{'fraction_non_alphanumeric': 0.028487641390867197, 'fraction_numerical': 0.007121910347716799, 'mean_word_length': 5.764872521246459, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Glycosaminoglycans: a new paradigm in the prevention of proteinuria and progression of glomerular disease.

Heparin as a therapeutic option in glomerular disease In the late 1960s, Priscilla Kincaid-Smith first proposed the therapeutic use of heparin in nephrology based on the putative pathogenetic role of the coagulative cascade in acute kidney rejection and in rapidly progressive glomerulonephritis. Small series of anecdotal observation on patients treated with triple or quadruple therapy comprising heparin, or oral anticoagulants (the so-called Melbourne cocktail) were reported by Kincaid-Smith and others. At that time it was not clearly recognized that heparin has activities other than anticoagulation, so that oral anticoagulants were gradually substituted for heparin. The high frequency of side-effects and disappointing results gradually relegated heparin, anticoagulants, and the Melbourne cocktail to the nephrology museum [1], Recently there has been a renaissance in heparin with a novel rationale. Studies in 'non-immunological' models gave strong evidence that heparin and glycosaminoglycans are effective in ameliorating the natural progression of a number of nephropathies, puromycin and habu snake-venom-induced nephrosis [2,3], antiThyl.l experimental mesangioproliferative glomerulonephritis [4], glomerulosclerosis in the GH-transgenic mouse [5], and nephropathy in the streptozotocin (STZ)-induced diabetic rat [6-8]. Purkerson et al. demonstrated that progression of glomerulosclerosis in subtotally nephrectomized rats is prevented by heparin, but not by other anticoagulant drugs such as coumadin [9]. This was the first observation to support the idea that the renoprotective effect of heparin depends on mechanisms other than the coagulation cascade. It is now clear that anticoagulation is not needed for these actions of heparin. In fact, Diamond and Karnovsky [2] demonstrated that chronic aminoglycoside nephrosis is prevented by a non-anticoagulant heparin, and in the quite different model of subtotal nephrectomy, Purkerson et al. [10] showed that a chemically transformed heparin devoid of anticoagulant activity ameliorates the progression of renal disease in the same way as anticoagulant heparin. Finally, in the STZdiabetic rat, nephropathy is prevented by both modified heparins and a dermatan sulphate which are poor anticoagulants [6,7].