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Cadmium Exposure and Toxicity
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Soisungwan Satarug, Kenneth R. Phelps
Renal morphological and histological changes such as dilatation of interstitial veins with apparent paravenous lymphatic infiltrates were more pronounced in vitamin C-deficient guinea pigs compared with those fed sufficiently with the vitamin (Nagyova et al., 1994). This suggests a role for vitamin C in the prevention of Cd toxicity. People with diabetes are generally known to have marginally reduced vitamin C status (Will et al., 1999; Shim et al., 2010). In NHANES 1988–1994, mean serum vitamin C concentration was lower in persons with newly diagnosed diabetes, compared with those without diabetes. NHANES 1988–1994 showed that vitamin C-deficiency prevalence was 13% and that mean serum vitamin C concentrations in persons with newly diagnosed diabetes were lower than those without diabetes (Will et al., 1999; Schleicher et al. 2009). Likewise, in a study of 2,048 Koreans, aged ≥30 years, lower serum vitamin C levels were observed in both non-smokers and smokers who had diabetes, compared with non-smokers and smokers without diabetes (Shim et al., 2010). In another study, diabetes patients with clinical nephropathy were found to have lower mean plasma vitamin C due to higher renal clearance of vitamin C compared to those with microalbuminuria (Hirsch et al., 1998). Low vitamin C levels may be one of the factors explaining increased susceptibility to renal Cd toxicity among people with diabetes (Buchet et al., 1990; Akesson et al., 2005; Barregard et al., 2014; Haswell-Elkins et al., 2008; Hwangbo et al., 2011; Madrigal et al., 2019).
A new one-dimensional copper(II) coordination polymer: crystal structure and treatment activity on diabetic nephropathy
Published in Inorganic and Nano-Metal Chemistry, 2021
Pan-Pan Lin, Qiao-Ling Xie, Ling-Wei Chen
Diabetes is the main cause of end-stage renal disease, and diabetic nephropathy is a disease characterized by persistent microalbumin in diabetic patients. At first, the glomerular filtration rate of patients is high, which is twice over that of normal people.[1] Some patients occasionally combined with microalbuminuria, and after about 20 years, the patient gradually develops a decline in glomerular filtration rate, mild proteinuria, followed by moderate proteinuria;[2] in the final stage, this disease will develop into severe urine protein, accompanied by chronic renal insufficiency and nephrotic syndrome, eventually develops into end-stage renal disease.
Molecularly imprinted based surface plasmon resonance nanosensors for microalbumin detection
Published in Journal of Biomaterials Science, Polymer Edition, 2019
Meltem Koca Esentürk, Semra Akgönüllü, Fatma Yılmaz, Adil Denizli
Albumin excretion increase in patients is a marker of generalized vascular disease and is associated with stroke and heart disease. Thus, there is a need for addressing small amounts of urinary albumin excretion (in the range of 30-300 mg/day, i.e., microalbuminuria). An albumin excretion rate >30 mg/24 hours is considered to be microalbuminuria. By definition, the upper end of microalbuminuria is thought to be 300 mg/24 hours. Thus, microalbuminuria has been defined as an albumin/creatinine ratio of 17 to 299 for males and 25 to 299 for females [40].