Abstract: FR-PO382

Augmented Association between Blood Pressure and Proteinuria in Hyperuricemic Patients with Non-Nephrotic Chronic Kidney Disease

Session Information

Category: Chronic Kidney Disease (Non-Dialysis)

  • 301 CKD: Risk Factors for Incidence and Progression

Authors

  • Kohagura, Kentaro, University of the Ryukyus, Nishihara-cho, OKINAWA, Japan
  • Miyagi, Tsuyoshi, University of the Ryukyus, Nishihara-cho, OKINAWA, Japan
  • Zamami, Ryo, University of the Ryukyus, Nishihara-cho, OKINAWA, Japan
  • Ohya, Yusuke, University of the Ryukyus, Nishihara-cho, OKINAWA, Japan
Background

High serum uric acid levels (HU) may enhance susceptibility to hypertensive renal damage via disrupted autoregulation system of glomerular hemodynamics. However, effect of HU on the relationship between blood pressure (BP) levels and proteinuria is unknown in patients with chronic kidney disease (CKD).

Methods

A total of 109 patients with non-nephrotic CKD (55 men and 54 women) who underwent renal biopsy were recruited. Arteriolar hyalinosis was semiquantitatively assessed via arteriole grading. We examined the correlation between BP and urine protein levels (g/gCr) according to the presence of higher uric acid (HU) levels (mg/dl), defined as ≥7 in men and 5≥ in women, which were the levels from which risk of hyalinosis is increased in our previous study.

Results

The median for age, BP, estimated glomerular filtration rate (eGFR), and urine protein were as follows: 38 years, 124/74 mmHg, and 82 ml/min/1.73 m2, and 0.8 g/gCr, respectively. In the patients with HU (n=58), log-transformed systolic BP was significantly correlated with log-transformed urine protein (r=0.49, p<0.0001). In contrast, there was no significant correlation between them in those without it (n=51). In the multiple regression model (R2=0.18, p=0.0009), interaction of HU and log-transformed systolic BP for proteinuria was significantly correlated with logarithm-transformed urine protein (β=3.0, p=0.04) independent of age, sex and potential confounding factors. However, its statistical significance was completely disappeared after additional adjustment with arteriolar hyalinosis index.

Conclusion

These results suggested that HU might potentiate the susceptibility for hypertensive glomerular damage via disrupted autoregulation in non-nephrotic CKD patients.