Intestinal phosphorus absorption in moderate ckd and healthy adults determined using a radioisotopic tracer

Background Reducing intestinal phosphorus absorption is a cornerstone in CKD-MBD management. Yet, knowledge gaps include how CKD pathophysiology affects intestinal phosphorus absorption. In vivo rodent studies suggest that intestinal phosphorus absorption remains inappropriately normal in early-moderate CKD, despite declining 1,25-dihydroxyvitamin D (1,25D). We measured intestinal phosphorus absorption in patients with moderate CKD versus healthy adults using a direct radiotracer method. Methods Patients with CKD and healthy adults matched for age, sex, and race were enrolled in this 8-day controlled diet study: The first 6 days outpatient and the final 2 days inpatient. Oral and intravenous doses of 33P and serial blood and urine sampling determined intestinal phosphorus absorption during the final 2 days. Secondary outcomes included fasting biochemistries and 24-hour urine phosphorus (uP). Results In total, n58 patients with CKD (eGFR529-55 ml/min per 1.73 m2) and n58 matched healthy controls completed the study. On a controlled diet, no difference in fractional intestinal phosphorus absorption was detected between patients with CKD and healthy adults (0.69 versus 0.62, respectively; P50.52), and this was similar for 24-hour uP (884 versus 935 mg/d, respectively; P50.70). Fractional intestinal phosphorus absorption was not significantly related to 24-hour uP. Patients with CKD had higher serum intact PTH and intact FGF23 and lower 1,25D. The relationship between 1,25D and fractional intestinal phosphorus absorption was not statistically significant. Conclusions Intestinalphosphorus absorptionwith typicaldietary intakedid notdiffer inpatientswithmoderate CKD compared with controls, despite lower serum 1,25D levels. In this setting, a relationship between 24-hour uP and fractional or absolute intestinal absorptionwas not evident. Further investigation is needed to determine what factors influence intestinal phosphorus absorption inCKDand the apparent lack of compensation by the intestine to limit phosphorus absorption in the face of declining kidney function and reduced 1,25D.Whether this is evident across a range of dietaryphosphorus intakes, aswell asCKDseverity, also needs to be determined.