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. Author manuscript; available in PMC: 2012 Jul 1.
Published in final edited form as: J Hypertens. 2012 Jul;30(7):1453–1459. doi: 10.1097/HJH.0b013e328353e807

TABLE 2.

Histological changes in IgAN vs. controls

IgAN (n = 40) Control (n = 4) P value
Proximal tubular AGT 0.40 ± 4.24 0.08 ± 5.02 0.04

Glomerular lesionsa
 Glomerular obsolescence 0.1 ± 0.1 0.1 ± 0.1 0.6
 Glomerular sclerosis 0.6 ± 0.6 0.0 ± 0.0 0.02
 Mesangial proliferation 0.4 ± 0.5 0.0 ± 0.0 0.01
 Mesangial matrix increase 0.4 ± 0.5 0.0 ± 0.0 0.005

Tubulo-interstitial and vascular lesions
 Interstitial fibrosis No. of patients (%)
  0 (absent) 24 (60.0) 3 (75.0) 0.7
  1 (≤25%) 10 (25) 1 (25.0)b
  2 (26–50%) 6 (15) 0
  3 (>50%) 0 0
 Tubular atrophy No. of patients (%)
  0 (absent) 31 (77.5) 3 (75.0) 0.8
  1 (≤25%) 6 (15.0) 1 (25.0)b
  2 (26–50%) 3 (7.5) 0
  3 (>50%) 0 0
 Arteriolar hyalinosis No. of patients (%)
  0 (absent) 36 (90.0) 4 (100) 0.5
  1 (mild) 4 (10.0) 0
  2 (severe, any) 0 0
  3 (severe, many) 0 0
 Arterial intimal thickening No. of patients (%)
  0 (absent) 33 (82.5) 4 (100) 0.4
  1 (≤25%) 7 (17.5) 0
  2 (26–50%) 0 0
  3 (>50%) 0 0

Values are means ± SD. AGT, angiotensinogen (arbitrary unit); IgAN, IgA nephropathy.

a

Glomeruli were scored individually and the mean scores calculated for all nonsclerosed glomeruli semiquantitatively.

b

Less than 10% was involved. An adequate specimen for the light microscopy containing sufficient cortical area was considered as a biopsy with at least 10 glomeruli. Consequently, a total of 1290 and 70 glomeruli in the specimens from IgAN and control individuals, respectively, were observed.