Summary The behaviour of the kidney concerning glucose excretion is defined, for high levels of blood glucose, by a straight line relationship (Shannon and Fisher). For a given filtration rate (F) to each value of TmG (tubular maximal reabsorption capacity for glucose) corresponds a definitive value of the mean threshold which is equal to TmG/F. The concept of threshold has been recently discussed by Govaerts. In order to understand the laws of glucose excretion when hyperglycemia is moderate (between 0,15 and 0,3 gr % in man) it is necessary to define a minimal and a maximal threshold. This is due to the fact that the nephrons being structurally unequal, their reabsorptive capacity for glucose is also unequal. The minimal threshold is the level of blood glucose at which enough glucose is filtered to saturate the nephrons with the smallest reabsorption power. The maximal threshold is the level of hyperglycemia at which enough glucose is filtered to saturate the nephrons with the largest reabsorptive power. The mean threshold ((TmG/F) is the level of hyperglycemia at which all the nephrons would be saturated if their reabsorptive power was uniform for all and equal to the statistical mean of the individual reabsorptive capacity of the nephrons. Renal diabetes may be characterized by the fact that glucosuria exists at normal or nearly normal blood levels (which means that the minimal threshold is lowered). Furthermore, Govaerts and Cambier have found that patients with a renal diabetes, when their blood glucose rose, excreted more glucose than did other patients with similar hyperglycemia and filtration rate. This means that TmG and the mean threshold are decreased in renal diabetes. However, Friedman has claimed that in patients with renal diabetes and a low minimal threshold, the reabsorption capacity TmG and the mean threshold were normal. The purpose of the present work was to control Friedman’s opinion. In two cases, we found decreased values of mean threshold and TmG. This confirms Govaerts and Cambier’s previous conclusions and recent findings of Nielsen. As in our cases the glomerular filtration was normal, the reduction of TmG could not be explained by inactivity or impairment of the glomeruli. Therefore renal diabetes has to be related to a tubular disorder. If such a dysfunction was due to a morphological damage, one should expect a similar decrease of glucose and both phosphorus and amino-acids reabsorption as all these substances are claimed to be reabsorbed at the same level of the proximal tubule. Such a picture has been described in what is called Fanconi’s syndrom, but it does not conform to what was found in our patients. In these, phosphorus reabsorption was the same as in patients with normal kidneys, even when the blood level was increased. Therefore we feel that the cause of renal diabetes is likely to be a disturbance in those enzymatic processes that make possible the reabsorption of glucose and the transfer of glucose through the cells.