Renal phosphate handling: Physiology

Prasad, Narayan; Bhadauria, Dharmendra

doi:10.4103/2230-8210.113752

Cited by 44 publications

(36 citation statements)

References 65 publications

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“…In the kidney, Klotho is expressed primarily in the distal tubules, and to a much lower extent in the proximal tubules. 16 However, renal phosphate is reabsorbed mainly in the proximal tubules [17][18][19] and activation of vitamin D occurs primarily in the proximal tubules. 20 It is currently unknown whether Klotho expressed in the proximal tubule is sufficient to mediate the phosphaturic and anti-vitamin D actions of FGF23, or whether cross talk between the distal and proximal tubules is needed for such regulation.…”

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In vivo evidence for a limited role of proximal tubular Klotho in renal phosphate handling

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Olauson

Sato

et al. 2016

Kidney International

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Klotho is a transmembrane protein expressed in the renal tubules where it acts as a permissive coreceptor for fibroblast growth factor 23 (FGF23). FGF23 signaling reduces the abundance of CYP27b1 and phosphate cotransporters NPT2a and NPT2c, leading to a decrease in 1,25(OH)2D3 synthesis and a rise in urinary phosphate excretion, respectively. Systemic or whole-nephron deletion of Klotho in mice results in renal FGF23 resistance characterized by high 1,25(OH)2D3 and phosphate levels and premature aging. Expression of Klotho is highest in the distal tubules, whereas 25OH vitamin D 1α hydroxylation and phosphate reabsorption predominantly occur in the proximal tubules. Currently, the segment-specific roles of Klotho in renal tubules are not fully understood. Here we have generated mice with Klotho specifically ablated from the proximal tubules using 3 different Cre mouse strains. All 3 models displayed impaired urinary phosphate excretion and increased abundance of NPT2a in the brush border membrane. Notably, hyperphosphatemia in knockout mice was mild or nonexistent under basal conditions but occurred upon high phosphate loading, indicating the presence of compensatory mechanisms. Effects on 1,25(OH)2D3 varied between mouse strains but were modest overall. Thus, Klotho expressed in the proximal tubules has a defined but limited role in renal phosphate handling in vivo.

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confidence: 99%

In vivo evidence for a limited role of proximal tubular Klotho in renal phosphate handling

Ide

Olauson

Sato

et al. 2016

Kidney International

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“…Serum phosphate levels are maintained by intestinal absorption, intracellular and bone storage pool exchange, and renal tubular absorption. Approximately 65% of ingested phosphate is absorbed in the duodenum and jejunum (Prasad & Bhadauria, 2013). Under the influence of calcitriol, phosphate is transported from the small intestine into the blood where it can be used for bone deposition and remodeling.…”

Section: Figurementioning

confidence: 99%

Hypophosphatemic Rickets

O'Mara

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Hypophosphatemic rickets is a rare, renal phosphate wasting disorder that presents various skeletal deformities. Although there are specific clinical presentations and biochemical findings used to identify hypophosphatemic rickets, there are various underlying renal phosphate wasting disorders that can lead to hypophosphatemic rickets making diagnosis extremely difficult. A targeted literature review through electronic search engines (e.g., BMC, PubMed, Google Scholar) was conducted to: 1) consolidate and summarize currently available data regarding the various renal phosphate wasting disorders, 2) identify current obstacles of successful diagnosis and treatment, and 3) propose directions for future hypophosphatemic rickets research into new biomarkers.

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“…FGF-23 is a bone-derived regulatory factor that acts to increase the fractional excretion of phosphorus in the kidneys (7). Conversely, its cofactor klotho is decreased and may initiate the early increase in FGF-23 concentrations (10,11).…”

Section: Renal Phosphorus Handling In Health and Ckdmentioning

confidence: 99%

Phosphate Additive Avoidance in Chronic Kidney Disease

et al. 2017

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IN BRIEF Dietary guidelines for patients with diabetes extend beyond glycemic management to include recommendations for mitigating chronic disease risk. This review summarizes the literature suggesting that excess dietary phosphorus intake may increase the risk of skeletal and cardiovascular disease in patients who are in the early stages of chronic kidney disease (CKD) despite having normal serum phosphorus concentrations. It explores strategies for limiting dietary phosphorus, emphasizing that food additives, as a major source of highly bioavailable dietary phosphorus, may be a suitable target. Although the evidence for restricting phosphorus-based food additives in early CKD is limited, diabetes clinicians should monitor ongoing research aimed at assessing its efficacy.

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Renal phosphate handling: Physiology

Cited by 44 publications

References 65 publications

In vivo evidence for a limited role of proximal tubular Klotho in renal phosphate handling

In vivo evidence for a limited role of proximal tubular Klotho in renal phosphate handling

Hypophosphatemic Rickets

Phosphate Additive Avoidance in Chronic Kidney Disease

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