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IntroductionNephrotic syndrome is a kidney disorder marked by excessive protein loss in the urine, leading to various systemic complications. This condition often results from damage to the glomeruli—the kidney's filtering units—causing proteinuria, low blood protein levels, and fluid retention. Understanding the assessment, diagnosis, and management of nephrotic syndrome is essential for effective treatment and prevention of further kidney damage.AssessmentPatient History: Document...
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Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of...
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Concomitant Nephrotic Syndrome with Diffuse Large B-cell Lymphoma: A Case Report.

Keisuke Kidoguchi1, Hiroo Katsuya1, Hiroshi Ureshino1

  • 1Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University.

The Tohoku Journal of Experimental Medicine
|October 8, 2020
PubMed
Summary

This case report highlights a rare instance of nephrotic syndrome (NS) co-occurring with diffuse large B-cell lymphoma (DLBCL). The findings suggest DLBCL may be a potential cause of secondary membranous nephropathy (MN).

Keywords:
anti-PLA2R antibodyautoantibodiesdiffuse large B-cell lymphomamembranous nephropathynephrotic syndrome

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Area of Science:

  • Nephrology
  • Oncology
  • Pathology

Background:

  • Membranous nephropathy (MN) is a leading cause of nephrotic syndrome (NS), often linked to underlying malignancies, though hematological cancers are rare associations.
  • Diffuse large B-cell lymphoma (DLBCL) is an aggressive hematological malignancy.

Observation:

  • A 68-year-old man with diabetes presented with fatigue, subsequently diagnosed with pancreatic DLBCL.
  • The patient concurrently developed NS, characterized by severe proteinuria, hypoalbuminemia, edema, and hyperlipidemia.
  • Renal biopsy revealed membranous nephropathy (MN) with spike lesions and interstitial lymphocyte infiltration; negative for anti-GBM, ANCA, HBsAg, and anti-PLA2R antibodies.

Findings:

  • A diagnosis of secondary MN induced by DLBCL was established.
  • Treatment with rituximab-based chemotherapy for DLBCL led to the improvement of both the lymphoma and the nephrotic syndrome.
  • This case supports the hypothesis that DLBCL can be a cause of secondary MN, particularly when primary MN markers are absent.

Implications:

  • This case underscores the importance of investigating hematological malignancies, such as DLBCL, in patients presenting with secondary MN.
  • Early diagnosis and treatment of DLBCL may lead to the resolution of associated nephrotic syndrome.
  • Further research is needed to elucidate the precise mechanisms linking DLBCL to secondary MN.