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Am. J. Trop. Med. Hyg., 75(5), 2006, pp. 864-868
Copyright © 2006 by The American Society of Tropical Medicine and Hygiene

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CYSTATIN C AS A MARKER OF IMMUNE COMPLEX–ASSOCIATED RENAL IMPAIRMENT IN A SUDANESE POPULATION WITH VISCERAL LEISHMANIASIS

AMIR IBRAHIM ELSHAFIE, GEHAD ELGHAZALI, JOHAN RÖNNELID, AND PER VENGE*
Department of Clinical Pathology and Microbiology, Alribat University Hospital, Khartoum, Sudan; Department of Immunology, King Fahad Medical City, Riyadh, Kingdom of Saudi Arabia; Department of Microbiology and Immunology, University of Khartoum, Khartoum, Sudan; Department of Oncology, Radiology and Clinical Immunology, University of Uppsala, Uppsala, Sweden; Department of Medical Sciences, University of Uppsala, Uppsala, Sweden

Renal function was studied in visceral leishmaniasis (VL) and post-kala-azar dermal leishmaniasis (PKDL) by means of the specific marker cystatin C and related to circulating immune complexes and cytokine production. Forty patients with VL (23 with sub-acute disease and 17 with acute disease), 17 patients with PKDL, and 22 healthy controls were included. Cystatin C, but not creatinine, was significantly raised in VL (P = 0.004). The highest levels of cystatin C were found in those with acute disease (P < 0.0001). In VL, cystatin C levels were positively correlated to circulating immune complexes and production of granulocyte-macrophage colony stimulating factor (GM-CSF), but negatively correlated to aspartate aminotransferase and lactate dehydrogenase. We conclude that cystatin C is a superior marker of glomerular function in leishmaniasis and that immune complex deposition and GM-CSF are two functions that most likely are causally involved in the mechanisms leading to glomerular dysfunction in leishmaniasis.


Received November 1, 2005. Accepted for publication July 11, 2006.

Acknowledgments: For the completion of this study, we wish to acknowledge the great support and inspiration of Profs. A. Ashmage, Hashim Erwa, and A. G. Eltahir, Dr. Anwar Alkordofani, Dr. Maria Satti, and all colleagues in the fields of Clinical Pathology and Medicine in Sudan. Special thanks to the patients and doctors in charge at the Tabarakalla rural hospital.

* Address correspondence to Per Venge, Department of Clinical Chemistry and Pharmacology, University Hospital, SE-751 85 Uppsala, Sweden. E-mail: per.venge{at}akademiska.se

Authors’ addresses: Amir ElShafie, Department of Clinical Pathology and Microbiology, Alribat University Hospital, Khartoum, Sudan, Telephone: 2499-12590192, E-mail: amirel1970{at}hotmail.com. Gehad Elghazali, Department of Immunology, King Fahad Medical City, Riyadh, Kingdom of Saudi Arabia, and Department of Microbiology and Immunology, University of Khartoum, Khartoum, Sudan, E-mail: gelghazali{at}KFMC.med.sa. Johan Rönnelid, Unit of Clinical Immunology, Rudbeck Laboratory, SE-751 85 Uppsala, Sweden, Telephone: 46-186114182, E-mail: johan.ronnelid{at}klinimm.uu.se. Per Venge, Department of Clinical Chemistry and Pharmacology, University Hospital, SE-751 85 Uppsala, Sweden, Telephone: 46-186114246, Fax: 46-186613703; E-mail: per.venge{at}akademiska.se.







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Copyright © 2006 by the American Society of Tropical Medicine and Hygiene.