| PMC full text: | Published online 2023 Jul 3. doi: 10.3389/fimmu.2023.1192941
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Table 1
Summary references of mononuclear phagocyte system in IgA nephropathy.
| Author | Year | Age | Sex (M/F) | Renal biopsy | Blood test | Urinalysis | Hypertension | Infiltration of mononuclear macrophages | Outcome | Conclusion |
|---|---|---|---|---|---|---|---|---|---|---|
| Glomeruli and tubulointerstitium | ||||||||||
| Caliskan Y (12) | 2022 | 37 ± 13 | 31/16 | M1: 26 E1: 16 S1: 27 T0: 32 T1: 14 C0: 25 C1: 11 | Scr (mg/dl) median (IQR): 1.2 (1.0–1.6) ALB (g/L) median (IQR): 42 (36–44) eGFR (ml/min/1.73 m2): 70.3 ± 35.6 Serum Gd-IgA1 (µg/µl) median (IQR): 6.18 (3.16–12.44) Serum AOPP (µmol/L) median (IQR): 90 (47–169) | Macroscopic hematuria, n = 5 Microscopic hematuria, n = 30 Proteinuria (g/day) median (IQR): 1.9 (1.0–4.0) | Systolic BP (mmHg): 131 ± 14 Diastolic BP: 78 ± 9 Hypertension presentation: n = 15 | CD68+ cell count (glomerular) median (IQR): 4.4 (2.8–11.1) CD68+ cell count (tubulointerstitium) median (IQR): 10 (5–30) | The number of CD68+ cells per glomerulus is linked to C (r = 0.346), M (r = 0.325), final MEST-C sum scores (r = 0.337) Tubulointerstitial CD68+ cell count with T score (r = 0.302) MEST-C score (r = 0.322), proteinuria (r = 0.410) | Macrophages, in the tubulointerstitial compartment, were paralleled to tubular atrophy, interstitial fibrosis, and the degree of proteinuria, while macrophages in glomeruli were related with crescent formation. |
| Xie D (11) | 2021 | Responders: 33.5 ± 9.8 Non-responders: 35.5 ± 9.2 | Responders: 119/146 Non-responders: 61/92 | Responders/non-responders M1: 248/146 E1: 31/14 S1: 227/132 T1: 103/55 T2: 63/61 C1: 115/59 | Responders eGFR (ml/min/1.73 m2): 85.2 ± 28.9 ALB (g/L): 36.6 ± 6.7 Hemoglobin (g/L): 130.7 ± 20.1 Non-responders eGFR (ml/min/1.73 m2): 74.0 ± 30.3 ALB (g/L): 36.7 ± 5.8 Hemoglobin (g/L): 126.4 ± 19.9 | Responders 24-h proteinuria (g/day): 1.4 Non-responders 24-h proteinuria (g/day): 1.3 | Hypertension presentation (n) Responders: 41 Non-responders: 25 | Responders/Non-responders Glomeruli (cells per glomerulus): CD68+ macrophages: 4.7/1.5 (p < 0.001) CD206+ macrophages: 3.3/1.4 (p < 0.001) Tubulointerstitium (cells per 100 mm2) CD68+ macrophages: 2.4/1.9 (p = 0.01) CD206+ macrophages: 2.4/2.1 (p < 0.001) | Macrophages, in the tubulointerstitium positively related with T scores, tubulointerstitial fibrosis, and eGFR attenuation, were the marker of chronic kidney damage. | The quantity of glomerular macrophage can reflect the possibility of reaction to immunosuppression in IgAN patients with a high risk of renal injury. |
