Table 2

Baseline pathological characteristics stratified by eGFR declining speed

IncreasingControlDecreasingTotalInc
vs Cont
Dec vs Cont
MeanMedian2575MeanMedian2575MeanMedian2575MeanMedian2575P valueP value
Diff1.722122.112132.323232.17213
Nodu0.200000.300010.531010.43001
Double0.430010.89101.51.211021.00102<0.05
Exda0.280010.370010.581010.48001
MesL0.160000.250010.480010.38001
Pola0.521010.781110.791110.74101
GScle16.8010.0029.624.5820.06.634.427.2824.010.040.024.8520.06.339.0<0.05
SScle1.790002.90003.33.800.00.05.63.260.00.04.3
GMega0.300010.380010.450010.41001
IFTA1.271121.652122.032131.82213
ICell0.921011.271121.311121.23112<0.05
Hyali1.912132.303232.272232.21313
Athero1.001021.221121.311121.24112
  • Data are mean and median (25th, 75th percentile) of pathological score or %.

  • Baseline pathological characteristics stratified by eGFR declining speed were shown. After propensity score matching with urinary albumin, Hb, and systolic blood pressure, three pathological findings (subendothelial space widening, global glomerulosclerosis, and interstitial cell infiltration) have a lower score in eGFR increasing group than control group. There was no statistical significance in any pathological financing between control and declining group.

  • Athero, intimal thickening; Cont, control group; Dec, eGFR declining group; Diff, diffuse lesion; Double, subendothelial space widening (or duplication of basement membrane); eGFR, estimated glomerular filtration rate; Exda, exudative lesion; GMega, glomerulomegaly; GScle, global glomerulosclerosis, collapsing glomerulopathy, and ischemic nephropathy; Hyali, arteriolar hyalinosis; ICell, interstitial cell infiltration; IFTA, interstitial fibrosis and tubular atrophy; Inc, eGFR increasing group; MesL, mesangiolysis/microaneurysm; Nodu, nodular lesion; Pola, perihilar neovascularization (polar vasculosis); SScle, segmental sclerosis.