# Rapidly Progressive IgA Nephropathy in a Patient with Systemic Lupus Erythematosus and Chronic Hepatitis B: A Case Report

**Authors:** Patrícia Kleinová, Karol Graňák, Tímea Blichová, Matej Vnučák, Ivana Dedinská

PMC · DOI: 10.3390/reports8040220 · Reports - Clinical Practice and Surgical Cases · 2025-10-31

## TL;DR

A rare case of rapidly progressive IgA nephropathy in a patient with lupus and hepatitis B highlights the complexity of managing overlapping autoimmune and infectious conditions.

## Contribution

This case report presents a rare clinical scenario of IgA nephropathy complicated by systemic lupus erythematosus and active hepatitis B.

## Key findings

- The patient's renal biopsy showed crescentic glomerulonephritis with IgA deposits.
- Treatment with corticosteroids and cyclophosphamide failed to recover renal function due to active hepatitis B.
- Management required a multidisciplinary approach to balance immunosuppression and infection risk.

## Abstract

Background and Clinical Significance: Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis in adults, typically following a chronic course that often leads to end-stage kidney disease. Rapidly progressive glomerulonephritis is a rare and severe variant of IgAN with a poor prognosis. Case Presentation: We present the clinical case of a 68-year-old Caucasian female with a history of systemic lupus erythematosus and untreated chronic hepatitis B, who was admitted to the Transplant-Nephrology Department, University Hospital Martin, with acute kidney injury and nephrotic syndrome accompanied by hematuria. The clinical picture was marked by lower limb oedema and poorly controlled hypertension, both of which responded well to conservative management. Extrarenal causes were excluded through otolaryngologic, stomatologic, and gynecologic assessments, and autoantibody screening was negative. Renal biopsy revealed crescentic glomerulonephritis with endocapillary and mesangial proliferation and IgA deposits. Due to active hepatitis B, initial treatment was limited to corticosteroids. Following a decrease in viral load, pulse therapy with cyclophosphamide was administered, followed by mycophenolic acid; however, renal function did not recover. Conclusions: The rapidly progressive form of IgA nephropathy in the context of active hepatitis B presents a rare and challenging clinical case. Management requires a highly individualised, multidisciplinary approach due to the risk of infectious complications and the need to preserve renal function.

## Linked entities

- **Diseases:** Systemic lupus erythematosus (MONDO:0007915), Chronic hepatitis B (MONDO:0005344), nephrotic syndrome (MONDO:0005377), acute kidney injury (MONDO:0002492)

## Full-text entities

- **Genes:** CD79A (CD79a molecule) [NCBI Gene 973] {aka IGA, IGAlpha, MB-1, MB1}
- **Diseases:** oedema (MESH:C536897), glomerulonephritis (MESH:D005921), hypertension (MESH:D006973), Chronic Hepatitis B (MESH:D019694), acute kidney injury (MESH:D058186), hematuria (MESH:D006417), Systemic Lupus Erythematosus (MESH:D008180), active hepatitis B (MESH:D006509), nephrotic syndrome (MESH:D009404), infectious complications (MESH:D003141), IgA Nephropathy (MESH:D005922), end-stage kidney disease (MESH:D007676)
- **Chemicals:** cyclophosphamide (MESH:D003520), mycophenolic acid (MESH:D009173)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12643444/full.md

## References

17 references — full list in the complete paper: https://tomesphere.com/paper/PMC12643444/full.md

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Source: https://tomesphere.com/paper/PMC12643444