Chronic tubulointerstitial nephropathy induced by glucosamine: a case report and literature review

Causal Effect of Chondroitin, Glucosamine, Vitamin, and Mineral Intake on Kidney Function: A Mendelian Randomization Study

“…In this regard, our findings suggest that clinicians should carefully monitor long-term chondroprotective agent use, particularly in patients at high risk of kidney function impairment. Our results are supported by pre-vious reports that raised concerns regarding the nephrotoxic effects of chondroprotective drugs and their impact on kidney function [15][16][17]. A few patients who regularly ingested glucosamine exhibited a decline in kidney function without any other precipitating factors, and acute or chronic tubulointerstitial nephritis was confirmed in kidney biopsies.…”

“…Chondroitin and glucosamine are associated with a reduction in joint pain, improvement of joint function, and reduction in joint space narrowing in patients with OA [6,7,9,10]. Despite a protective effect against various pathological conditions, including inflammation [11,12], cardiovascular disease [13], and diabetes [14], there have been some reports of non-specific kidney injury and toxicity associated with these chondroprotective drugs [15][16][17]. Nevertheless, the causal association between chondroitin or glucosamine intake and kidney function has not been established yet.…”

IL versus DES: Impact on chitin pretreatment to afford high quality and highly functionalizable chitosan

“…It is worth noting that the BE-2-DES, HI-2-DES and S-2-DES CrI are higher than 90 %. These values are similar to the one owned by chitin nanocrystals (Gueye et al 2016). These results are fully in line with those obtained by FTIR where α-structures are maintained for these samples after the DES pretreatment.…”

Dietary supplement use among patients with chronic kidney disease

“…Aristolochic acid, found in some herbal supplements, is an acknowledged cause of 'Chinese herbs' nephropathy and is involved in the pathomechanism of Balkan endemic nephropathy (Jadot et al, 2017). Experimental data, as well as some clinical reports, point to the possibility of kidney injury caused by glucosamine through induction of apoptosis in the tubular and mesangial cells of the kidney (Gueye et al, 2016). High vitamin E consumption leads to increased content of biomarkers of tissue toxicity and oxidative stress in the kidneys of mice (Jansen et al, 2016).…”