Serum Phosphate Levels Research Articles

Effects of intravenous sodium thiosulfate on vascular calcification in dialysis patients with end-stage renal disease: a systematic review and meta-analysis.

In dialysis patients, vascular calcification is a common complication and is closely related to the morbidity and mortality of cardiovascular disease. We performed a systematic review to determine the efficacy and safety of sodium thiosulfate (STS) in the progression of vascular calcification in dialysis patients with end-stage renal disease. The PubMed, Web of Science, Embase, Cochrane Library, Wanfang, CNKI, China Biology Medicine disc and Weipu databases were searched up to 9 March 2022 for clinical trials to synthesise findings on the efficacy and safety of STS in the progression of vascular calcification in dialysis patients. The primary outcome was coronary artery calcification scores (CACS) or abdominal aortic calcification scores (AACS) or Kauppila index. The secondary outcome was pulse-wave velocity (PWV). Laboratory data were shown in safety data. A random-effect model was used to provide the summary measures of effect [standardised mean difference (SMD) and 95% confidence interval (CI)]. Seven randomised, controlled trials and one nonrandomised, controlled trial involving 370 patients were included. Six studies reported that the progression of CACS or AACS was slower in the intravenous STS group compared with the control group (SMD -3.24, 95% CI: -5.29, -1.18, p = 0.002). Two studies showed the increase in PWV was less in the STS group compared with the control group (SMD -0.52, 95% CI: -0.92, -0.13, p = 0.009). During the trial period, a lower high-sensitivity C-reactive protein level (SMD 1.61, 95% CI: 0.19, 3.04, p = 0.03), a decrease in serum bicarbonate level (SMD 0.67, 95% CI: 0.22, 1.11, p = 0.003) and an increase in serum phosphate level (SMD -0.32, 95% CI: -0.62, -0.03, p = 0.03) were noted in the intravenous STS group compared with the control group. However, serum calcium and parathyroid hormone levels showed no difference between the two groups after the trials. The most common adverse events were temporary nausea and vomiting, which occurred in 12.5 to 75% of patients. Intravenous STS may slow down the progression of vascular calcification and ameliorate arterial stiffness in dialysis patients. Reliably defining the efficacy and safety of intravenous STS in attenuating the progression of vascular calcification requires a high-quality trial with a large sample size.

The Association Between the Levels of Serum Phosphate and Mortality Rates in Pre-Dialysis and Dialysis Patients

Introduction: Discovering predictors to reduce morbidity and mortality in chronic kidney disease (CKD) is now a critical global priority. Serum phosphate level is considered to be a potential marker for mortality rate in patients with CKD. Previous studies examined the independent pathogenic role of phosphorus in the development of CKD and dialysis patients but have yielded contradictory findings. This study aims at evaluating the relationship between serum phosphate levels and death rates in pre-dialysis CKD and maintenance of dialysis patients. Method: PubMed, Scopus, and Web of Science were searched by using MeSH term keywords. The authors did screening, data extraction, and quality assessment in accordance with the inclusion criteria. STATA 14.2 was used for statistical analyses. The analysis was performed using the random- and fixed-effects model when the heterogeneity was >50% and ≤50%, respectively. For evaluating publication bias, Funnel plots and Egger tests were used. Result: Eleven original studies between 2005 and 2021 met the eligibility criteria. The overall estimate of unadjusted HR of all-cause mortality each 1 mg/dL increase in the serum phosphate concentration using the random-effects model in pre-dialysis CKD and dialysis patients was 1.33 (95% CI: 0.97, 1.82, I2 = 99.1%, P = 0.074), and for adjustment, Hazard ratio was 1.27 (95% CI: 1.15, 1.39, I2 = 75.4%, P < 0.001). Conclusion: The findings showed the association between serum phosphate levels and death rates in pre-dialysis individuals with CKD and dialysis patients.

Hyperphosphatemia Contributes to Skeletal Muscle Atrophy in Mice.

