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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.
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Abstract titles should be brief and reflect the content of the abstract.
Nephritic syndrome is a clinical syndrome characterized by the acute onset of hematuria, red blood cell casts, varying degrees of proteinuria, azotemia, hypertension, and oliguria, reflecting glomerular inflammation and injury [1].
Complement level assessment serves as a valuable tool in differentiating the various etiologies of nephritic syndrome. Some forms of thrombotic microangiopathy (TMA), particularly complement- mediated TMA, also present with low complement levels. [2-5]
Genetic mutations or acquired abnormalities in complement-regulating proteins (e.g., CFH, CFI, MCP/CD46, C3, FHR 1-FHR5) are implicated in atypical hemolytic uremic syndrome (aHUS), a prototypical complement-mediated TMA [6] and C3 glomerulopathy(C3G).
This was a prospective, descriptive study in patients with azotemia, active urinary sediments were included in the study presenting to a tertiary care centre in Western India. Kidney biopsy was performed as per indication and processed for light microscopy (LM), immunofluorescence (IF). Genetic analysis by MLPA (Multiplex Ligation- dependent Probe Amplification) method was carried out.
Ten patients presented to our department with nephritic syndrome, out of which two were post-transplant. Seven (70%) were males, six (60%) had pedal oedema, five (50%) had dyspnea and one each with gross hematuria (10%), fever (10%) and rash (10%). Four (40%) had oliguria, three (30%) had anuria and rest three had urine output >800ml/day. eGFR by CKD- EPI was less than 15ml/min/1.73m2 in eight (80%) patients, one had eGFR of 21ml/min/1.73m2 and one presented with 120ml/min/1.73m2. C3 levels were low in four (40%) (Ref. range 80-120 mg/dL), but C4 levels were normal in all patients (Ref. range 10-40 mg/dL) [Table no.: 1].
Out of 10 kidney biopsies, seven (70%) had mesangial proliferation, three (30%) revealed changes of TMA. Immunofluorescence revealed ‘3+’ C3 staining in three (30%), ‘2+’ C3 staining in one (10%), ‘1+’ C3 staining in two (20%) and ‘3+’ IgG in one patient. In two graft biopsy, LM exhibited no active glomerular lesions & IF was negative, but showed ct1, ci1 as per Banff classification. Genetic abnormalities were evident in seven (70%). Four (40%) patients had heterozygous deletions, out of which three patients with FHR1& FHR3 heterozygous deletions, one with FHR1,FHR3 & FHR5 heterozygous deletions. Homozygous FHR 1& FHR3 deletions were observed in three (30%) patients, rest three had no mutations.
MLPA analysis (70%) was more sensitive in diagnosing disease spectrum of proliferative GN, compared to serological complement levels (40%) and histopathological finding (30%) TMA & (40%) C3 deposition. Both post transplant patient presented with requirement of renal replacement therapy. They had heterozygous deletion, hence genetic analysis may help in predicting graft survival, also prognosticating risk for patients awaiting renal transplant and donor selection.
Limitations:
The study with large sample size will help in supporting our conclusion, due to rarity of the disease and economical constrain large study will pose us challenge.
