# A Clot and a Clue: When Pulmonary Embolism Leads to a Renal Diagnosis

**Authors:** Valter Duarte, Jéssica Krowicki, Miguel Martins, Telma Santos, Gorete Jesus

PMC · DOI: 10.7759/cureus.94389 · Cureus · 2025-10-12

## TL;DR

A case study shows how a pulmonary embolism led to the diagnosis of primary membranous nephropathy, highlighting the importance of early treatment to prevent kidney disease progression.

## Contribution

This case highlights the rare but important connection between pulmonary embolism and undiagnosed primary membranous nephropathy.

## Key findings

- A patient with pulmonary embolism was found to have primary membranous nephropathy through lab tests and antibody detection.
- Treatment with rituximab led to improvement and disappearance of anti-PLA2R antibodies after six months.
- Early conservative treatment and monitoring are crucial to prevent complications of nephrotic syndrome.

## Abstract

Primary membranous nephropathy (PMN) is one of the leading causes of nephrotic syndrome (NS) in non-diabetic adults, potentially progressing to end-stage renal disease. The detection of specific antibodies, such as anti-phospholipase A2 receptor (anti-PLA2R), is useful for diagnosis, risk stratification, and monitoring therapeutic response. Clinical presentation is usually insidious, with edema, malaise, fatigue, and anorexia, but may be complicated by NS complications as thrombotic events. We present the case of a 45-year-old man with bilateral pleuritic chest pain and hemoptoic cough for the past week, and peripheral edema over six months. Contrast-enhanced chest computed tomography (CT) revealed bilateral pulmonary embolism (PE). Laboratory tests highlighted hypoalbuminemia (2.4 g/dL), nephrotic-range proteinuria (12 g/24h) with preserved renal function, and positive anti-PLA2R antibodies (80 RU/mL). Secondary membranous nephropathy was excluded and renal biopsy was deferred. Treatment with rituximab was initiated, resulting in analytical improvement and disappearance of anti-PLA2R antibodies at six months. Close monitoring of renal function and early initiation of conservative treatment are essential to prevent disease progression and complications of NS, with immunosuppressive therapy potentially required in selected cases.

## Linked entities

- **Diseases:** nephrotic syndrome (MONDO:0005377), end-stage renal disease (MONDO:0004375), pulmonary embolism (MONDO:0005279)

## Full-text entities

- **Genes:** PLA2R1 (phospholipase A2 receptor 1) [NCBI Gene 22925] {aka CLEC13C, PLA2-R, PLA2G1R, PLA2IR, PLA2R}
- **Diseases:** thrombotic (MESH:D013927), PE (MESH:D011655), PMN (MESH:D015433), cough (MESH:D003371), diabetic (MESH:D003920), end-stage renal disease (MESH:D007676), hypoalbuminemia (MESH:D034141), chest pain (MESH:D002637), anorexia (MESH:D000855), edema (MESH:D004487), proteinuria (MESH:D011507), fatigue (MESH:D005221), NS (MESH:D009404)
- **Chemicals:** rituximab (MESH:D000069283)

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12604433/full.md

## References

8 references — full list in the complete paper: https://tomesphere.com/paper/PMC12604433/full.md

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Source: https://tomesphere.com/paper/PMC12604433