Summary.There is no evidence that acidosis is either a causal or associated factor in infantile rickets. There is an increased urinary output of ammonia but the fact that it is associated with a diminution in the titratable acidity of the urine renders it unlikely that there is a condition of acidosis present. This conclusion is further strengthened by the fact that healing of rickets as evidenced by increased retention of minerals and X‐ray signs, may take place during prolonged administration of an acid‐producing substance.Infantile tetany is characterised by an increased retention of chlorine but there is no evidence of any disturbance of acid‐base equilibrium as a causal or associated factor.The retentions of calcium and phosphorus may run parallel even in the presence of tetany. Furthermore the phosphorus retention may be proportionately greater than that of calcium during spontaneous healing or following vitamin D therapy without any manifestations of tetany. Even the administration of large doses of phosphate leading to a great increase in the retention of phosphorus with a diminution in that of lime does not necessarily lead to the appearence of tetany although the calcium stores of the body have been previously greatly depleted. These results indicate that tetany complicating rickets may occur without an excessive retention of phosphorus over calcium and that excessive retention of phosphorus may take place without any manifestation of tetany. It therefore seems justifiable to conclude that phosphate retention is not the dominating factor in the pathogenesis of infantile tetany.The authors are indebted to Prof. G. B. Flemingfor much helpful advice. They desire to express their thanks to the Medical Research Council for personal grants to two of them (S. G. and