A 22-year-old woman presents with bilateral lower limb swelling, and puffiness on her face for the past three months. A routine health examination revealed proteinuria (3+) and microscopic hematuria (1+), prompting evaluation by a local physician.
Vital parameters:
BP: 124/87 mmHg
HR: 75/min
SpO2: 98 %
Physical examination:
Mild bilaterally
Lower leg edema as well as an unremarkable abdominal examination and pulse status.
Laboratory:
Hemoglobin (12.4–16.1) g/dL: 11.2
White blood cells: (4.0–11.8) Mrd/L: 6.7
Albumin (34–50) g/L: 38
Creatinine (0.7-1.2) mg/dL: 1.72
Immunology:
C3 (90-170) mg/dL: 47
C4 (12-36) mg/dL: 10
ANA (< 1:80) Titer: 1:80
c-ANCA (< 1:20): negative
p-ANCA (< 1:20): negative
GBM-AB (< 7) U/mL: negative
Cryoglobulin (negative): negative
ASO：72IU/ml
Urine:
Urine protein-creatinine ratio (uPCR) mg/g: 2569
Urine sediment:
Some eumorphic red blood cells, few granulated cylinders, some epithelial cells.
Note related to annotations: To avoid obscuring the lesions, the annotations are deliberately positioned close to, but not directly over, the lesion areas.
Pathological diagnosis:
Immune complex-type membranoproliferative glomerulonephritis (IC-MPGN) with 2/19 segmental and 2/19 global glomerulosclerosis
Light microscopic findings:
Two renal cortex to medulla specimens (cortex:medulla = 7:3) contained about 16-19 glomeruli, of which 2 were obsolescent glomeruli. Glomerular hypertrophy was not conspicuous, but mild to moderate mesangial proliferative lesions. The glomerular basement membranes showed widespread double contours, indicating membranoproliferative glomerulonephritis (MPGN). Segmental sclerosis was present in 2-3 glomeruli, and including these glomeruli, adhesion to Bowman’s capsule was observed in 5-8 glomeruli. No acute active necrotic and crescentic lesions were observed.
Tubulointerstitial lesions were present, predominantly around the atrophic tubules, covering approximately 50% of the cortex.
Mild to moderate atherosclerotic lesions were observed in interlobular arteries. Mild to moderate hyaline arteriolosclerosis was also seen in small arterioles.
Immunofluorescence study (6 glomeruli):
Positive IgG, IgM, and C3c were observed as the mesangial and irregular peripheral granular pattern.
IgM (1+) mesangial and peripheral, granular
IgG (3+) mesangial and peripheral, granular
IgA (-)
C1q (-)
C3c (3+) mesangial and peripheral, granular
C4 (-)
Electron microscopy findings:
Electron dense deposits were observed in the subendothelial and mesangial regions of the glomeruli. Abundant subendothelial deposits were observed in the glomeruli, along with enlargement of the subendothelial space and double contour of the glomeruli basement membrane. Extensive effacement of the foot processes of the podocytes was observed. Mesangial proliferative lesions, swelling of glomerular endothelial cells, loss of fenestrae, and narrowing of the capillary lumens are observed, indicating endocapillary proliferative lesions.
Pathological diagnosis:
Light microscopy findings revealed MPGN pattern of injury, and immunofluorescence findings revealed positive for IgG, IgM, and C3c as mesangial, peripheral, and granular pattern, corresponding to immune complex-type MPGN (IC-MPGN). Segmental sclerotic lesions with exudative lesions were observed in some glomeruli with fibrous adhesions to Bowman’s capsule. Regarding the cause of IC-MPGN, the cause of secondary MPGN is uncertain, so considered to be primary MPGN.