Increased oxidative stress generated by hyperglycaemia, hyperlipidaemia or the presence of advanced glycation endproducts (AGEs) or both is regarded as an important mediator of late diabetic complications [1]. A clear relation between the quality of glycaemic control and the presence of free radicals has been shown thereby relating the appearance of oxidative stress to the underlying metabolic disorder rather than to the complication itself [2]. The presence of oxygen free radicals and the simultaneous decline of antioxidative defence mechanisms observed in diabetic patients could therefore promote the development of late diabetic complications [1, 3±5].Oxidative stress has been proposed as a major cause of diabetic nephropathy [6±9]. Animal models implicate that oxidative stress accompanying the early onset of diabetes increases the kidney's susceptibility to develop diabetic nephropathy [10]. One possible mechanism for this is the activation of the oxidative stress sensitive transcription factor NF-kB [6, 11±13]. Translocation of activated NF-kB into the nucleus results in gene expression of NF-kB controlled Diabetologia (1999) 42: 222±232 Peripheral blood mononuclear cells isolated from patients with diabetic nephropathy show increased activation of the oxidative-stress sensitive transcription factor NF-kB

Hyperhomocyst(e)inemia is common in nephropathic diabetic patients and may contribute to the enhanced morbidity and mortality from cardiovascular diseases characteristically observed in IDDM patients with diabetic nephropathy.

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Hyperhomocyst(e)inemia is common in nephropathic diabetic patients and may contribute to the enhanced morbidity and mortality from cardiovascular diseases characteristically observed in IDDM patients with diabetic nephropathy.