Sentence examples for phosphorus reabsorption from inspiring English sources

PTH interferes with renal tubular phosphorus reabsorption, causing an enhanced renal excretion of phosphorus.

The purpose of the present study is to examine the effect of cinacalcet treatment on determinants of renal phosphorus reabsorption under steady-state conditions.

In postmenopausal women, administration of estrogen suppresses bone resorption and produces a transient decrease in serum calcium and phosphorus and in renal reabsorption of phosphorus, as well as positive calcium balance effects that help to stabilize the total skeletal bone mass.

It is an inhibitor of proximal tubular reabsorption of phosphorus.

The tubular maximum reabsorption of phosphorus per glomerular filtration rate (TmP/GFR [mg/dL]) can be calculated by the following equation [ 22]: If TRP is ≤ 0.86 (86%), then TmP/GFR = TRP × (serum phosphate).

Fractional excretion of calcium (FEca) was calculated by the formula: FEca = ([urine calcium] × [serum creatinine])/([serum calcium] × [urine creatinine]).Tubular fractional reabsorption of phosphorus (TRP) was calculated by the formula: TRP = 1- [urine phosphate] × [serum creatinine])/([serum phosphate] × [urine creatinine]); and percent TRP was calculated by multiplying TRP by 1- [urine

Hyperphosphatemic familial tumoral calcinosis is a relatively rare genetic disease characterized by enhanced renal tubular phosphate reabsorption and elevated serum phosphorus, as well as paraarticular calcific tumors.

A number of factors influence the renal tubular reabsorption of Pi, such as dietary phosphorus content, and parathyroid hormone (PTH), growth hormone (insulin-like growth factor 1) and thyroid hormone concentrations, although these latter two hormones probably do not play a major role in the short-term control of serum Pi concentrations, but, rather, determine long-term concentrations.

To compare 24-h U-P/CCr with common markers of urinary phosphorus excretion, we examined for the association of fractional excretion of phosphorus (FeP), tubular reabsorption of phosphate (TRP), and maximum tubular reabsorption of phosphorus per unit volume of glomerular filtration rate (TmP/GFR) with primary outcomes.

This mechanism, which serves to lower levels of phosphorus in the bloodstream, is significant because high phosphate levels inhibit and low levels enhance osteoclastic reabsorption.

Additionally, low levels of vitamin D and parathyroid hormone increase the transport of phosphorus out of the renal cells through 3NA-HPO4 co-transporter type 2a (NPT-2a) and limit renal tubular reabsorption additionally resulting in hyperphosphatemia [ 47, 48].