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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2015  |  Volume : 26  |  Issue : 3  |  Page : 572-579
Herb-induced acute bone marrow intoxication and interstitial nephritis superimposing glomerular C1q deposition in a patient with paroxysmal nocturnal hemoglobinuria


1 Department of Pathology and Laboratory Medicine, King Abdulaziz Medical City and College of Medicine, King Saud University for Health Sciences, Riyadh, Saudi Arabia
2 Department of Pathology, King Khalid University Hospital, College of Medicine, King Saud University, Riyadh, Saudi Arabia

Correspondence Address:
Dr. Khalid S Alkhairy
Department of Pathology and Laboratory Medicine, King Abdulaziz Medical City, King Saud University for Health Sciences, P. O. Box 22490, Riyadh 11426
Saudi Arabia
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DOI: 10.4103/1319-2442.157384

PMID: 26022031

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Paroxysmal nocturnal hemoglobinuria is a rare disease of the red blood cell membrane that renders it lyzable by the complement system, leading to chronic intravascular hemolysis. Renal hemosiderosis is a well-known complication of intravascular hemolytic anemia and can lead to acute kidney injury and renal failure. The use of herbal medicine is common worldwide. The nephrotoxicity of herbal remedies can take several forms, which include acute kidney injury and acute and chronic interstitial nephritis. In addition, the use of herbal remedies can result in bone marrow toxicity and suppression. C1q nephropathy is an uncommon form of glomerular disease characterized by dominant or co-dominant glomerular immunofluorescence positivity for C1q in the absence of clinical and serological evidence of systemic lupus erythematosus, and has various clinical presentations and outcome. Here, we report a patient of undiagnosed paroxysmal nocturnal hemoglobinuria who consumed herbal medicine of unknown constituents and clinically presented with anemia and acute kidney injury. The pathological findings of bone marrow and renal biopsies that include bone marrow intoxication, severe renal hemosiderosis and acute interstitial nephritis and kidney injury, as well as co-dominant glomerular deposition of C1q, are discussed. In addition, we discuss and hypothesize the possible pathogenesis of glomerular C1q deposition in the setting of paroxysmal nocturnal hemoglobulinuria.


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