| Yang M (24) | 2021 | NA | NA | Lee grade III: n = 17 IV: n = 12 V: n = 11 | Scr (mmol/L): III: 79.31 ± 19.73 IV: 113.59 ± 24.07 V: 145.40 ± 36.40 eGFR (ml/min/1.73 m2) III: 94.59 ± 28.05 IV: 71.18 ± 19.93 V: 49.84 ± 16.41 | Proteinuria (g/day) III: 0.92 ± 0.63 IV: 1.50 ± 0.98 V: 3.08 ± 1.62 Urinary RBC (HP) III: 43.47 ± 45.38 IV: 91.49 ± 91.78 V: 88.90 ± 88.59 | NA | IgAN patients: Location: macrophages mainly infiltrated the interstitium of the renal tubules and some in the glomerular capillaries and lumen of the renal tubules. M0 macrophages were mainly polarized into M2 macrophages. Control: no distribution | The infiltration of M2 macrophage is related with Scr (r = 0.447) and 24-h proteinuria (r = 0.436) and eGFR (r = −0.332) and fibrotic area (r = 0.777) NS between M0 and M1 and clinical indicator normal | M2 macrophages, AIM, and TGF-β1 play pivotal roles in the course of IgAN fibrosis, which is influenced mutually. M2 macrophage is related with AIM (r = 0.900) and TGF-β1 (r = 0.888). AIM is related with TGF-β1 (r = 0.913). |
| Hu W (20) | 2019 | 38.76 ± 12.89 | 22/27 | M0: n = 19 E0: n = 48 S0: n = 23 T0/T1: n = 22/27 C0/C1: n = 32/17 Lee grade (n): II: 5 III: 18 IV: 6 V: 13 | Scr (μmol/L): 166.19 ± 88.06 ALB (g/L): 37.62 ± 5.67 BUN (mmol/L): 8.96 ± 3.79 | Proteinuria (g/day): 1.871 ± 1.865 | Systolic BP: 131.88 ± 19.22 Diastolic BP: 81.88 ± 12.70 Hypertensive patients: 55.1% | The numbers of macrophages in the glomerular: Glomerular macrophage: 12.84 ± 7.94 M2a: 7.24 ± 4.39 M2b: 10.72 ± 6.58 M2c: 3.50 ± 1.98 The numbers of macrophages in the tubulointerstitium: Tubulointerstitial macrophage: 26.13 ± 17.68 M2a: 14.47 ± 8.60 M2b: 15.14 ± 12.24 M2c: 6.02 ± 3.68 | Macrophages in the tubulointerstitium were related with glomerular sclerosis (r = 0.283), and tubulointerstitial fibrosis (r = 0.400). In tubulointerstitium, the quantities of M2a were positively pertinent to Scr (r = 0.363), 24-h proteinuria (r = 0.329), degree of focal sclerosis (r = 0.457), and tubulointerstitial fibrosis (r = 0.327). M2a macrophages that mainly migrated to tubulointerstitium were related with M1, S1, and T1 in line with the Oxford MEST-C and Lee grade IV–V. The number of M2c macrophages in glomeruli was related with T0, G0, and Lee grade II–III. M2b macrophages were NS. | In IgAN, the counts of M2a and M2b macrophages were higher than those of M2c. M2a macrophages were pertinent to more serious tubulointerstitial pathological features and kidney function, but M2c was negatively associated with glomerular sclerosis and tubulointerstitial fibrosis. |
| Li J (18) | 2015 | With crescents: 35 ± 20 Without crescents: 42 ± 10 | With crescents: 3/7 Without crescents: 6/8 | With/without crescents (mean rank) E: 13.7/12.01 M: 12.55/12.46 S (glomerular): 11.93/12.11 S (focal): 12.65/12.39 T: 12.7/12.36 | Scr (g/l) With crescents: 34 ± 7 Without crescents: 41 ± 7 eGFR (ml/min/1.73 m2) With crescents: 58 ± 27 Without crescents: 88 ± 22 | Proteinuria (g/day) With crescents: 1.8 ± 1.1 Without crescents: 1.0 ± 0.7 | NA | CD163+ macrophages in tubulointerstitium: With crescents: 26 ± 8 Without crescents: 9 ± 4 CD163+ macrophages in glomeruli: