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Association of fibroblast growth factor 23 and hypophosphatemia in well‐suppressed HIV‐infected patients receiving antiretroviral therapy
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IntroductionProlong hypophosphatemia may result in future bone loss which will have effect on patient's quality of life. Hypophosphatemia is observed in 4–31% of HIV‐infected patients receiving highly active antiretroviral therapy (HAART). Fibroblast growth factor 23 (FGF‐23), a potent phosphaturic hormone, has not been well studied in HIV‐infected Thai patients. We aimed to investigate whether FGF‐23 is involved in the etiology of hypophosphatemia in our HIV‐positive patients on HAART.MethodThis study was a case‐controlled study at HIV‐NAT, Thai Red Cross AIDS Research Centre, Bangkok, Thailand during June 2011‐May 2012. Serum and urine phosphate was studied in 696 well‐suppressed HIV‐infected patients. Hypophosphatemia was defined as a serum phosphate level <2.5 mg/dl. All fasting blood and urine samples were taken between 7.00 and 10.00 hr to measure serum phosphate, calcium, 1,25 OHD, parathyroid hormone (PTH), FGF‐23 and urinary phosphate excretion. The renal phosphate threshold tubular maximum phosphate reabsorption per glomerular filtration rate (TmP/GFR) was calculated. eGFR was calculated using the MDRD.ResultsTotally 65 (9.3%) subjects were identified for hypophosphatemia. The prevalence of hypophosphatemia was not difference between TDF exposure [(46/544: 8.5%) and TDF unexposure (19/154: 12.5%), p=0.13]. However, only 56 subjects for a case group (hypophosphatemia group) and 65 subjects with normal phosphate (normophosphatemia group were included in this analysis. In the hypophosphatemia group, they were more likely younger, less female, and lower CD4 cell counts than the control group. About 80% and 74% of the case and control group had TDF exposure, respectively. The renal phosphate reabsorption threshold was significantly lower in hypophosphatemia group than in the control [43 (2.19–2.6) vs 3.16 (2.92–3.61) mg/dl, p<0.001]. FGF‐23 was significantly higher in hypophosphatemia group [31.9 (24.7–40.0) vs 26.2 (19.3–34.1) pg/dl, p<0.017]. TmP/GFR was strongly related to FGF‐23 levels (p<0.04), but not for PTH (p<0.06), and urine calcium (p<0.07).ConclusionFGF‐23 is involved in pathogenesis of hypophosphatemia in our HIV‐positive patients on HAART.
Title: Association of fibroblast growth factor 23 and hypophosphatemia in well‐suppressed HIV‐infected patients receiving antiretroviral therapy
Description:
IntroductionProlong hypophosphatemia may result in future bone loss which will have effect on patient's quality of life.
Hypophosphatemia is observed in 4–31% of HIV‐infected patients receiving highly active antiretroviral therapy (HAART).
Fibroblast growth factor 23 (FGF‐23), a potent phosphaturic hormone, has not been well studied in HIV‐infected Thai patients.
We aimed to investigate whether FGF‐23 is involved in the etiology of hypophosphatemia in our HIV‐positive patients on HAART.
MethodThis study was a case‐controlled study at HIV‐NAT, Thai Red Cross AIDS Research Centre, Bangkok, Thailand during June 2011‐May 2012.
Serum and urine phosphate was studied in 696 well‐suppressed HIV‐infected patients.
Hypophosphatemia was defined as a serum phosphate level <2.
5 mg/dl.
All fasting blood and urine samples were taken between 7.
00 and 10.
00 hr to measure serum phosphate, calcium, 1,25 OHD, parathyroid hormone (PTH), FGF‐23 and urinary phosphate excretion.
The renal phosphate threshold tubular maximum phosphate reabsorption per glomerular filtration rate (TmP/GFR) was calculated.
eGFR was calculated using the MDRD.
ResultsTotally 65 (9.
3%) subjects were identified for hypophosphatemia.
The prevalence of hypophosphatemia was not difference between TDF exposure [(46/544: 8.
5%) and TDF unexposure (19/154: 12.
5%), p=0.
13].
However, only 56 subjects for a case group (hypophosphatemia group) and 65 subjects with normal phosphate (normophosphatemia group were included in this analysis.
In the hypophosphatemia group, they were more likely younger, less female, and lower CD4 cell counts than the control group.
About 80% and 74% of the case and control group had TDF exposure, respectively.
The renal phosphate reabsorption threshold was significantly lower in hypophosphatemia group than in the control [43 (2.
19–2.
6) vs 3.
16 (2.
92–3.
61) mg/dl, p<0.
001].
FGF‐23 was significantly higher in hypophosphatemia group [31.
9 (24.
7–40.
0) vs 26.
2 (19.
3–34.
1) pg/dl, p<0.
017].
TmP/GFR was strongly related to FGF‐23 levels (p<0.
04), but not for PTH (p<0.
06), and urine calcium (p<0.
07).
ConclusionFGF‐23 is involved in pathogenesis of hypophosphatemia in our HIV‐positive patients on HAART.
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