Chronic kidney disease (CKD) is associated with various pathologic changes, including elevations in serum phosphate levels (hyperphosphatemia), vascular calcification, and skeletal muscle atrophy. Elevated phosphate can damage vascular smooth muscle cells and cause vascular calcification. Here, we determined whether high phosphate can also affect skeletal muscle cells and whether hyperphosphatemia, in the context of CKD or by itself, is associated with skeletal muscle atrophy. As models of hyperphosphatemia with CKD, we studied mice receiving an adenine-rich diet for 14 weeks and mice with deletion of Collagen 4a3 (Col4a3-/-). As models of hyperphosphatemia without CKD, we analyzed mice receiving a high-phosphate diet for three and six months as well as a genetic model for klotho deficiency (kl/kl). We found that adenine, Col4a3-/-, and kl/kl mice have reduced skeletal muscle mass and function and develop atrophy. Mice on a high-phosphate diet for six months also had lower skeletal muscle mass and function but no significant signs of atrophy, indicating less severe damage compared with the other three models. To determine the potential direct actions of phosphate on skeletal muscle, we cultured primary mouse myotubes in high phosphate concentrations, and we detected the induction of atrophy. We conclude that in experimental mouse models, hyperphosphatemia is sufficient to induce skeletal muscle atrophy and that, among various other factors, elevated phosphate levels might contribute to skeletal muscle injury in CKD.

Genetic association of serum calcium, phosphate, vitamin D, parathyroid hormone, and FGF23 with the risk of aortic stenosis

Disorders of mineral metabolism, including elevated levels of serum calcium, phosphate, 25-hydroxyvitamin D (25OH-VitD), parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23), have been reported in patients with calcific aortic valve stenosis (CAVS). However, evidence of the causal role of mineral metabolism in CAVS is still lacking. In this study, we employed a systematic pipeline combining Mendelian randomization (MR), Steiger directionality test, colocalization analysis, protein-protein network, and enrichment analysis to investigate the causal effect of mineral metabolism on CAVS. Genome-wide association study (GWAS) and protein quantitative trait loci data for mineral metabolism markers were extracted from large-scale meta-analyses. Summary statistics for CAVS were obtained from two independent GWAS datasets as discovery and replication cohorts (n = 374,277 and 653,867). In MR analysis, genetic mimicry of serum FGF23 elevation was associated with increased CAVS risk [ORdiscovery = 3.081 (1.649–5.760), Pdiscovery = 4.21 × 10−4; ORreplication = 2.280 (1.461 – 3.558), Preplication = 2.82 × 10−4] without evidence of reverse causation (Psteiger= 7.21 × 10−98). Strong colocalisation association with CAVS was observed for FGF23 expression in the blood (PP.H4 = 0.96). Additionally, we identified some protein-protein interactions between FGF23 and known CAVS-associated genes. Serum calcium, phosphate, 25OH-VitD, and PTH failed to show causal effects on CAVS at Bonferroni-corrected significance (all P > 0.05/5 = 0.01). In conclusion, elevated serum FGF23 level may act as a causal risk factor for CAVS, and its mechanism of action in CAVS development may be independent of its function in regulating mineral metabolism. Hence, FGF23 may serve as a circulating marker and a promising preventive target for CAVS, warranting further investigation.

Item Response Theory Quantifies the Relationship Between Improvements in Serum Phosphate and Patient-Reported Outcomes in Adults With X-Linked Hypophosphatemia.

Burosumab is indicated for treatment of a rare bone disease, X-linked hypophosphatemia (XLH). The aim of this analysis was to evaluate the relationship between a treatment response biomarker and patient-reported outcomes (PROs). Longitudinal data for PROs were obtained from adults with XLH from a phase III study. Individual rich time profiles of the biomarker, serum phosphate were simulated using a prior population pharmacokinetic-pharmacodynamic model to calculate serum phosphate exposure metrics for each 28-day treatment cycle, which were then merged with PROs data. Item response theory parameters were first estimated to map a latent variable, ψ, that is, disability score, relative to baseline. Next, the relationships between serum phosphate exposures and ψ were modeled using a nonlinear mixed-effect (NLME) modeling approach. A combined item response theory-NLME model with average serum phosphate as a predictor of ψ described PROs data well. The model estimates suggested 28%, 31%, and 25% reduction in Western Ontario and McMaster Universities Osteoarthritis Index, brief pain inventory, and brief fatigue inventory scores, respectively, with every unit increase in average serum phosphate from the lower limit of normal (2.5 mg/dL). Additionally, a time effect of ~ 0.08% improvements each week was estimated. The analysis suggested that burosumab treatment-induced improvements in serum phosphate levels are associated with improvements in PROs in adults with X-linked hypophosphatemia. The analyses confirmed the importance of prolonged serum phosphate level correction in adult patients with XLH. These results can be useful to guide the design of further studies and to design treatment optimization strategies.

The Impact of Prescription Time Limits on Phosphate Administration in the Intensive Care Unit: A Before-After Quality Improvement Study.