With crescents: 4 ± 1 Without crescents: 2 ± 1 | CD163+ macrophage in tubulointerstitium is related with ALB (r = −0.574), eGFR (r = −0.718), proteinuria (r = 0.520), and with glomeruli crescents (r = 0.821). CD163+ macrophage in glomeruli is related with eGFR (r = −0.523) and with glomeruli crescents (r = 0.730). | More CD163+ macrophages infiltrated the glomeruli and acute tubulointerstitial lesions in IgAN patients with Formation of crescents. |
| Ikezumi Y (13) | 2011 | Children (<10 years): n = 14 Children (> 12 years): n = 15 Adults (26–35 years): n = 27 | Children (<10 years): 8/6 Children (>12 years): 6/9 Adults (26–35 years): 11/6 | Children (<10 years): Glomerular hypercellularity increased cells in the mesangial and endocapillary cells. Children (>12 years): glomerular lesion more akin to the adult IgAN Adults: glomerular matrix expansion, segmental glomerulosclerosis | eGFR (ml/min/1.73 m2): Children (<10 years): 107.4 ± 17.3 Children (>12 years): 121.1 ± 14.1 Adults: 104.3 ± 28.2 | Proteinuria (g) (1.73 m2 /day): Children (<10 years): 1.2 ± 1.3 Children (>12 years): 0.9 ± 0.4 Adults: 0.8 ± 0.4 Hematuria (score): Children (<10 years): 2.9 ± 1.3 Children (>12 years): 3.0 ± 1.0 Adults: 2.8 ± 1.3 | Hypertension presentation (n): Children (<10 years): 0 Children (>12 years): 0 Adults: 5 | The accumulation of CD68+ macrophages was evident in glomeruli and tubulointerstitium and greater in adults than in the young pediatric group. CD163+ is higher in adults (65%) and the older than younger pediatrics (29%). CD204+ is higher in adults than in the two groups of pediatrics. | CD68+ and CD163+ macrophages are related with proteinuria in all groups (r) Children (<10 years)/children (>12 years)/adults CD68+ macrophages: 0.71/0.79/0.69 CD163+ macrophages: 0.67/0.77/0.73 In children (<10 years) groups the CD68+ macrophage is correlated with glomerular hypercellularity (r = 0.86), in children (>12 years) (r = 0.66), CD204+ is correlated with it (r = 0.56) | In early phase of IgAN, the alternatively activated macrophages infiltrated the glomeruli and tubulointerstitium, and M2 macrophages were correlated with glomerular matrix expansion. |
| Zhu G (25) | 2006 | 23–66 (average 42.7) | 26/10 | Hypercellular glomerulus n: Grade 0 (none)/grade 1 (<25%)/grade 2 (25%–50%): 3/29/4 Mild–moderate glomerulosclerosis n: Grade 0/grade 1/grade 2/grade 3: 3/11/13/9 Tubular atrophy n: Grade 1/grade 2 (<25%):22/14 Tubulointerstitial fibrosis, n: Grade 1/grade 2: 19/17 | Median (range) Scr: 130 (91–180) μmol/L eGFR: 66 (40–91) ml/min | Mean proteinuria: 2.3 ± 1.8 g/day 31% of patients had proteinuria > 3 g/day Microscopic hematuria: n = 32 (89%) | Hypertension presentation, n = 16 | The number of activated macrophages (27E10) in glomeruli is related with Scr (r2 = 0.1) and tubulointerstitium Scr (r2 = 0.34). The number of macrophage (Mac387) and CD25+ cell in interstitial is related with Scr (r2 = 