Hydralazine Induces Myeloperoxidase and Proteinase 3 Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Leads to Pulmonary Renal Syndrome

We report a case of hydralazine-induced ANCA-associated glomerulonephritis with pulmonary hemorrhage. A 62-year-old Hispanic man with hypertension, who was being treated with hydralazine 100 mg three times a day for four and half years, presented to the hospital with severe anemia. He had acute kidn...

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Main Authors: Gaurav Agarwal, Ghayyath Sultan, Sherry L. Werner, Claudia Hura
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:Case Reports in Nephrology
Online Access:http://dx.doi.org/10.1155/2014/868590
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author Gaurav Agarwal
Ghayyath Sultan
Sherry L. Werner
Claudia Hura
author_facet Gaurav Agarwal
Ghayyath Sultan
Sherry L. Werner
Claudia Hura
author_sort Gaurav Agarwal
collection DOAJ
description We report a case of hydralazine-induced ANCA-associated glomerulonephritis with pulmonary hemorrhage. A 62-year-old Hispanic man with hypertension, who was being treated with hydralazine 100 mg three times a day for four and half years, presented to the hospital with severe anemia. He had acute kidney injury and urinalysis showed proteinuria, dysmorphic RBCs, and rare RBC cast. CT scan of the chest revealed bilateral pulmonary ground-glass infiltrates. Transbronchial biopsy was consistent with pulmonary hemorrhage. Serologic tests showed high titer PR3 ANCA and, to a lesser extent, MPO ANCA. Kidney biopsy revealed focal segmental necrotizing glomerulonephritis with crescents, without evidence of immune complex deposits. Hydralazine was discontinued and the patient was treated with corticosteroids and intravenous cyclophosphamide. At one-year follow-up, he had no symptoms and anemia had resolved. Kidney function improved dramatically. Serology showed undetectable PR3 ANCA and minimally elevated MPO ANCA. To our knowledge, hydralazine-associated PR3 ANCA has not been previously reported. The possibility of ANCA systemic vasculitis should be included in the differential diagnosis of any patient with hydralazine use and pulmonary renal syndrome. This is a potentially life threatening condition requiring prompt cessation of the drug and treatment with glucocorticoids and immunosuppression.
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spelling doaj-art-be1356112bd048939ac40f17ea26f5ab2025-08-20T03:23:31ZengWileyCase Reports in Nephrology2090-66412090-665X2014-01-01201410.1155/2014/868590868590Hydralazine Induces Myeloperoxidase and Proteinase 3 Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Leads to Pulmonary Renal SyndromeGaurav Agarwal0Ghayyath Sultan1Sherry L. Werner2Claudia Hura3Division on Nephrology, University of Texas Health Science Center at San Antonio, MC 7882, 7703 Floyd Curl Drive, San Antonio, TX 78229, USADivision on Nephrology, University of Texas Health Science Center at San Antonio, MC 7882, 7703 Floyd Curl Drive, San Antonio, TX 78229, USADepartment of Pathology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USADivision on Nephrology, University of Texas Health Science Center at San Antonio, MC 7882, 7703 Floyd Curl Drive, San Antonio, TX 78229, USAWe report a case of hydralazine-induced ANCA-associated glomerulonephritis with pulmonary hemorrhage. A 62-year-old Hispanic man with hypertension, who was being treated with hydralazine 100 mg three times a day for four and half years, presented to the hospital with severe anemia. He had acute kidney injury and urinalysis showed proteinuria, dysmorphic RBCs, and rare RBC cast. CT scan of the chest revealed bilateral pulmonary ground-glass infiltrates. Transbronchial biopsy was consistent with pulmonary hemorrhage. Serologic tests showed high titer PR3 ANCA and, to a lesser extent, MPO ANCA. Kidney biopsy revealed focal segmental necrotizing glomerulonephritis with crescents, without evidence of immune complex deposits. Hydralazine was discontinued and the patient was treated with corticosteroids and intravenous cyclophosphamide. At one-year follow-up, he had no symptoms and anemia had resolved. Kidney function improved dramatically. Serology showed undetectable PR3 ANCA and minimally elevated MPO ANCA. To our knowledge, hydralazine-associated PR3 ANCA has not been previously reported. The possibility of ANCA systemic vasculitis should be included in the differential diagnosis of any patient with hydralazine use and pulmonary renal syndrome. This is a potentially life threatening condition requiring prompt cessation of the drug and treatment with glucocorticoids and immunosuppression.http://dx.doi.org/10.1155/2014/868590
spellingShingle Gaurav Agarwal
Ghayyath Sultan
Sherry L. Werner
Claudia Hura
Hydralazine Induces Myeloperoxidase and Proteinase 3 Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Leads to Pulmonary Renal Syndrome
Case Reports in Nephrology
title Hydralazine Induces Myeloperoxidase and Proteinase 3 Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Leads to Pulmonary Renal Syndrome
title_full Hydralazine Induces Myeloperoxidase and Proteinase 3 Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Leads to Pulmonary Renal Syndrome
title_fullStr Hydralazine Induces Myeloperoxidase and Proteinase 3 Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Leads to Pulmonary Renal Syndrome
title_full_unstemmed Hydralazine Induces Myeloperoxidase and Proteinase 3 Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Leads to Pulmonary Renal Syndrome
title_short Hydralazine Induces Myeloperoxidase and Proteinase 3 Anti-Neutrophil Cytoplasmic Antibody Vasculitis and Leads to Pulmonary Renal Syndrome
title_sort hydralazine induces myeloperoxidase and proteinase 3 anti neutrophil cytoplasmic antibody vasculitis and leads to pulmonary renal syndrome
url http://dx.doi.org/10.1155/2014/868590
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