In 1984 we first reported that human serum albumin (HSA) in its denatured form was present in a large amount, up to 25% in terms of fully denaturated protein, in the serum of patients with chronic renal failure (CRF) and patients with the nephrotic syndrome (NS).1 These results were obtained by studying urea levels in hydrolysates (supernatants) of HSA sampled from patients with CRF or NS.1 A comparison of our findings with the literature led to a concept that changed our understanding of the pathophysiologic mechanisms and the nature of glomerulonephritis (GN).
Kozhevnikov AD. Modified Serum Albumin in the Pathogenesis of Glomerular Diseases: A New Hypothesis. Arch Intern Med. 2002;162(3):356–358. doi: