-nephron GFR (SNGFR) and associated changes in glomerular ultrafiltration pressure during recovery from acute ischemic renal injury (AKI) and whether this is affected by pre-existing chronic kidney disease (CKD). Method: Glomerular hemodynamics assessed by renal micropuncture (MP) in 527 nephrons from 53 male Wistar Froemter rats. CKD was by subtotal nephrectomy (STN) (ablation/ infarction). AKI was by 60-minutes bilateral pedicle clamp done 3-weeks after STN. MP was performed 1 day, 1 week or 4 weeks after AKI in controls. MP was performed 1 or 4 weeks after AKI in CKD. Pressure in glomerular capillary (PGC) and Bowman space (PBS) and afferent effective filtration pressure (EFPa) were determined from tubular stop-flow pressure, free-flow pressure, and plasma oncotic pressure. Pairwise comparisons were made after Tukey test including all 7 groups. Results: Results in sham were not different between time points, so Shams are pooled across time points. *p<0.05 vs respective Sham. †<0.05 vs Control. Comparisons after Tukey test including all 7 groups. [Table: see text] Conclusion: Low SN(GFR) after AKI is associated with reduced filtration pressure due to reduced PGC in both Controls and STN. Renal recovery from AKI in STN is more rapid, but less complete. Increased heterogeneity of function persists between nephrons in kidneys recovered from AKI. Contrary to expectation, glomerular capillary hypertension, which is normally associated with this model of CKD, was absent in the CKD kidney after 4 weeks of recovery from AKI. NIDDK R01 DK 132690 and UAB/UCSD O'Brien Center for Acute Kidney Injury Research Grant U54-DK 137307 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

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Journal
Physiology
Published
2025-05-01
DOI
https://doi.org/10.1152/physiol.2025.40.s1.1267
Primary Topic
Acute Kidney Injury Research
Type
article
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article

Glomerular Ultrafiltration Pressure Following Acute Kidney injury in Rats with Pre-existing Chronic Kidney Disease

Scott C. Thomson, Volker Vallon
Physiology
Acute Kidney Injury Research
article

Glomerular Ultrafiltration Pressure Following Acute Kidney injury in Rats with Pre-existing Chronic Kidney Disease

Scott C. Thomson, Volker Vallon
article en

Abstract

Background: GFR emerges from physical determinants, but GFR does not imply values for those determinants. It is unknown what happens to individual determinants of GFR in previously healthy, or chronically diseased, kidneys as they recover from acute injury. Objective: To define changes in single-nephron GFR (SNGFR) and associated changes in glomerular ultrafiltration pressure during recovery from acute ischemic renal injury (AKI) and whether this is affected by pre-existing chronic kidney disease (CKD). Method: Glomerular hemodynamics assessed by renal micropuncture (MP) in 527 nephrons from 53 male Wistar Froemter rats. CKD was by subtotal nephrectomy (STN) (ablation/ infarction). AKI was by 60-minutes bilateral pedicle clamp done 3-weeks after STN. MP was performed 1 day, 1 week or 4 weeks after AKI in controls. MP was performed 1 or 4 weeks after AKI in CKD. Pressure in glomerular capillary (PGC) and Bowman space (PBS) and afferent effective filtration pressure (EFPa) were determined from tubular stop-flow pressure, free-flow pressure, and plasma oncotic pressure. Pairwise comparisons were made after Tukey test including all 7 groups. Results: Results in sham were not different between time points, so Shams are pooled across time points. *p<0.05 vs respective Sham. †<0.05 vs Control. Comparisons after Tukey test including all 7 groups. [Table: see text] Conclusion: Low SN(GFR) after AKI is associated with reduced filtration pressure due to reduced PGC in both Controls and STN. Renal recovery from AKI in STN is more rapid, but less complete. Increased heterogeneity of function persists between nephrons in kidneys recovered from AKI. Contrary to expectation, glomerular capillary hypertension, which is normally associated with this model of CKD, was absent in the CKD kidney after 4 weeks of recovery from AKI. NIDDK R01 DK 132690 and UAB/UCSD O'Brien Center for Acute Kidney Injury Research Grant U54-DK 137307 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

PhysiologyVol. 40(S1)
UC San Diego Health System (US)
Openalex Percentile: Top 82%
Acute Kidney Injury Research
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