THE EFFECT OF PARATHYROID HORMONE ON PHOSPHATE EXCRETION IN THE RAT

1953 ◽  
Vol 9 (3) ◽  
pp. 292-300 ◽  
Author(s):  
BERYL M. A. DAVIES ◽  
A. H. GORDON

The magnitude of the decrease in serum inorganic phosphate and the increase in urine phosphate of parathyroidectomized rats caused by injected parathyroid hormone has been studied. About 3 u.s.p. units of this hormone have been found to cause maximum changes in both serum and urine phosphate. Both responses depend on the respective initial phosphate level. Urine phosphate levels too high for more than minimal changes in phosphate excretion have been reduced by diets containing aluminium sulphate.

1984 ◽  
Vol 246 (4) ◽  
pp. F373-F378 ◽  
Author(s):  
R. F. Wideman

Parathyroid hormone (PTH) stimulates a secretory component of avian renal inorganic phosphate (Pi) transport, but the secreted Pi does not appear to be derived directly from peritubular (plasma) Pi. In the present study, experiments were conducted to determine whether differences in parathyroid status during 32P infusion influenced entry of the isotope into the Pi secretory pool. Fractional excretion values for Pi (FEPi) and 32P (FE32P) were compared in normal and parathyroidectomized (PTX) anesthetized birds that had been preinfused with 32P for 0, 90, and 240 min before PTH infusion. The results demonstrate that in the absence of exogenous PTH, FEPi is identical to FE32P in normal and PTX birds, reflecting full equilibration of 32P with excreted Pi under these conditions; and, regardless of the duration of 32P preequilibration or the parathyroid status of the experimental animals, exogenous PTH always causes FEPi to exceed FE32P. It is concluded that the Pi secretory pool is inaccessible to 32P under conditions that should markedly alter cellular Pi influx and efflux.


2015 ◽  
Vol 23 (1) ◽  
pp. 37-40
Author(s):  
Gobinda Chandra Saha ◽  
Ekramul Mustafa ◽  
Masood Salehin ◽  
T Alam ◽  
M Akhtaruzzaman ◽  
...  

Background: Glomerular filtration rate (GFR) reflects renal function and in chronic kidney disease (CKD) stage 3-5, there is electrolyte imbalance which is reflected by changes in serum creatinine and phosphate level. The aim of this study was to determine GFR in advanced stages of CKD and its relation with serum creatinine and serum inorganic phosphate. Methods: This was a cross sectional study which was done in Rajshahi Medical College, Rajshahi. A total of 120 patients were taken. Among them ninety were with advanced stages of CKD and thirty were as control group. Results: Mean GFR in healthy control was 104.953±16.663 ml/min., mean GFR in CKD3 group was 36.256±5.582, in CKD4 group was 21.142±5.420 ml/min. and in CKD5 group was 10.304±2.694 ml/min. Mean serum creatinine in healthy control was 0.936±0.116 mg/dl and 2.226±0.272, 3.698±0.915 & 6.906±2.439 mg/dl in CKD3, CKD4 & CKD5 respectively. While, the mean serum inorganic phosphate level in healthy control group was 1.23±0.17 mmol/L, and 1.79±0.11, 2.09±0.27 & 3.04±0.33 mmol/L in CKD3, CKD4 & CKD5 respectively. Conclusion: Serum creatinine and phosphate levels are increased with the severity of CKD. DOI: http://dx.doi.org/10.3329/jdmc.v23i1.22692 J Dhaka Medical College, Vol. 23, No.1, April, 2014, Page 37-40


2020 ◽  
Vol 16 (7) ◽  
pp. 674-689 ◽  
Author(s):  
Ronald B. Brown

This article presents a scoping review and synthesis of research findings investigating the toxic cellular accumulation of dysregulated inorganic phosphate—phosphate toxicity—as a pathophysiological determinant of diabetes and diabetic complications. Phosphorus, an essential micronutrient, is closely linked to the cellular metabolism of glucose for energy production, and serum inorganic phosphate is often transported into cells along with glucose during insulin therapy. Mitochondrial dysfunction and apoptosis, endoplasmic reticulum stress, neuronal degeneration, and pancreatic cancer are associated with dysregulated levels of phosphate in diabetes. Ectopic calcification involving deposition of calcium-phosphate crystals is prevalent throughout diabetic complications, including vascular calcification, nephropathy, retinopathy, and bone disorders. A low-glycemic, low-phosphate dietary intervention is proposed for further investigations in the treatment and prevention of diabetes and related diabetic pathologies.


2019 ◽  
Author(s):  
Forough Saki ◽  
Seyed Reza Kassaee ◽  
Azita Salehifar Salehifar ◽  
gholamhossein Ranjbar omrani

Abstract Background:phosphate homeostasis is mediated through complex counter regulatory feed-back balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium- phosphate cotransporters II a and II c . However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods:In this case-control study, 19 patients with hypoparathyroidism and their age- and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results:The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group(P<0.001 and P<0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P<0.001 and P<0.001,respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal individuals (P <0.001, r = 0.79). Conclusions:Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.


2017 ◽  
Vol 42 (3) ◽  
pp. 104-110
Author(s):  
Ismat Jahan ◽  
MA Mannan ◽  
Sanjoy Kumer Dey ◽  
Sadeka Choudhury Moni ◽  
Mohammod Shahidullah

Osteopaenia of prematurity (OOP) imposes the risk of fractures and growth failure to premature infants. Studies have investigated the validity of biochemical markers of osteopaenia but till date it is not established. So, this study was intended to examine the diagnostic performance of biochemical markers in early detection of osteopaenia of prematurity. This prospective study was conducted in the Neonatal Intensive Care Unit (NICU), Department of Neonatology, Bangabandhu Sheikh Mujib Medical University during June 2013 to February 2014. A total of 100 premature infants with gestational age ? 34 weeks were consecutively included over 9 months period. Serum alkaline phosphatase, serum calcium and serum inorganic phosphates were measured from 1 week of chronological age until corrected term age. At corrected term age, radiologic examination was done for the assessment of osteopaenia. Of the enrolled infants, 36/78 (46%) developed radiological evidence of osteopaenia. Serum inorganic phosphate level was significantly less in osteopaenic infants than non-osteopaenic infants throughout first two months of life (p <0.001). The area under ROC curve for serum inorganic phosphate was 85% (p = 0.001). If the cut off value of serum inorganic phosphate was set at 3.6 mg/dl, then a sensitivity of 86% and a specificity of 49% were obtained. Low serum inorganic phosphate at 3 weeks of life can be used as a marker for early detection of osteopaenia of prematurity. 


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