“…Abnormalities of proximal tubular function in the nephrotic syndrome are not generally seen until end-stage renal failure has been reached (Bruck et al, 1954), but there are well documented cases of proximal tubular abnormalities and nephrotic syndrome in the absence of end-stage uraemia in children (Shwayder et al, 1976;Stanbury and Macaulay, 1957;Burke et al, 1971) and adults (Sherman and Becker, 1971;Weinreb et al, 1970. The pathophysiological mechanisms underlying tubular damage in this context remain unknown, but many have been proposed, including the damaging effect of heavy proteinuria (Pabico et al, 1976;Weinreb et al, 1970), hypokalaemic nephropathy (Stanbury and Macauley, 1957), glycogen deposition in distal tubule cells (Kovnat and Lin, 1974), specific autoimmune tubular and glomerular disease (Shwayder et al, 1976;Naruse et al, 1976) and the general tissue damage associated with end-stage glomerulonephritis and uraemia (Sherman and Becker, 1971). A variety of histological patterns has been described in this mixed syndrome, the most common of which is MCGN with immune complex deposition (Dreher, Zimmerman and Simpson, 1977;Vitacco et al, 1970).…”