Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Proliferative glomerulonephritis with monoclonal immunoglobulin deposition (PGNMID) is a type of monoclonal immunoglobulin-related renal injury associated with clonal proliferation of B lymphocytes or plasma cells. This study summarizes and analyzes the renal pathological morphology and clinical characteristics of PGNMID patients in our department over the past 10 years, providing a basis for the precise treatment of this disease.
We retrospectively analyzed the clinical, renal pathological, and follow-up data of PGNMID patients diagnosed by renal biopsy in the Department of Nephrology, Zhongshan Hospital, Fudan University, from January 2015 to June 2025.
During the study period, 10,927 renal biopsies were performed, identifying 29 (0.30%) PGNMID patients. 24.1% of patients presented with nephrotic syndrome, 65.5% exhibited renal dysfunction, and 31.0% had hypocomplementemia. Four patients were diagnosed with hematological diseases. 37.9% of patients had positive serum immunofixation electrophoresis, while the rest had abnormal serum or urine or bone marrow flow cytometry κ/λ ratio. In terms of renal pathology, 69.0% of patients had membranous proliferative glomerulonephritis, and 34.5% had IgG3-κ monoclonal deposition. Fourteen patients received cytotoxic/chemotherapy/targeted therapy, with a median follow-up time of 77.5 (9, 125.5) weeks. Five(35.7%) patients achieved renal remission.
Table 1 Clinical and laboratory examination data of 29 patients with PGNMID
Total
N=29
eGFR≤60ml/min/1.73m2
N=19
eGFR>
60ml/min/1.73m2
N=10
P Value
Gender
0.4311
Male/[n(%)]
20（69.0%）
12（41.4%）
8（27.6%）
Female/[n(%)]
9（31.0%）
7（24.1%）
2（6.9%）
Age
59.66±12.60
61.11±11.16
56.9±15.22
0.4027
Urine protein/（g/d）
2.98(1.14,5.67)
4.86(1.64,7.03)
1.23(0.56,3.26)
0.0051
Hematuria/[n(%)]
0.2023
Yes
19（65.5%）
14（48.3%）
5（17.2%）
No
10（34.5%）
Hemoglobin/(g/L)
107.0±21.99
101.9±21.61
116.6±20.36
0.0882
BUN/（mmol/L）
9.0(6.55,12.15)
11.5(8.0,13.2)
6.7(4.6,8.7)
0.0069
Scr/（μmol/L）
121(99,192)
197.3±114.1
85.60±18.84
eGFR/(ml/min/1.73m2)
52.10±28.70
35.21±14.25
84.20±20.26
<0.0001
AKI/[n(%)]
0
CKD/[n(%)]
27（93.1%）
17（58.6%）
CKD G1/[n(%)]
3（10.3%）
CKD G2/[n(%)]
CKD G3/[n(%)]
CKD G4/[n(%)]
6（20.7%）
CKD G5/[n(%)]
1（3.4%）
CysC/(mg/L)
1.72±0.73
2.03±0.65
1.10±0.41
0.0012
UA/（μmol/L）
374.7±110.3
386.9±119.5
348.9±88.63
0.4049
Serum albumin（g/L）
32.93±6.92
31.53±5.78
35.89±8.49
0.1213
LDH/(U/L)
198.0(179.5,275.8)
206.0(189.0,284.0)
181.0(153.0,246.0)
0.1457
β2-MG/(mg/L)
5.62±3.58
6.75±3.62
2.78±0.97
0.0171
Serum calcium/(mmol/L)
2.18(2.03,2.28)
2.18(2.02,2.28)
2.23(2.04,2.38)
0.5058
IgG/(g/L)
7.40(4.74,10.30)
7.40(4.41,10.59)
7.51(6.45,10.30)
0.6073
C3/(g/L)
0.91±0.20
0.90±0.21
0.93±0.21
0.7159
C4/(g/L)
0.21±0.07
0.22±0.06
0.21±0.10
0.7312
CH50/(IU/mL)
59.86±18.65
64.74±18.62
50.10±15.40
0.0687
Serum immunofixation electrophoresis [n(%)]
0.6926
Positive
11（37.9%）
Negative
18（62.1%）
Serum freeκ/λlight chain ratio abnormal[n(%)]
5/20
4/20
1/20
Urine freeκ/λlight chain ratio abnormal [n(%)]
10/28
8/28
2/28
Bone marrow κ/λlight chain ratio abnormal [n(%)]
14/20
9/20
cTnT/(ng/mL)
0.018(0.01,0.039)
0.027(0.013,0.038)
0.009(0.006,0.016)
0.0028
NT-proBNP/(pg/mL)
256.0(82.7,701.0)
462.0(183.0,2057)
143.3(28.93,251.30)
0.0104
Table 2 Renal biopsy pathological characteristics of 29 patients with PGNMID
χ2
IF
C3 positive
21
14
7
*1.00
C4 positive
4
3
*0.65
C1q positive
11
Ig subgroup and light chain
5.245
0.81
IgG1-κ
2
1
IgG1-λ
IgG2-κ