0.33, r2 = 0.23) Correlation of the number of tubulointerstitial Mac387 (r2 = −0.21) and 27E10 (r2 = −0.19) with eGFR | The number of activated macrophages in the glomeruli is weakly related with follow-up Scr (r2 = 0.15). Activated macrophage and macrophage in the tubulointerstitium are related with the follow-up Scr (r2 = 0.34, r2 = 0.33). | The quantities of activated macrophages (27E10) in the glomeruli and tubulointerstitium reflected a poor kidney prognosis. |
| Utsunomiya Y (26) | 1999 | Stable group: 30.0 ± 7.9 ESRD group: 30.5 ± 8.5 | Stable group: 7/6 ESRD group: 9/5 | Mesangial cell cellularity (score) Stable group: 0.8 ± 0.3 ESRD group: 1.4 ± 0.7 | NA | Proteinuria (g/day): Stable group: 0.7 ± 0.5 ESRD group: 1.3 ± 0.8 | Stable group: Systolic BP: 124.3 ± 22.9 Diastolic BP: 75.2 ± 13.3 ESRD group: Systolic BP: 124.6 ± 21.5 Diastolic BP: 72.6 ± 15.9 | CD68+ M/C (mesangial localization index) With/without mesangial expression of α-SMA: 1.6 ± 0.3/0.8 ± 0.2 Mesangial expression of α-SMA Stable group/ESRD: 0.3 ± 0.1/1.1 ± 0.3 (p < 0.0005) Location: distributed in the mesangial area in IgAN patients with the expression of α-SMA. | Mesangial localization of macrophages is able to drive the phenotypic modulation of mesangial cells correlated with renal damage progression. | Macrophages distributed in the mesangial induced phenotypic modulation of mesangial cells and the expression of α-SMA in mesangial predicted the progressive attenuation in kidney function in IgAN patients. |
| Arima S (27) | 1991 | 18–66 (average 42.3) | 21/24 | Controls: n = 8 Mes-Grade 1: n = 20 Mes-Grade 2: n = 14 Mes-Grade 3: n = 11 | NA | NA | NA | FMC32+ cells (per glomerulus) Controls: 1.32 ± 0.094 Mes-Grade 1: 1.00 ± 0.077 Mes-Grade 2: 2.21 ± 0.153 Mes-Grade 3: 3.85 ± 0.462 FMC32+ cells (capillary lumen:Bowman’s:mesangial area) Controls: 100%:0:0, Mes-Grade 1: 52%:39%:9% Mes-Grade 2–3: 40%:40%:19% | The counts of FMC32+ cells per glomerulus were correlated with severity of proteinuria (r = 0.387) and the number of cellular crescent (r = 0.779). | The monocyte/macrophages infiltrating the glomeruli were the markers of the high level of mesangial proliferation and glomerular sclerosis. The monocyte/macrophages infiltrating the tubulointerstitium were correlated with tubulointerstitial damage, especially around the sclerosis of glomeruli. |
| Alexopoulos E (28) | 1989 | 27 ± 14.8 | 31/3 | 70% of patients: tubular atrophy and tubulointerstitial fibrosis 38% of patients: small segmental crescents | Pcr (μmol/1): 109.3 ± 64.4 35% of patients: IgM 29% of patients: IgG 91% of patients: C3 | Microscopic hematuria Patients: n = 28 Macroscopic hematuria Patients: n = 19 Proteinuria patients: n = 27 | Hypertensive patients %: 32.3% | FMC32+ macrophages Intraglomerular cells (per glomerular cross-section): Controls (n = 8): 0.9 ± 0.4 IgAN (n = 34): 1.1 ± 0.9 Tubulointerstitial cells (per mm2) Controls (n = 