Prediction of small-diameter arterial fibrosis in patients with hypertension and primary chronic glomerulonephritis

Abstract

<jats:p><jats:bold>Aim</jats:bold>. To study clinical, laboratory, and morphological risk factors for small-diameter renal arterial fibrosis in patients with hypertension (HTN) and primary chronic glomerulonephritis (CGN).</jats:p><jats:p><jats:bold>Material and methods</jats:bold>. 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.</jats:p><jats:p><jats:bold>Results</jats:bold>. 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&lt;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.</jats:p><jats:p><jats:bold>Conclusion</jats:bold>. 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.</jats:p>