(1) Background: We aim to examine and improve phosphate prescribing as part of a quality assurance program by examining the change in the proportion of patients receiving phosphate with normal or high preceding serum phosphate concentrations before and after the introduction of the 24 h time limit to default phosphate prescription. (2) Methods: This was a quality assurance study conducted across three Australian adult intensive care units (ICUs). All adult patients with ICU lengths of stay greater than or equal to 48 h who had their serum phosphate concentrations measured were included. A 24 h time limit was introduced to the protocolised prescription in the electronic clinical information system for enteral and intravenous phosphate at participating ICUs. Patient characteristics, phosphate administration, and outcomes were compared before and after this time limit was introduced. The primary outcome was the proportion of patients to whom phosphate was prescribed after measurement of a normal or high serum phosphate level. Secondary outcomes were ICU length of stay, mortality, and discharge destination. (3) Results: A total of 1192 patients were included from three ICUs over the two periods. The proportion of patients with a normal or high measured phosphate level who then received phosphate supplementation was significantly lower in the second study period (30.3% vs. 9.9%; p < 0.001). This difference persisted when adjusted for potential confounders in a mixed-effects logistic regression model (an adjusted odds ratio for receiving phosphate with normal or high serum concentration 0.214, 95% confidence interval of 0.132-0.347; p < 0.001). No significant difference was seen in the typical ICU length of stay, in-hospital case-fatality rate, and hospital discharge destination between these groups. (4) Conclusions: This multicentre before-after study has demonstrated that the introduction of a 24 h limit on electronic phosphate prescriptions resulted in significantly fewer patients receiving phosphate when their serum phosphate concentration was normal or high, without any adverse impact on patient outcomes.

Improved Clinical Outcomes Associated With Hungry Bone Syndrome Following Parathyroidectomy in Dialysis Patients

ObjectiveHungry bone syndrome (HBS) is a common complication after parathyroidectomy in dialysis patients with severe secondary hyperparathyroidism. The rapid decline in parathyroid hormone (PTH) levels diminishes bone resorption and accelerates bone formation. This causes a significant influx of calcium and phosphate into the bone, resulting in severe and prolonged hypocalcemia. While previous studies have established risk factors for HBS, the outcomes beyond the reduced recurrence rate of hyperparathyroidism have been largely unexplored. MethodsThis single-center retrospective study analyzed 322 cases in 314 dialysis patients who underwent parathyroidectomy between 2012 and 2022. The study examined baseline factors associated with HBS, adverse events, and clinical outcomes, including changes in blood pressure and hematologic and nutritional parameters over 3-12 months of follow-up, stratified by HBS status. ResultsTotal parathyroidectomy was performed in 28 cases (8.7%), total parathyroidectomy with implantation in 98 cases (30.4%), and subtotal parathyroidectomy in 196 cases (60.9%). HBS occurred in 207 cases (64%). Independent predictors of HBS included male sex, lower serum calcium levels, higher PTH levels, and lack of active vitamin D treatment at baseline. Patients with HBS had longer hospital stays but did not experience an increase in other adverse events. Following parathyroidectomy, the HBS group showed a greater reduction in blood pressure and more significant increases in hemoglobin, total lymphocyte count, and serum creatinine. This group also saw a more substantial decrease in the proportions of patients with hemoglobin <11 g/dL and serum creatinine/body surface area <380 μmol/L/m2. Although the HBS group showed a more significant decline in PTH levels from baseline, similar proportions achieved the target PTH level by the end of the study. Serum calcium levels remained substantially lower in the HBS group throughout the follow-up, while serum phosphate and PTH levels were comparable. ConclusionHBS was associated with more pronounced improvements in blood pressure, anemia, and nutritional parameters. The presence of HBS could indicate greater achievement in controlling hyperparathyroidism following parathyroidectomy.

Differences of Efficacy Between Tenofovir Alafenamide Fumarate and Tenofovir Disoproxil Fumarate in Pregnant Women with Different Hepatitis B Virus DNA Loads