8): 75 ± 12 IgAN (n = 34): 278 ± 24 | Monocytes/macrophages with plasma creatinine (r = 0.34) T cells and leucocytes in the tubulointerstitium have a positive relationship with tubular atrophy, tubulointerstitial fibrosis, and crescents (p < 0.05). T cells and leucocytes in the interstitial with Pcr are positive (p < 0.005) | T cells and macrophages played an important role in the pathogenesis of tubulointerstitial lesions and indicated the severity of renal function impairment. |
| Glomerular | ||||||||||
| Kawasaki Y (9) | 2009 | Favorable group: 11.5 ± 2.7 Unfavorable group: 12.1 ± 3.7 | Favorable group: 9/8 Unfavorable group: 4/4 | Favorable group: normal urine or minor abnormal urine Unfavorable group: persistent nephropathy | Favorable group/unfavorable group ALB (g/L): First renal biopsy: 42 ± 7/40 ± 6 Second renal biopsy: 44 ± 4/42 ± 3 Scr (μmol/L): First renal biopsy: 48.6 ± 13.3/49.5 ± 11.5 Second renal biopsy: 42.9 ± 9.7/45.1 ± 8.8 Serum IgA (mg/dl): First renal biopsy 262.4 ± 80.3/259.8 ± 77.5 Second renal biopsy 214.1 ± 77.9/277 ± 85.4 | Favorable group/unfavorable group Urinary protein excretion (mg/m2/h): First renal biopsy Favorable group: 18.6 ± 13.2 Unfavorable group: 20.4 ± 10.6 Second renal biopsy Favorable group: 0.8 ± 1.2 Unfavorable group: 8.3 ± 5.0 Frequency of hematuria (%): First renal biopsy: 100/100 Second renal biopsy: 23.5/100 | NA | Favorable group/unfavorable group Glomerular macrophage MPR8+ First renal biopsy 6.3 ± 2.2/7.8 ± 3.5 Second renal biopsy 1.7 ± 1.2/5.9 ± 1.6 Glomerular macrophage MPR14+ First renal biopsy 1.7 ± 1.4/2.5 ± 1.5 Second renal biopsy 0.4 ± 0.6/0.5 ± 0.5 | MPR14+ macrophages are the marker of acute-stage inflammation, and MPR8+ macrophages are the marker of the chronic stage. MPR8+ might reflect a predilection for chronic inflammation and a poor prognosis in children with IgAN. | Renal macrophages expressing MPR8+ participated in the progression of sclerotic changes in children with IgAN. |
| Nagata M (29) | 1995 | MGA: 12.1 ± 1.1 FGN: 12.7 ± 0.7 DPUN: 12.9 ± 0.9 SCL: 11.8 ± 0.7 Total: 13 ± 0.4 | MGA: 5/3 FGN: 11/4 DPUN: 8/5 SCL: 3/2 Total: 27/14 | MGA: N = 8 FGN: N = 15 DPGN: N = 13 SCL: N = 5 | Serum IgA (mg/dl): MGA: 279 ± 34 FGN: 312 ± 19 DPGN: 247 ± 28 SCL: 243 ± 20 | Proteinuria: (g/day) MGA: 0.1 ± 0.04, FGN: 0.6 ± 0.2 DPGN: 1.5 ± 0.4, SCL: 3.1 ± 1.1 URBC (degree): MGA: 1.4 ± 0.3, FGN: 2.3 ± 0.3 DPGN: 2.4 ± 0.2, SCL: 1.8 ± 0.4 UWBC (HPF): MGA: 1.9 ± 0.4, FGN: 5.7 ± 1.5 DPGN: 8.2 ± 1.9, SCL: 4.0 ± 1.3 | NA | ANM/P (glomerulus): MGA: 1.4 ± 0.3 FGN: 5.6 ± 1.3 DPGN: 6.9 ± 0.9 SCL: 0.4 ± 0.3 | The relationship of ANM/P with the severity of hematuria and leukocyturia (p < 0.01) ANM/GL in MOD and SEV is higher than MIN or SCL (p < 0.05). SEV is higher than MOD (p < 0.05) | During an active site of glomerular inflammation, macrophages that infiltrated the glomeruli take part in mesangial hypercellularity and are involved in the process of par mesangial destructive lesions, decline of GBM, or injury of the integrity of podocyte. |
