Context Dietary consumption of phosphate is increasing, and elevated serum phosphate is associated with increased cardiovascular disease (CVD) risk. Sex differences in phosphate homeostasis and response to changes in dietary phosphate intake, which are not captured by clinically measured analytes, may contribute to differences in CVD presentation and bone disease. Objective To assess sex differences in acute phosphate homeostasis in response to a single oral phosphate challenge. Design Cross-sectional. Setting General community. Participants : 78 participants (40-76y) with measured GFR >60 mL/min/1.73m2 and no clinically diagnosed CVD and 14 young healthy adults. Main Outcome Measures To elucidate subtle alterations in phosphate homeostasis, we employ an acute challenge whereby the hormonal response, circulating mineral levels, and urinary excretion are assessed following an oral challenge of phosphate. Results Although both males and females had similar changes in circulating phosphate, calcium, and parathyroid hormone in response to the challenge, females excreted ∼1.9x more phosphate and ∼2.7x more calcium than males, despite not consuming calcium. These sex differences were recapitulated in healthy young adults. This excretion response did not correlate to age, serum phosphate, or estradiol levels. The females with greater excretion of phosphate had higher levels of bone resorption markers compared to formation markers. Conclusions Taken together, these data identify sex differences in acute phosphate homeostasis, specifically that females may mobilize and excrete endogenous sources of calcium and phosphate in response to oral phosphate compared to males. While high levels of dietary phosphate negatively impact bone, our results suggest that females may incur more risk from these diets.

Spreading depression (SD) is associated with large changes in extracellular ion concentrations and can be induced by impairing mechanisms of K + ion homeostasis. We tested activity dependence of SD in the locust model of ouabain-induced SD in the metathoracic ganglion. Wind activation of thoracic circuitry resulted in small increases of K + concentration that took 5-10 s to be cleared from the extracellular space. In the presence of the Na + /K + -ATPase inhibitor ouabain, wind stimulation every 30 s halved the latency to the first SD event and increased its duration. Wind stimulation was able to trigger the first event, suggesting that local activity could determine the origin of successive SD events. Perfusion with calcium-free saline blocked neural activity in the ganglion and prevented the occurrence of ouabain-induced SD. We conclude that ouabain-induced SD in the locust CNS is strongly dependent on the existing level of neural activity.

Background: While dietary intake is known to influence serum markers of chronic kidney disease–mineral and bone disorder (CKD-MBD), the effects of recent food and beverage intake, particularly phosphorus consumption on these serum markers (phosphate, calcium, and parathyroid hormone [PTH]), are unknown in hemodialysis patients. An understanding of these effects could have direct and important implications on the management of CKD-MBD. Objective: To determine whether serum phosphate, calcium, and PTH levels were higher in hemodialysis patients who had consumed dietary phosphorus within 1 hour prior to their routine dialysis-related blood work (non–phosphorus-fasted) compared with patients who did not (phosphorus-fasted). Design: Observational, cross-sectional study. Setting: Kingston Health Sciences Center—Kingston General Hospital Site and its affiliated satellite hemodialysis units. Patients: Two hundred fifty-four adult patients receiving outpatient hemodialysis treatment for end-stage kidney disease were recruited. Measurements: The main measurements for this study included an assessment of dietary phosphorus intake as well as serum phosphate, calcium, PTH, albumin, Kt/V, and urea reduction ratio. Methods: A direct patient interview was performed to assess dietary phosphorus intake within 1 hour prior to routine dialysis-related blood work. The Canadian Nutrient File was then used to estimate dietary phosphorus based on the specific foods and beverages (including portion sizes and brands where applicable) identified in the interview. Serum measures of phosphate, PTH, calcium, albumin, and dialysis adequacy (Kt/V and urea reduction ratio) were obtained from participants’ routine dialysis-related blood work. Results: Non–phosphorus-fasted participants had nonsignificantly higher serum PTH levels compared to phosphorus-fasted participants (61.2 ± 64.7 vs 47.9 ± 39.7, P = .05). Non–phosphorus-fasted participants with PTH levels at the Kidney Disease Improving Global Outcomes (KDIGO) “target” (between 15 and 60 pmol/L) had significantly higher serum phosphate levels relative to phosphorus-fasted participants (1.6 ± 0.3 vs 1.4 ± 0.4, P = .006). In non–phosphorus-fasted participants, there was a nonsignificant association between the number of items containing inorganic phosphate additives and higher levels of serum phosphate and lower levels of serum calcium. Limitations: Some limitations include the cross-sectional nature of this study, self-reporting biases and estimates (as opposed to direct measurements) related to the dietary assessment, and the use of single (and not serial) assessments of serum measures. Conclusions: Dietary phosphorus intake in close proximity to blood work may contribute to subtle alterations in some key serum CKD-MBD parameters in adult outpatient hemodialysis patients but may not meaningfully alter CKD-MBD management.

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