Renal Handling of Phosphate and Sulfate

Abstract

In the kidney, both anions, phosphate and sulfate, are almost freely filtered and afterwards reclaimed (reabsorbed) to a large extent from tubular fluid along the proximal tubules. Under normal dietary conditions, fractional excretion of these anions is approximately 10%. Reabsorption of both anions occurs along the proximal tubules by active, saturable, and regulated transepithelial processes. Most of the transporters involved in renal handling of phosphate and sulfate have been identified and their transport functions as well as their cellular localizations have been described in detail. The role of these transporters in the renal handling of phosphate and sulfate has been investigated by the use of several mice knock out models and also by analysis of several inherited human diseases. Numerous hormonal and nonhormonal factors, have been described that alter renal excretion of phosphate or sulfate by mechanisms that alter the abundance of known phosphate/sulfate transporters and consequently renal excretion. These mechanisms contribute to the homeostasis of the extracellular concentrations of phosphate and sulfate.

Current Understanding of Mineral and Bone Disorders of Chronic Kidney Disease and the Scientific Grounds on the Use of Exogenous Parathyroid Hormone in Its Management

“…In the kidney, PTH increases Ca reabsorption, Pi excretion and 1,25(OH)2D and FGF-23 production. [5] As part of the feedback loop, 1,25(OH)2D suppresses PTH production. It also increases Ca and Pi absorption in the intestine.…”

Chemical evidence for the tradeoff-in-the-nephron hypothesis to explain secondary hyperparathyroidism

“…Total [P] DCT and [Ca] DCT were estimated in this work under the following assumptions: the rate of phosphate delivery to the DCT equals the excretion rate of phosphorus (E P ) [ 29 ]; the rate of calcium delivery to this segment is 10% of the filtration rate of calcium, or 0.1(eGFR)[Ca uf ] s [ 30 ]; and fractional delivery of filtrate (FD f ) to the DCT is 0.2 in controls and 0.35 in subjects with CKD [ 31 – 33 ]. Accordingly, total [Ca] DCT was computed as 0.1(eGFR)[Ca uf ] s /(0.35)eGFR in CKD and as 0.1[(eGFR)[Ca uf ] s /(0.2)eGFR in CTRL.…”

Tubular and genetic disorders associated with kidney stones

“…SLC34A3 (solute carrier family 34, member 3) encodes the sodium-dependent phosphate co-transporter 2c (NPT2c), which is located in the proximal tubule and mediates phosphate reabsorption across the apical brush border membrane [21]. Homozygous or compound heterozygous mutations of SLC34A3 cause hereditary hypophosphatemic rickets with hypercalciuria (HHRH), which is characterized by hypophosphatemia from increased renal phosphate losses, hypercalciuria, elevated 1,25(OH)2-vitamin D levels, and rickets [22,23].…”

“…SLC34A1 (solute carrier family 34, member 1) encodes for the sodium-dependent phosphate co-transporter 2a (NPT2a), which is expressed mainly in the kidney proximal tubule, and like SLC34A3 is responsible for renal phosphate reabsorption [21].…”