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Modification of the impact of hypertension on proteinuria by renal arteriolar hyalinosis in nonnephrotic chronic kidney disease

Objective: Morphological analysis suggests that afferent arteriole hyalinosis reflects disturbed autoregulation of glomerular hemodynamics. However, the effect of arteriolar hyalinosis on the correlation between blood pressure (BP) levels and proteinuria is unknown in patients with chronic kidney disease (CKD). Therefore, we conducted a cross-sectional study to determine this correlation. Methods: A total of 109 patients with nonnephrotic 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 arteriolar hyalinosis. Result: Patients had a mean age, BP, estimated glomerular filtration rate, and urine protein level of 40 years, 126/75 mmHg, 86 ml/min per 1.73 m2, and 1.3 g/gCr, respectively. Patients with hyalinosis (n = 59) exhibited significant increases in median proteinuria (g/gCr) because the SBP increased (<130, 130–140, and ≥140 mmHg: 1.0, 1.3, and 2.3, respectively; P = 0.045); however, median proteinuria was comparable in patients without hyalinosis (n = 50), regardless of SBP. Multiple logistic analysis revealed that combined high BP and hyalinosis were significantly associated with increased proteinuria, defined as equal to or greater than the median value (odds ratio: 5.99, 95% confidence interval: 1.13–31.70, P < 0.05 vs. high BP−/hyalinosis−). Moreover, this combination was associated with the largest glomerular diameter. Conclusion: Renal arteriolar hyalinosis may potentiate susceptibility to BP-related glomerular damage in patients with nonnephrotic CKD. Dysregulated afferent arteriolar resistance via arteriolar sclerosis may affect hypertensive renal damage.