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What is the role of albumin in proteinuric glomerulopathies?

Albumin is a 69 kDa plasma protein (molecular radius 36 A) with a variety of functions, including maintenance of plasma oncotic pressure, buffering of plasma acid–base changes and functioning as a transport protein for hormones, fatty acids, phospholipids, ions and heavy metals [1]. Albumin was early identified as critical in regulating endothelial permeability, especially in studies on single perfused microvessels [2]. Later, plasma acidic glycoproteins, especially orosomucoid, were found to be (additional) crucial factors in maintaining normal microvascular permeability, particularly to negatively charged macromolecules (e.g. albumin) [3]. The critical role of albumin and orosomucoid in maintaining vascular permeability has also been demonstrated for glomerular capillaries [4,5]. Paradoxically, in Nagase analbuminaemic rats (NARs), a mutant of the Sprague–Dawley strain devoid of circulating albumin, the clearance of proteins (albumin and IgG) to the interstitium was, however, only moderately increased [6]. Furthermore, in a recent study, the glomerular permeability to macromolecules was only slightly altered in this rat strain [7]. Albumin and its ligands have also been implicated in the progression of proteinuric renal disease, by direct or indirect tubulotoxic effects [8]. This tubulotoxicity, during continuous protein overload, apparently results not only in injury to the tubular cells, but also in overall tubulointerstitial damage [8–10]. Although proteinuria is an established risk factor for the progression of glomerular disorders, the concept that albumin may be tubulotoxic is partly controversial. Also, the concept of albumin regulating microvascular (glomerular) permeability has been questioned [11]. Moreover, the classic concept of the glomerular barrier functioning as a highly sizeand charge-selective filter has been put into serious doubt recently [12].