Abstract
Hyperphosphatemia is a secondary issue associated with chronic kidney disorder. Use of phosphate binders and dialysis are the treatments for hyperphosphatemia, albeit with harmful side effects and high cost, respectively. A safer and healthier approach is attempted to administer phosphate-accumulating organisms (PAOs) from probiotics to prevent hyperphosphatemia. However, screening and isolation of PAOs are limited by inefficient enrichment of relevant metabolism and contamination. Therefore, we devised a novel strategy to isolate elite PAOs from Lactobacillus casei JCM 1134 and Bifidobacterium adolescentis JCM 1275 (previously reported PAOs). PAOs were first enriched for phosphate uptake and incubated in low-pH phosphate-free media to dormant non-PAOs, and then purified using Percoll density gradient centrifugation. Subsequently, elite PAOs were isolated from centrifuged pellet on a toluidine blue O-supplemented agar-based media. Using this technique, elite PAOs could not only be isolated, but also semi-quantitatively scored for their phosphate accumulation capabilities. Additionally, these scores correlated well with their accumulated phosphate values. The elite PAOs isolated from L. casei and B. adolescentis showed 0.81 and 0.70 [mg-phosphate/mg-dry cell], respectively (23- and 4.34-fold increase, respectively). Thus, our method can be used to successfully isolate elite PAOs, which might be of use to prevent hyperphosphatemia at early stages.
Highlights
Pervasive phosphate-rich food habits and work pressure co-exist with chronic kidney disorder (CKD), one of the major causes of hyperphosphatemia due to deficiencies in kidney function[1]
We developed a novel and comprehensive method that involved the enrichment of phosphate accumulation metabolism in phosphate-accumulation media, subsequent inactivation of non-phosphateaccumulating organisms (PAOs) in a low-pH phosphate-free media, and separation via centrifugation on a Percoll density gradient
The cultures contained strains with diverse range of phosphate accumulating abilities, as low potential PAOs as well as non-PAOs were observed in DAPI micrographs
Summary
Pervasive phosphate-rich food habits and work pressure co-exist with chronic kidney disorder (CKD), one of the major causes of hyperphosphatemia due to deficiencies in kidney function[1]. According to the National Kidney Foundation-Kidney Disease Quality Outcome Initiative, CKD patients on dialysis should maintain serum phosphate levels between 3.5 to 5.5 mg/dL (National kidney foundation, accessed on 1st feb, 2018)[3]. Chemotherapy using phosphate binders such as calcium carbonate, lanthanum carbonate, ferric citrate, and Sevelamer can elicit hypercalcemia, deposition of lanthanum in the bone, and gastric issues such as constipation and vomiting, respectively[5]. All these treatments are prescribed typically at advanced stages of CKD when kidney damage is almost irreversible and the maintenance of normal serum phosphate levels becomes a lifelong challenge with associated side effects
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