Abstract Tenofovir alafenamide fumarate (TAF) has been endorsed by guidelines for blockade of mother-to-child transmission of hepatitis B virus (HBV), given that its efficacy and safety are comparable to tenofovir disoproxil fumarate (TDF). However, there is a lack of comparative studies regarding the treatment efficacy in patients with diverse viral loads. This study retrospectively analyzed 96 hepatitis B e antigen (HBeAg)-positive pregnant women with HBV DNA levels ≥2 × 105 IU/mL. Based on viral loads (HBV DNA levels), participants in the TAF and TDF groups were stratified into three subgroups, namely the High-G (titer ≥8 log10 IU/mL), Middle-G (7 log10 IU/mL ≤ titer &lt;8 log10 IU/mL) and Low-G (titer &lt;7 log10 IU/mL) subgroups. The primary endpoint was effectiveness of TAF and TDF in patients with varying viral loads, while secondary endpoints were hepatitis B surface antigen (HBsAg) positivity in infants at 7 -12 months and the safety profile for mothers and children. Compared to baseline levels, median HBV DNA levels in mothers were decreased by 4.51 and 4.09 log10 IU/mL in the TAF and TDF groups (P = 0.04) pre-delivery, respectively. In the High-G subgroup, the titers were significantly lower in the TAF group (P = 0.045), a higher proportion of patients experienced a virus decline of ≥4 log10 IU/mLin the TAF group compared with the TDF group, with rates of 78.26% versus 58% (P = 0.034), respectively. Moreover, the median serum phosphate levels significantly decreased from baseline to pre-delivery in the TDF group (P = 0.04). Finally, infants in both cohorts tested negative for HBsAg at 7-12 months after delivery. Overall, our findings indicated that TAF can be considered the preferred option for treatment of HBeAg-positive pregnant women with HBV DNA levels ≥8 log10 IU/mL.

Is there a relationship between hyperchloremia status and the risk of developing acute kidney injury in pediatric patients with diabetic ketoacidosis?

Diabetic ketoacidosis (DKA) is a life-threatening complication of type 1 diabetes mellitus (T1DM). Prerenal acute kidney injury (AKI) is associated with profound hypovolemia and reduced renal perfusion. Results regarding hyperchloremia-associated AKI in patients with DKA are conflicting; we therefore investigated the potential relationship between hyperchloremia status and the risk of developing AKI. This single-center cohort study included 113 newly diagnosed T1DM patients with DKA admitted to the pediatric intensive care unit. Laboratory parameters, including Na, K, urea, creatinine, and chloride levels, were retrospectively reviewed at the time of presentation and at 12, 24 and 36h. AKI was defined using the eGFR according to the pediatric RIFLE classification criteria. Twenty-two (19.5%) of the 113 patients were in the AKI group. Two-way repeated-measures ANOVA showed significant (P values ≤ 0.01) time interaction effects within the groups based on the eGFR and the serum chloride, hyperchloremia, and phosphate levels. Serum chloride levels did not differ between the groups during the first 12h (p > 0.05) but were significantly greater in the AKI group than in the non-AKI group at 24h and 36h (p < 0.01). The final DKA resolution time was significantly greater in the AKI group than in the non-AKI group [22.2 (9.5) vs. 17.0 (12.0) h, respectively; p = 0.03]. However, the groups had similar lengths of hospital stay [13.0 (8.0) days vs. 12.0 (4.0) days, respectively; p = 0.17].Conclusions: Hyperchloremia may be iatrogenic rather than causative during treatment. This may worsen renal failure and prolong the recovery and treatment time for DKA patients. What is Known? • Acute kidney injury resulting from severe volume depletion is a common occurrence in diabetic ketoacidosis and typically requires significant volume replacement therapy. • In recent years, hyperchloremia has been associated with increased risks of AKI, morbidity, and mortality in some conditions, such as diabetic ketoacidosis. What is New? • The incidence of hyperchloremia increases over time during the treatment of diabetic ketoacidosis. • Hyperchloremia may be an iatrogenic element rather than a cause of acute kidney injury during the treatment of diabetic ketoacidosis.

Description of Pre-Hemodialysis Serum Phosphate in Late-Stage Kidney Disease Patients of Productive Age (15-64 Years) at the Indonesian Christian University General Hospital

In Indonesia, end-stage kidney disease is still a health problem that needs attention. End-stage kidney disease or abbreviated as PGTA reflects the fifth stage of chronic kidney disease, at this stage, there is a buildup of toxins, fluids, electrolytes, and the remains of the body's metabolism. In stage 5 chronic kidney disease, the glomerular filtration rate decreases &lt; 15 ml/minute / 1.73 m2 and has occurred for 3 months or more. One of the clinical complications of end-stage renal disease is an increase in phosphate levels in the patient's blood serum (hyperphosphatemia), this occurs due to disruption of the kidney's phosphate excretion function. Hyperphosphatemia in PGTA patients can result in hyperparathyroidism, soft tissue, and cardiovascular calcification, and affect bone mineral disorders. In kidney disease patients with a glomerular filtration rate &lt; 30 ml/minute / 1.73m2, the prevalence of hyperphosphatemia complications increased to 23%. This study aims to determine the description of pre-hemodialysis inorganic phosphate levels in the serum of PGTA patients of productive age (15-64 years) undergoing hemodialysis at the Indonesian Christian University General Hospital for the period January 2022. The research conducted was a descriptive study, to determine the description of phosphate levels serum of PGTA patients. The data used in this study is primary data by directly taking the blood of 20 pre-hemodialysis patients with end-stage kidney disease and then examining it in the laboratory. In this study, the results showed that 10 PGTA patients (50%) experienced an increase in serum inorganic phosphate levels above normal (&gt;5 mg/dl). Meanwhile, 9 people (45%) had normal serum phosphate levels (2.5 - 5 mg/dl), and 1 other person had below normal serum phosphate levels (&lt;2.5 mg/dl). Keywords: Inorganic Phosphate, Hemodialysis, Hyperphosphatemia, End Stage Renal Disease

