Abstract: FR-PO1000
Impact of Nephron Number on Renal Uric Acid Excretion in Patients with IgA Nephropathy
Session Information
- Pathology and Lab Medicine: Basic
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: CKD (Non-Dialysis)
- 2102 CKD (Non-Dialysis): Clinical, Outcomes, and Trials
Authors
- Marumoto, Hirokazu, The Jikei University School of Medicine, Tokyo, Japan
- Tsuboi, Nobuo, The Jikei University School of Medicine, Tokyo, Japan
- Sasaki, Takaya, The Jikei University School of Medicine, Tokyo, Japan
- Okabayashi, Yusuke, The Jikei University School of Medicine, Tokyo, Japan
- Haruhara, Kotaro, The Jikei University School of Medicine, Tokyo, Japan
- Kanzaki, Go, The Jikei University School of Medicine, Tokyo, Japan
- Koike, Kentaro, The Jikei University School of Medicine, Tokyo, Japan
- Ichida, Kimiyoshi, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan
- Yokoo, Takashi, The Jikei University School of Medicine, Tokyo, Japan
Background
Hyperuricemia is a risk factor for the progression of chronic kidney disease (CKD), which is characterized by a progressive loss of functioning nephrons. Uric acid (UA) induces renal tubular cell injury. To date, renal UA handling has not been examined in relation to nephron number in patients with CKD due to technical difficulties in counting nephrons in a clinical setting.
Methods
The relationships between parameters related to UA handling and clinically relevant factors, including total nephron number, were examined in patients with biopsy-proven IgA nephropathy (IgAN). The total nephron number was estimated by the combined use of unenhanced computed tomography and stereology-based estimation of non-sclerotic glomerular density in biopsy specimens (Sasaki T et al. 2018 ASN).
Results
A total 87 patients were included in the study (mean age, 39.7 years; 47.1% male; estimated glomerular filtration rate [eGFR], 67.1 ± 22.1 ml/min/1.73 m2). The total nephron number in the patients ranged from 78,000 to 1,989,000 per kidney. The serum UA level and total nephron number showed a significant inverse correlation (r = −0.395, p < 0.01) (Figure A). Multivariate analysis showed that the association between the serum UA and nephron number was independent of gender, BMI, and renal function. The single-nephron excretion of urinary UA (urinary UA/urinary creatinine per total nephron number) was markedly increased in patients with advanced CKD at stage 3b or higher (Figure B).
Conclusion
The results of this study suggest that the total number of nephrons is an important determinant of the serum UA level in patients with IgAN. Abnormally concentrated UA in renal tubules due to compensatory failure may play additional roles in the progression of renal injury in patients with advanced-stage CKD.