| Tubulointerstitium | ||||||||||
| Wang Q (22) | 2018 | IgAN: 31.8 ± 11.6 Normal control: 32.9 ± 8.5 | IgAN: 36/35 Normal control: 3/3 | Normal control/IgAN (n): M0: 5/49 S0: 6/54 E0: 6/59 T0: 6/41 T1: 0/9 Tubular interstitial inflammation (1/2/3/4): Normal control: 6/0, IgAN: 30/21/14/6 | NA | Proteinuria g/24 h: Normal control: 0.102 ± 0.41 IgAN patients: 3.6 ± 1.9 sEH +: 1.5 ± 1.04 sEH ++: 2.9 ± 1.7 sEH +++: 4.1 ± 3.9 sEH ++++: 5.4 ± 2.6 | MAP IgAN: 109.7 ± 9.4 Normal control: 90.4 ± 9.2 | IgAN patients have a greater number of CD68+ macrophage cells and higher sEH (enzyme) than control people. sEH facilitated M1 polarization via NF-κB pathway activation, and EET accelerated M2 polarization via the activation of the PI3K pathway. | Tubular atrophy and tubulointerstitial fibrosis are correlated with kidney tubular sEH expression degree R = 0.221 Tubular interstitial inflammation is correlated with renal tubular sEH expression levels R = 0.247, p = 0.038. sEH is positively related with proteinuria R = 0.452. | sEH promotes M1 polarization, which is related to inflammation and fibrosis. IgAN patients have higher levels of sEH. |
| Gutiérrez E (30) | 2012 | Complete recovery: 45.48 ± 19.5 Incomplete recovery: 64.38 ± 12.7 | Complete recovery: 13/3 Incomplete recovery: 12/5 | Complete recovery/incomplete recovery Mesangial proliferation: 71% (+), 21% (++), 8% (+++)/42% (+), 58% (++) % GS:5.7 ± 9.4/15.5 ± 25.3 % Glomeruli with crescents: 3.8 ± 9.4/5.1 ± 9.6 % Tubules with RBC casts: 41.1 ± 19.2/55.3 ± 17.9 Tubular necrosis: 8% (−), 57% (+), 35% (++)/8% (+), 75% (++) 17% (+++) Interstitial fibrosis: 29% (−), 71% (+)/21% (−), 58% (+), 21% (++) | Complete recovery/incomplete recovery Scr (mg/dl) Initial: 2.9 ± 2.1/4.7 ± 1.9 Peak: 3.6 ± 2.1/7.1 ± 3.2 6 months post-AKI: 1.2 ± 0.9/2.4 ± 1.3 eGFR Initial: 33.7 ± 19.9/15.9 ± 10 Peak: 25.4 ± 15.0 6 months post-AKI: 76.5 ± 27.4/32.0 ± 12.8 | Complete recovery/Incomplete recovery Proteinuria (g/day): Initial (at admission): 1.8 ± 1.6/3.2 ± 2.7 Peak: 1.9 ± 1.6/4.9 ± 4.4 6 months post-AKI: 0.4 ± 0.4/1.6 ± 2.2 | Complete recovery Systolic BP: 127.5 ± 22.5 Diastolic BP: 73.9 ± 9.8 Incomplete recovery Systolic BP: 125.3 ± 12.6 Diastolic BP: 72.8 ± 11.7 | Macrophage-positive area, %/CD163+ macrophage score (ρ, p) % GS: (0.44, 0.02)/(0.24, 0.22) % Glomeruli with crescents: (0.17, 0.41)/(0.18, 0.36) % Tubules with RBC casts: (0.39, 0.05)/(0.48, 0.01) Tubular necrosis: (0.42, 0.03)/(0.54, 0.003) Interstitial fibrosis: (0.33, 0.09)/(0.29, 0.13) eGFR 6 months post-AKI: (−0.66, 0.001)/(−0.72, 0.001) Proteinuria 6 months post-AKI: (0.08, 0.69)/(0.50, 0.01) | The CD163+ macrophage is activated by Hb and ROS; therefore, some anti-inflammation reactions are activated. The CD163+ macrophage is related with tubular necrosis and higher proteinuria. | CD163+ macrophages can predict the patients with IgAN at high risk for worse renal outcomes with macroscopic hematuria-related acute kidney injury. |
