“…Most of the childhood cases progressed rapidly to renal failure (McVicar, et al, 1974;Burke et al, 1971) and in these patients it seemed reasonable to explain tubular dysfunction as being secondary to gross renal damage and uraemia. Some authors have considered that this may always be the case; there is indeed a growing body of experimental evidence that in nephrotic syndrome with good renal function, both tubular function (Maddox et al, 1974;Andreucci et al, 1973;Oken and Flamenbaum, 1971) and morphology (Ryabov et al, 1978) are essentially normal and able to compensate appropriately for the changed intraluminal and peritubular environment. Sherman and Becker (1971) showed in 22 adult patients with nephrotic syndrome that glycosuria and lysozymuria were correlated with the degree of renal function rather than urinary or serum protein concentrations.…”