MO467SINGLE NEPHRON GFR AND GLOMERULAR HYDROSTATIC PRESSURE IN JAPANESE HEALTHY SUBJECTS

Abstract

Abstract Background and Aims Hemodynamic abnormalities such as intraglomerular hypertension and glomerular hyperfiltration associated with the nephron loss are deeply involved in renal damage progression. Recent studies in humans have described a new method to calculate single nephron GFR (SNGFR), which is defined as GFR divided by the estimated total number of non-sclerosed glomeruli. We have previously shown that a higher SNGFR, which indicates glomerular hyperfiltration, is associated with CKD risk factors. However, it is still unknown that the hemodynamic changes in humans within the glomerulus in response to SNGFR. In the present study, we analysed the renal microcirculatory dynamics with SNGFR in healthy individuals without CKD. Method We retrospectively identified 51 living kidney donors who underwent enhanced computed tomography and kidney biopsy at the time of donation from January 2007 till December 2020. Nglom was calculated as the cortical volume of both kidneys assessed on computed tomography times the 1-hour posttransplant renal biopsy-determined glomerular density. SNGFR was calculated by dividing GFR (calculated from the corrected creatinine clearance) by the non-sclerosed Nglom. Glomerular hydrostatic pressure (Pglom) and afferent / efferent arteriolar pressure were calculated from the Gomez / Ohm's formula. Results Age was 57.0 ± 10.4 years, mean blood pressure was 88.7 ± 13.2 mmHg, GFR was 73.3 ± 16.7 mL/min, and Nglom was 807,774 ± 401,0352 / kidney. SNGFR was significantly associated with renal blood flow and Pglom (p for trend = 0.02, and 0.02, respectively), but not with age, mean blood pressure, renal plasma flow, filtration fraction, afferent / efferent arteriolar pressure (Table1). Conclusion Our results showed that the increase in SNGFR is associated with elevated Pglom, indicating that glomerular hyperfiltration may lead to intraglomerular hypertension.