IgG2-λ
IgG3-κ
10
6
IgG3-λ
5
IgA-κ
IgA-λ
IgM-κ
κ
LM
10.19
0.07
MPGN
20
15
Atypical MN
Crescentic nephritis
MsPGN
MsPGN+LCPT
MsPGN+LCCN
Glomerulosclerosis ratio
3.881
0.14
<25%
12
8
25%~50%
>50%
Crescent existing
*0.13
Ratio of crescentic glomerular
&am ConclusionPGNMID is associated with clonal proliferation of B lymphocytes or plasma cells, and pathogenic clones can be identified by combining immunofixation electrophoresis, serum/urine free light chain ratio, and bone marrow pathological examination. Renal biopsy pathology is a key indicator for the diagnosis of PGNMID. Clonal targeted therapy is currently a new direction for the treatment of PGNMID, with a certain rate of renal remission, and long-term efficacy remains to be observed. Future prospects: regarding the controversy over whether the PGNMID-IgG3 subtype should be removed from MGRS, we believe that there is still insufficient evidence at present. Recent studies suggest that both immune dysregulation and chronic inflammation can cause bone marrow changes, thereby mediating epigenetic and transcriptional reprogramming of monocytes, leading to the secretion of pro-inflammatory factors and causing kidney disease. Inflammation, immunity, and tumors cannot be completely distinguished in the pathogenesis pathway of kidney disease, and current treatment methods targeting these mechanisms are converging and have achieved good results. We should examine PGNMID from the following perspectives: through what mechanisms do factors such as infection induce cloning? Is there a correlation between the abundance and species of clones producing nephrotoxic IgG3? Are there different treatment plans for different subtypes of PGNMID? Therefore, there is an urgent need to expand the sample size, further conduct molecular research based on different subtypes, and evaluate the optimal treatment strategy. Kewords
PGNMID is associated with clonal proliferation of B lymphocytes or plasma cells, and pathogenic clones can be identified by combining immunofixation electrophoresis, serum/urine free light chain ratio, and bone marrow pathological examination. Renal biopsy pathology is a key indicator for the diagnosis of PGNMID. Clonal targeted therapy is currently a new direction for the treatment of PGNMID, with a certain rate of renal remission, and long-term efficacy remains to be observed.
Future prospects: regarding the controversy over whether the PGNMID-IgG3 subtype should be removed from MGRS, we believe that there is still insufficient evidence at present. Recent studies suggest that both immune dysregulation and chronic inflammation can cause bone marrow changes, thereby mediating epigenetic and transcriptional reprogramming of monocytes, leading to the secretion of pro-inflammatory factors and causing kidney disease. Inflammation, immunity, and tumors cannot be completely distinguished in the pathogenesis pathway of kidney disease, and current treatment methods targeting these mechanisms are converging and have achieved good results. We should examine PGNMID from the following perspectives: through what mechanisms do factors such as infection induce cloning? Is there a correlation between the abundance and species of clones producing nephrotoxic IgG3? Are there different treatment plans for different subtypes of PGNMID? Therefore, there is an urgent need to expand the sample size, further conduct molecular research based on different subtypes, and evaluate the optimal treatment strategy.