Clinical Characteristics and Outcomes of Hyperphosphatemia in Patients with Chronic Kidney Disease Stages 1-2.

There was limited research on the epidemiology of hyperphosphatemia in early-stage chronic kidney disease (CKD) patients. We aimed to explore the clinical characteristics and prognostic value of hyperphosphatemia in patients with CKD stages 1-2. We enrolled adult patients with CKD stages 1-2 from 24 regional central hospitals across China. Hyperphosphatemia was defined as a serum phosphate level exceeding 1.45 mmol/L. The study outcomes included all-cause and cardiovascular (CV) mortality. Cox proportional hazard models were used to investigate the association of hyperphosphatemia with all-cause and CV mortality. Among 99,266 patients with CKD stages 1-2 across China, the prevalence of hyperphosphatemia was 8.3%. The prevalence of hyperphosphatemia was increased with the level of urinary protein and was higher in younger and female patients. Among 63,121 patients with survival information, during a median of 5.2 years follow-up period, there were 436 (8.0%) and 4,695 (8.1%) deaths in those with and without hyperphosphatemia, respectively. After adjusting for potential confounders, compared with patients without hyperphosphatemia, patients with hyperphosphatemia were associated with a higher risk of all-cause mortality (hazard ratio: 1.28, 95% CI: 1.16-1.41). Although nearly 60.3% of hyperphosphatemia could be relieved without phosphate-lowering drug therapy among patients with CKD stages 1-2, transient hyperphosphatemia was also associated with an increased risk of all-cause mortality (p = 0.048). Hyperphosphatemia was not rare in patients with CKD stages 1-2 and was associated with an increased risk of mortality. Clinicians should closely monitor serum phosphorus levels in patients with CKD, even in those with normal kidney function.

Beneficial Effects of Ketoanalogues on the Evolution of Renal Function and Bone Mineral Disorders in Patients with Advanced Chronic Kidney Disease: A Pilot Study.

The supplementation with Ketoanalogues in patients on very low-protein diets has shown a favorable effect on the evolution of renal function. The aim of the present study was to evaluate the progression of renal function in advanced chronic kidney disease patients on a low-protein diet (&lt;0.8 g/kg/d) with or without additional Ketoanalogues. The primary criterion is the evolution of the renal function at 6, 12, and 24 months for the two groups. The secondary criteria comprise the evolution of the body weight, mean blood pressure, 24-h proteinuria, salt and protein consumption, energy consumption, hemoglobin levels, serum albumin, prealbumin, C-reactive protein, liver function tests, serum electrolyte and phosphate levels, parathormone as well as calcium levels at the same time periods. There was a significant nephroprotective effect of the Ketoanalogues after 12 and 24 months with no differences in the protein consumption between the two groups. Mean blood pressure, hemoglobin levels, 24-hour proteinuria, serum electrolyte, liver function tests, salt and protein consumption, and serum albumin and prealbumin did not present any significant differences. Serum bicarbonate and calcium levels were higher while serum phosphate and parathormone levels were lower in the Ketoanalogue group at all follow-up time points. During the 24-month follow-up period, 4 patients from the Ketoanalogue group and 8 patients from the control group quit the study. A low-protein diet supplemented with Ketoanalogues exerts significant nephroprotective effects and better bone mineral metabolism parameters compared to a low-protein diet only.

A meta-analysis of the impact of a phosphate-specific diet on serum phosphate levels in people receiving hemodialysis

