Since the presentation of a case of nephritis associated with rachitic changes in the long bones by Lucas1 in 1883, the subject of renal rickets has been widely discussed in English and American literature. Its pathology and chemical physiology, as well as the various etiologic factors involved, have been carefully considered by Parsons,2 Mitchell,3 Schoenthal and Burpee,4 Hamperl and Wallis,5 Shelling and Remsen6 and others. In brief, this disturbance is characterized by chronic renal disease, dwarfism, hyperphosphatemia, azotemia, changes in the skeleton simulating those in infantile rickets, chronic acidosis and, finally, uremia and death.
Of late, several cases have been reported in which the clinical and roentgenologic findings simulated those of renal rickets, except for the absence of azotemia and the presence of hypophosphatemia instead of the usual hyperphosphatemia. De Toni7 presented an unusual case of rickets associated with albuminuria, glycosuria, hypophosphatemia and