Secondary failure of plasma therapy in factor H deficiency View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2006-08-15

AUTHORS

Sylvie Nathanson, Tim Ulinski, Véronique Frémeaux-Bacchi, Georges Deschênes

ABSTRACT

We report a patient with homozygous factor H deficiency leading to permanent alternate complement activation and early onset of the hemolytic uremic syndrome. He was successfully treated with weekly infusions of fresh frozen plasma over 4 years, displaying normal blood pressure while only treated with an angiotensin converting enzyme (ACE) inhibitor, a steady level of haptoglobin, low-range proteinuria and normal creatinine clearance. By the end of the fourth year of treatment, he dramatically developed a relapse of hemolytic and uremic syndrome, displaying undetectable haptoglobin, nephrotic range proteinuria and progressive renal failure. Despite a ten-fold increase in the dosage of plasma infusion through daily plasma exchange, haptoglobin remained undetectable while circulating antigenic factor H levels reached 22–24% (normal values 65–140%). Three months following the biological onset of the relapse, a bilateral nephrectomy was performed owing to uncontrolled hypertension and rapidly progressive renal failure. The molecular mechanism of plasma resistance remained unclear while antifactor H antibodies were not detected in the plasma. We suggest that protracted administration of exogenous factor H might not be a long-term strategy in homozygous factor H deficiency. More... »

PAGES

1769-1771

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00467-006-0237-9

DOI

http://dx.doi.org/10.1007/s00467-006-0237-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1048718146

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16909242


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