Renal tubular absorption of β2 microglobulin

Abstract

125Iodinated human beta 2 microglobulin (beta 2m, 5 to 30 mg) was administered to anesthetized rats. Clearance studies showed a low threshold of excretion of injected beta 2m and a high Tm of 400 to 600 micrograms X min-1 X kg-1. A glomerular sieving coefficient of 0.97 was calculated as the slope of the curve: beta 2m excretion rate = F (plasma beta 2m X glomerular filtration rate) for values above saturation. Electrophoresis analysis of proteinuria in agarose gel and sodium dodecyl sulfate polyacrylamide gel showed that injection of saturating doses of beta 2m induced the excretion of proteins of similar size but different charge and that of other proteins of different size. Among the latter, some were excreted transiently in association with beta 2m, whereas others had a delayed excretion suggesting existence of a complex mechanism of reabsorption whose steps remain to be elucidated.

Urine Beta2-Microglobulin Is an Early Marker of Renal Involvement in LPI

“…Therefore, it might represent an ideal marker of GFR in patients with renal diseases (Wibell et al 1973;Trollfors and Norrby 1981;Acchiardo et al 1989;Shea et al 1981;Bianchi et al 2001). Furthermore, beta2-microglobulin is reabsorbed almost completely in renal tubules, and therefore, increased urinary excretion is a sign of decreased tubular reabsorption and damage of tubular structures (Gauthier et al 1984). In our study, urine beta2-microglobulin was elevated in 90% of the patients.…”

Competition between Albumin and Low-Molecular-Weight Proteins for Renal Tubular Uptake in Experimental Nephropathies

“…Four arguments suggest that this massive elevation of low-Mr urinary proteins results from a competitive inhibition of their tubular uptake by the high filtered load of albumin [I], No significant increase was detected in the urinary excretion of the tubular enzyme NAG which makes unlikely the possibility of cytotoxic effects decreasing the protein reabsorptive capacity of proximal tubules [2], The rise in |)2-m and cystatin occurred in parallel with that of albuminuria but with a delay of a few days and at each time about a 10-fold difference in the magnitude of the increase [3]. In both models of glomerular injury, low-Mr proteins and albumin in urine were associ ated through the same nonlinear relationship characterized by a threshold around 100 mg of albumin per 24 h above which the 2 low-Mr proteins were invariably increased [4].…”

“…Two theories are presently in opposition. The first one considers that the tubular transport of proteins is governed by differ ent modes of selectivity based on the charge, size of the proteins or the site of reabsorption [1][2][3]. This theory as sumes that low-and high-molecular-weight (Mr) proteins are reabsorbed by different mechanisms and that cationic and anionic proteins can not compete with each other because of constraints in the access to endocytotic sites.…”

Effects of Extracorporeal Shock Wave Lithotripsy on Renal Function in Patients with Kidney Stone Disease

“…The kidney is the principal organ of its elimination, a place where β 2 m is freely filtered by the glomeruli [13]. Ninety-nine percent of the filtered load of β 2 m is catabolized by proximal tubular cells, leaving only a small amount of this protein in the urine [12, 13]. In patients with renal tubular disorders, an increased urinary β 2 m excretion was observed which suggests a defective tubular catabolism of filtered protein.…”

“…The β 2 m is a small protein with a molecular weight of 11,800 daltons which is present in the cell membrane of most nucleated cells [11, 12]. The kidney is the principal organ of its elimination, a place where β 2 m is freely filtered by the glomeruli [13]. Ninety-nine percent of the filtered load of β 2 m is catabolized by proximal tubular cells, leaving only a small amount of this protein in the urine [12, 13].…”