Related Experiment Video
Updated: May 28, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
Published on: June 8, 2022
Absence of glomerular IgG4 deposition in patients with membranous nephropathy may indicate malignancy
1Renal Division, Department of Medicine, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Beijing, China.
Background:
The renal pathological manifestations of malignancy-associated membranous nephropathy (M-MN) and idiopathic membranous nephropathy (I-MN) are similar. It has been suggested that glomerular IgG4 deposition may play an important role in the pathogenesis of I-MN. In the present study, we compared the IgG subclass of immune complex deposition, clinical data and pathological data of patients with M-MN and I-MN.
Methods:
Eight patients with M-MN and 42 patients with I-MN diagnosed between 1997 and 2009 in our hospital were enrolled. The clinical and pathological data were retrospectively collected, and glomerular IgG subclass deposition was detected by immunohistochemistry.
Results:
Patients with M-MN were older (P = 0.003), with lower serum albumin (P = 0.034) and higher serum C-reactive protein (CRP) level (P = 0.003) than patients with I-MN. The majority of patients with M-MN had earlier pathological stages (P = 0.003) and less IgG deposition in glomeruli (P = 0.029). Absence of IgG4 deposition in glomeruli was notably observed in patients with M-MN (7/8 in M-MN versus 6/42 in I-MN, P < 0.001) and it was an independent predictor for occurrence of malignancy (hazard ratio 0.065, 95% confidence intervals 0.007-0.571, P = 0.014).
Conclusion:
Absence of glomerular IgG4 deposition, together with older age, severe hypoalbuminemia and high serum CRP level could be useful clues to differentiate M-MN from I-MN.
Insights
Absence of glomerular IgG4 deposition helps differentiate malignancy-associated membranous nephropathy (M-MN) from idiopathic membranous nephropathy (I-MN). This finding, along with older age and specific lab markers, aids in distinguishing these conditions.
Area of Science:
- Nephrology
- Immunopathology
- Oncology
Background:
- Malignancy-associated membranous nephropathy (M-MN) and idiopathic membranous nephropathy (I-MN) share similar renal pathological features.
- Glomerular IgG4 deposition is implicated in the pathogenesis of I-MN.
- Distinguishing between M-MN and I-MN is clinically important.
Purpose of the Study:
- To compare IgG subclass immune complex deposition between M-MN and I-MN patients.
- To analyze clinical and pathological data differentiating M-MN from I-MN.
- To identify predictors for malignancy in membranous nephropathy.
Main Methods:
- Retrospective analysis of 8 M-MN and 42 I-MN patients diagnosed between 1997-2009.
- Immunohistochemistry used to detect glomerular IgG subclass deposition.
- Comparison of clinical and pathological data between the two groups.
Main Results:
- M-MN patients were older with lower serum albumin and higher C-reactive protein (CRP) levels compared to I-MN patients.
- M-MN cases showed earlier pathological stages and less glomerular IgG deposition.
- Absence of glomerular IgG4 deposition was significantly more common in M-MN (7/8) than I-MN (6/42) and predicted malignancy.
Conclusions:
- Absence of glomerular IgG4 deposition is a key differentiator between M-MN and I-MN.
- Older age, severe hypoalbuminemia, and high serum CRP levels are additional clues for M-MN.
- These findings can aid in the clinical differentiation of M-MN from I-MN.
Related Concept Videos
Nephrotic Syndrome I : Introduction
Renal Corpuscle
Glomerulus: Structure and Function
The glomerulus is a tiny, intricate network of capillaries located at the beginning of the nephron. It's enveloped by the Bowman's capsule and receives its blood supply from an afferent arteriole, which divides into numerous capillaries...
Nephrotic Syndrome II : Assessment and Medical Management
Diabetic Nephropathy
Myasthenia Gravis ll: Pathophysiology