&lt;p class="MsoNormal"&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi; background: white;"&gt;Background &lt;/span&gt;&lt;/p&gt; &lt;p class="MsoNormal" style="mso-layout-grid-align: none;"&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi; background: white;"&gt;We performed a meta-analysis to &lt;/span&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi;"&gt;evaluate the influence of a phosphate-specific intake on serum phosphate levels in hemodialysis subjects.&lt;/span&gt;&lt;/p&gt; &lt;p class="MsoNormal"&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi;"&gt;Methods&lt;/span&gt;&lt;/p&gt; &lt;p class="MsoNormal"&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi;"&gt;A systematic literature search up to November 2021 was done and 14 studies included 1284 hemodialysis subjects at the start of the study; 671 of them were provided with phosphate-specific intake, and 613 were control. We calculated the mean difference (MD) with 95% confidence intervals (CIs) to evaluate the influence of phosphate-specific intake on serum phosphate levels in hemodialysis subjects by the contentious method with a random or fixed-influence model. &lt;/span&gt;&lt;/p&gt; &lt;p class="MsoNormal"&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-fareast-font-family: Calibri; mso-fareast-theme-font: minor-latin; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi;"&gt;Results&lt;/span&gt;&lt;/p&gt; &lt;p class="MsoNormal"&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi;"&gt;Phosphate-specific intake &lt;/span&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-fareast-font-family: Calibri; mso-fareast-theme-font: minor-latin; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi;"&gt;had significantly better &lt;/span&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi;"&gt;serum phosphate levels change (MD, -0.66; 95% CI, -0.95- -0.36, p&amp;lt;0.001) with moderate heterogeneity (I&lt;sup&gt;2&lt;/sup&gt; = 71%) compared to control in hemodialysis subjects&lt;/span&gt;&lt;/p&gt; &lt;p class="MsoNormal"&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi;"&gt;Conclusions&lt;/span&gt;&lt;/p&gt; &lt;p class="MsoNormal"&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi;"&gt;Phosphate-specific intake &lt;/span&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-fareast-font-family: Calibri; mso-fareast-theme-font: minor-latin; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi;"&gt;had significantly lower &lt;/span&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi;"&gt;serum phosphate levels change compared to control in hemodialysis subjects. Further studies are required.&lt;/span&gt;&lt;/p&gt;

The association between serum phosphate and length of hospital stay and all-cause mortality in adult patients: a cross-sectional study

BackgroundData is limited on the prevalence of hypophosphatemia in general hospitalized patients, and its association with length of hospital stay (LOS) and mortality remained unclear. We aimed to investigate the prevalence of admission phosphate abnormality and the association between serum phosphate level and length of hospital stay and all-cause mortality in adult patients.MethodsThis was a multi-center retrospective study based on real-world data. Participants were classified into five groups according to serum phosphate level (inorganic phosphorus, iP) within 48 h after admission: G1, iP < 0.64 mmol/L; G2, iP 0.64–0.8 mmol/L; G3, iP 0.8–1.16 mmol/L; G4, iP 1.16–1.45 mmol/L; and G5, iP ≥ 1.45 mmol/L, respectively. Both LOS and in-hospital mortality were considered as outcomes. Clinical information, including age, sex, primary diagnosis, co-morbidity, and phosphate-metabolism related parameters, were also abstracted from medical records.ResultsA total number of 23,479 adult patients (14,073 males and 9,406 females, aged 57.7 ± 16.8 y) were included in the study. The prevalence of hypophosphatemia was 4.74%. An “L-shaped” non-linear association was determined between serum phosphate level and LOS and the inflection point was 1.16 mmol/L in serum phosphate level. Compared with patients in G4, patients in G1, G2 or G3 were significantly associated with longer LOS after full adjustment of covariates. Each 0.1 mmol/L decrease in serum phosphate level to the left side of the inflection point led to 0.64 days increase in LOS [95% confidence interval (CI): 0.46, 0.81; p for trend < 0.001]. But there was no association between serum phosphate and LOS where serum levels of phosphate ≥ 1.16 mmol/L. Multivariable logistic regression analysis showed that adjusted all-cause in-hospital mortality was 3.08-fold greater in patients in G1 than those in G4 (95% CI: 1.52, 6.25; p for trend = 0.001). Similarly, no significant association with either LOS or mortality were found in patients in G5, comparing with G4.ConclusionsHypophosphatemia, but not hyperphosphatemia, was associated with LOS and all-cause mortality in adult inpatients. It is meaningful to monitor serum levels of phosphate to facilitate early diagnosis and intervention.

