Aim. To study clinical, laboratory, and morphological risk factors for small-diameter renal arterial fibrosis in patients with hypertension (HTN) and primary chronic glomerulonephritis (CGN).Material and methods. The study included 102 patients with primary CGN. The first group consisted of 62 patients with small-diameter renal arterial fibrosis according to renal biopsy; the second group included 40 patients without vascular fibrosis. All patients signed informed consent.Results. A comparative analysis revealed the most significant differences between groups 1 and 2: mean systolic blood pressure (SBP) — 131,85±17,56 mm Hg and 119,65±22,2 mm Hg, respectively (p=0,0008); mean diastolic blood pressure (DBP) — 84,11±10,7 and 79,63±9,7 mm Hg (p=0,03), respectively; peak SBP — 158,61±23,76 mm Hg and 144,25±23,56 mm Hg (p=0,002), respectively; peak DBP — 95,66±10,33 mm Hg and 90,63±10,74 mm Hg (p=0,02), respectively; HTN stage — 1,85 [1; 3] and 1,38 [1; 3] (p=0,03), respectively; HTN grade — 1,73 [1; 3] and 1,13 [1; 3] (p=0,004), respectively; left ventricular hypertrophy — 15 patients and 2 patients (p=0,006), respectively; blood urea nitrogen — 8,98±7,31 and 6,42±4,02 mmol/L (p=0,03), respectively. Significant morphological differences between first and second groups were as follows: tubulointerstitial fibrosis — 56% and 21% (p<0,001), respectively; tubulointerstitial inflamemation — 44% and 16% (p=0,002), respectively; interstitial fibrosis — 24,9±20,5% and 9,89±19,8% (p=0,001), respectively.Conclusion. The presented analysis emphasizes a significant contribution of hemodynamics in small-diameter renal arterial fibrosis in patients with HTN and CGN. It manifested by a persistent increase of SBP and involvement of target organs. Systemic hemodynamic changes are fundamental in the development of small-diameter renal arterial fibrosis in patients with HTN and primary CGN, while the isolated progression of CGN does not significantly affect the structure of small-diameter renal arteries.