| Silva GE (14) | 2012 | Favorable course: 27.7 ± 9.2 Unfavorable course: 27.2 ± 13.0 | Favorable course: 10/18 Unfavorable course: 22/12 | NA | Scr (mg/dl): At the time of biopsy: Favorable course: 1.4 ± 0.5 Unfavorable course: 1.9 ± 0.4 At the end of follow-up: Favorable course (n = 28): 2.2 ± 0.7 Unfavorable course (n = 34): 3.8 ± 1.3 | Proteinuria g/24 h: At the time of biopsy: Favorable course: 1.9 ± 0.8 Unfavorable course: 2.9 ± 1.0 At the end of follow-up: Favorable course: 1.1 ± 0.8 Unfavorable course: 1.0 ± 0.5 | NA | Unfavorable courses have more macrophages than favorable courses. | R1: the time of biopsy; R2: the end of the follow-up period Tubulointerstitial macrophages are related with Scr (R1 = 0.28, R2 = 0.46) and proteinuria (R1 = 0.44, R2 = 33), tubulointerstitial α-SMA and NF-kB expression (p = 0.01), tubulointerstitial lesions (p < 0.01), eGFR (r = −0.531), and renal function (p < 0.01) | CD68+ macrophages were positively related with the Scr, 24-h proteinuria, process of renal disease, and a worse outcome. The number of macrophages that increased in the tubulointerstitium was regarded as the predictor for poor prognosis in IgAN patients. |
| Blood | ||||||||||
| Esteve Cols C (31) | 2020 | 50.63 (mean age) | 14/8 | IgAN n (%): M1: 22 (100%) S1: 12 (54.54%) E1: 4 (18.18%) T1-2: 7 (31.82%) Group 1 (n = 13)/Group 2 (n = 9) M1: 13/9 S1: 10/2 (p = 0.0274) E1: 2/2 T1-2: 7/1 (p = 0.0669) | Scr (mg/dl): IgAN: 1.76 ± 3.03 Group 1 (patients with CD89+ MFI < 4000): 2.198 ± 0.389 Group 2 (patients with CD89+ MFI > 4000): 1.157 ± 0.193 | Proteinuria IgAN: 1.21 ± 1.81 (g/g creatinine) Group 1: 1049 ± 297.7 mg/L Group 2: 785.4 ± 368.6 mg/L IgAN: Hematuria: 7 ± 15.90 | NA | In group 1, patients had poor kidney function with higher Scr (p = 0.0440), lower eGFR (p = 0.0506), and a more severe renal biopsy, with more severe S1 (p = 0.0274) and T1-2 (p = 0.0669). | CD89+ on non-classical monocyte can be seen as the marker of diagnosis in IgAN. Low CD89+ monocytes have more severe pathology (S1 and T1-2) and clinical symptoms. | Low expression of CD89+ on monocytes, with higher serum degree of Gd-IgA1 and percentages of inflammatory leukocyte subclasses, increased the sensitivity of diagnosis and prognosis in IgAN. |
M, male; Scr, serum creatinine; ALB, serum albumin; eGFR, estimated glomerular filtration rate; BUN, urea nitrogen; AOPP, advanced oxidation protein product; ANM/P, average number of glomerular macrophages per patient; MAP, mean arterial pressure; Hb, hemoglobin; ROS, reactive oxygen species; NA, not available; MGA, minor glomerular abnormality; FGN, focal proliferative glomerulonephritis; DPGN, diffuse proliferative glomerulonephritis; SCL, sclerosis; sEH, soluble epoxide hydrolase; EET, epoxyeicosatrienoic acids.