Comparing early and delayed [99mTc]Tc-MIBI SPECT/CT parathyroid scans: agreement, confidence levels, and clinical predictive factors

BackgroundParathyroid scan is an important imaging modality for localizing hyperfunctioning parathyroid tissue in patients with hyperparathyroidism. Unfortunately, whether early or delayed timing is the optimal protocol for [99mTc]Tc-MIBI SPECT/CT parathyroid remains under debate. This study aimed to evaluate the agreement and compare the confidence levels of physicians when interpreting early and delayed [99mTc]Tc-MIBI SPECT/CT parathyroid scans. Additionally, it sought to identify clinical factors that related to positive scan result. We conducted a prospective study where the early and delayed [99mTc]Tc-MIBI SPECT/CT was separately interpreted as either positive or negative. Furthermore, these interpretations were categorized based on whether they fell within more or less confidence levels of the readers and were correlated with clinical information.ResultsWe enrolled 39 patients with hyperparathyroidism with 158 possible locations of parathyroid glands. The per-location agreement between the early and delayed scans was moderate (concordant rate: 80.3%, Kappa = 0.558), and the per-patient agreement was slight (concordant rate: 71.8%, Kappa = 0.093). The confidence of interpretation was significantly higher for the delayed scans. Calcium supplementation, low serum parathyroid hormone levels, and low serum phosphate levels were associated with positive early scans. High calcium level and high parathyroid hormone levels were associated with positive delayed scans.ConclusionsOur study highlights the impact of the timing of SPECT/CT in [99mTc]Tc-MIBI parathyroid scans. The different confidence levels between early and delayed scans, along with clinical factors, imply that various factors affect parathyroid scan interpretation, and individualized scanning protocols adjusted for specific settings may be needed to optimize the successful localization of hyperfunctioning parathyroid tissue.

Correlation of Parathyroid Hormone Values With Lung Function Parameters in Patients With Chronic Obstructive Pulmonary Disease.

The aim of this study was to determine the disturbances in the concentration of parathyroid hormone (PTH) and 25-hydroxyvitamin D (vitamin D) in patients with stable chronic obstructive pulmonary disease (COPD)and its correlation with airflow obstruction. A prospective study included 200 patients with a confirmed diagnosis of COPD in the Department of Lung Diseases and Tuberculosisand Pulmonology Polyclinic of University Clinical Hospital Mostar in the period of three years, between May 2021 and May 2024. Inclusion criteria were a stable phase of COPD, hemodynamically stable patients older than 40 years, forced vital capacities in the first second (FEV1)/forced vital capacities (FVC)<0.7, and patients with PTH, vitamin D, calcium, and phosphate measurements. Exclusion criteria wereacute exacerbation of COPD in the last month; current treatment with nutritional supplements, vitamins, and statins; lack of availability of lung function data; use of systemic corticosteroids in the previous three months; chronic renal insufficiency, respiratory diseases other than COPD (asthma, pneumonia, tuberculosis, and bronchiectasis), and other diseases (cancerand parathyroid disease). Medical records about demographic data (age and gender), pulmonary function test (FVC, FEV1, FEV1%FVC, mean expiratory flow (MEF)50), body mass index (BMI), COPD assessment test (CAT), Modified Medical Research Council(mMRC) Dyspnea Scale, and serum PTH, vitamin D, calcium, and phosphate levels were obtained. Patients with higher COPD stagehad lower spirometry values,most significantly MEF50. The higher the COPD group (Global Initiative for Chronic Obstructive Lung Disease (GOLD) D), the lower vitamin D ​​and the higher PTH levels were. Calcium and phosphate values ​​were the same for all groups. Vitamin D and PTH levels significantly ​​correlated with MEF50 values. The lower MEF50 level, the higher PTH levels, ​​and lower vitamin D levels were found (P<0.05). Our study showed that the patients in the higher COPD group have lower vitamin D levels ​​and higher PTH levels, indicating that they developed secondary hyperparathyroidism. The levels of vitamin D and PTH correlated the most with MEF50 values while other spirometry parameters did not significantly correlate with vitamin D and PTH levels.

Serum phosphate levels at diagnosis predict long-term risk for hypopituitarism in patients with acromegaly.

Excess growth hormone (GH) secretion in acromegaly has a major impact on mineral balance and serum phosphate levels. However, the clinical utilization of serum phosphate levels as a marker for long-term disease outcomes in acromegaly has not been evaluated. This is a retrospective study of patients with acromegaly who were followed in a tertiary center. Data were retrieved on patient characteristics, endocrine and biochemical evaluation, and tumor parameters. Comparisons were performed by measuring baseline phosphate levels and conductingcorrelation analysis and multivariable logistic regression. Sixty-one patients were followed for 4.5years (range 1-21). Patients with hyperphosphatemia (> 4.5mg/dl) at baseline had larger adenomas (15.0mm [8.0, 47.0] vs. 10.0mm [3.0, 24.0], p = 0.001), a rate chance of invasive adenoma (16 [80.0%] vs. 14 [46.7%], p = 0.02), and lower serum cortisol levels (226.0nmol/l [27.6, 516.0] vs. 294.0nmol/l [32.0, 610.0], p = 0.02). Baseline serum phosphate levels positively correlated with IGF-1 levels (r = 0.43, p = 0.003) and negatively correlated with morning plasma cortisol levels (r = -0.46, p = 0.002). Regarding long-term impact, baseline phosphate levels correlated with the number of pituitary axes involved 6months after diagnosis (r-0.34, p = 0.01). In multivariable analysis, baseline plasma phosphate levels were independently associated with risk for disease progression/recurrence (odds ratio [OR] 9.66, 95% confidence interval [CI] 1.5, 105.9, p = 0.03) and for invasive adenoma (OR 6.21, 95% CI 1.6, 28.7, p = 0.01). Elevated pretreatment serum phosphate levels are associated with a greater risk of disease persistence and recurrence and with altered pituitary function in patients with acromegaly.

