Our patient's clinical and biochemical features clearly oriented towards renal failure of tubular origin (metabolic acidosis, increased alpha-1 and beta-2 microglobulin levels, microalbuminuria, glycosuria and low urine osmolality), without any sign of significant glomerular involvement (normal serum immunoglobulins and complement and nonnephrotic proteinuria). This evidence concerns the gene B2M and Renal insufficiency.