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Chronic tubulointerstitial nephropathy induced by glucosamine: a case report and literature review
Serigne Gueye1, Morgane Saint-Cricq, Moussa Coulibaly
1Service de Néphrologie-Dialyse, CH de Cahors, Service d'Anatomopathologie CHU Toulouse, Département of Nephrology and Organ Transplantation, CHU Rangueil, INSERM U, IFR-BMT, CHU Purpan, and Université Paul Sabatier, Toulouse, France.
Abstract:
Glucosamine is a glycosylated amine and a slow-acting symptomatic treatment for osteoarthritis. Some experimental animal studies have shown that glucosamine can cause apoptosis in kidney tubular and mesangial cells as well as overexpression of transforming growth factor β1 (TGF-β1) and connective-tissue growth factor (CTGF), which are potent inducers of mesangial and interstitial tubulointerstitial fibrosis. We report the case of a 67-year-old patient who presented with non-proteinuric renal insufficiency and a reduction of the glomerularfiltration rate (GFR) from 86 to 46 mL/min within 3 months. A kidney biopsy showed noninflammatory 40 - 50% fibrosis of the renal cortex associated with acute tubular necrosis. The etiological investigation was negative apart from taking 1,200 mg of glucosamine daily for 3 years to treat osteoarthritic knee pain. Three weeks after stopping glucosamine, GFR increased from 47.5 to 60 mL/min. Reintroduction of glucosamine resulted in loss of kidney function after 3 weeks, with GFR reduced from 60 to 53 mL/ min. Thus, glucosamine was shown to cause renal toxicity. Referring to other reported cases, we conclude that toxicity is rare but may also be underreported.
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