Correspondence (reply): In Reply

Professor Maurer mentions the association of phosphate with abnormal behaviors. The mechanism of organophosphates that is being discussed in the context of the development of ADHD is due to the direct effect of these organophosphates and not due to dietary phosphate intake.

Dr Deixler rightly points out that in addition to hyperphosphatemia, hypophosphatemia affects the cardiovascular risk. This is undoubtedly true, and pronounced hypophosphatemia leads to a notably increased risk even in renal patients. The extent to which these rare cases of hypophosphatemia represent the result of reduced dietary intake is currently not known. The question of the extent to which problems such as sepsis, poorly controlled diabetes, alcoholism, etc, are due to a negative phosphate balance or poorly distributed extracellular and intracellular phosphate can currently not be answered.

Dr Deixler rightly also reminds us that the phosphate concentration in the extracellular space probably triggers pathological effects not directly, but perhaps indirectly, owing to intracellular metabolic cascades. This is correct; intracellular phosphate concentration itself is relevant for the problem of vascular calcification. Equally correct is the comment that because of the circadian rhythm, one individual reading of the serum phosphate concentration under non-standardized conditions is not 100% reliable. All the more remarkable is the fact that even in people with healthy kidneys a highly significant relation exists between cardiovascular risk and serum phosphate (that is, in blood samples taken under non-standardized conditions)—another reason for why, in spite of this potential source of error, the association between serum phosphate and cardiovascular risk is relevant.