Differential Serum Phosphate Levels in Pediatric Febrile Syndromes and Their Clinical Significance.

The potential of hypophosphatemia (HP) to differentiate between febrile syndromes and its clinical significance in children without sepsis were not previously described. Data were retrospectively collected of febrile children aged 3 months to 18 years, hospitalized at general pediatric wards during 2010-2019. Phosphate levels were compared between bacterial infection (BI), viral infection (VI), and Kawasaki disease (KD). Regression analyses were used to evaluate the relationship between HP and outcome. Of 3963 febrile children, 559 had BI, 3271 had VI, and 133 had KD. In BI compared to VI and KD, HP was more prevalent (49.2%, 19.7%, and 31.6%, respectively; P<0.001) and more severe [median (interquartile range) phosphate standard deviation score: -1.85 (2.08), -0.56 (2.08), and -1.20 (2.28), respectively; P<0.001]. In the BI group, Pi-SDS level was lower among patients with than without bacteremia (-2.33 ± 1.8 vs. -0.79 ± 1.68; P<0.001). Phosphate levels displayed discriminatory potential between bacterial and viral etiologies, with an area under the curve of 0.719 (95% CI, 0.697-0.742). Minimal phosphate standard deviation score values had a negative weak correlation with the maximal C-reactive protein levels and white blood cell count. Univariate and multivariate analyses showed an association of HP with a more severe disease course, manifested by longer hospital stay [+2.10 (95% CI, 0.75-3.46) days; P=0.003] and a higher rate of intensive care unit admission [odds ratio, 2.63 (95% CI, 1.94-3.56); P<0.001). Hypophosphatemia rates were highest in bacterial etiology, intermediate in KD, and lowest in viral etiology and were associated with poorer outcomes. Phosphate level may serve as a marker for ruling out a bacterial etiology.

The Effect of Periodontitis on Fibroblast Growth Factor 23 Levels in Predialysis Chronic Kidney Disease Patients.

Introduction Chronic kidney disease (CKD) is known to cause an increase in fibroblast growth factor 23 (FGF23). Periodontitis, a condition recognized as a risk factor for CKD, is also potentially associated with the increment of FGF23. This study aims to compare FGF23 levels in CKD patients with and without periodontitisand non-CKDpatients with and without periodontitis. Correlation with serum phosphate, calcium, and intact parathyroid hormone (iPTH) was assessed. Additionally, associations between FGF23, calcium, phosphate, iPTH, creatinine, urea, plaque score, and bleeding score with periodontitis in CKD patients were determined. Method A total of 124 participants were categorized into four groups: CKD patients with periodontitis (n=31), CKD patients without periodontitis (n=32), periodontitis patients without CKD (n=32), and healthy population (n=29). The selected CKD patients include those from stages 3 and 4 (predialysis) patients. Serum levels of FGF23, calcium, phosphate, iPTH, creatinine, and urea were analyzed. Oral examinations were conducted to determine the presence and absence of periodontitis and assess plaque and bleeding scores. Result A significantly higher level of FGF23 was found in CKD compared to non-CKD groups; however, no difference was observed with the presence of periodontitis in both CKD and non-CKD. There was no significant correlation found between FGF23 and serum calcium, phosphate, or iPTH concerning periodontal status. Apart from the bleeding score, there was no association between FGF23, calcium, phosphate, iPTH, creatinine, urea, and plaque score with the presence of periodontitis in CKD patients. Conclusion The presence of periodontitis was not associated with higher FGF23 levels in CKD patients. Changes in FGF23, calcium, phosphate, iPTH, creatinine, urea, and plaque score could not be attributed to the presence of periodontitis in CKD patients.

Impact of Calcium Phosphate Product on Acute Kidney Injury and Mortality: A Retrospective Cohort Study.

This study aims to assess the association between admission-corrected serum calcium phosphate (CaPO4) levels and the risks of in-hospital acute kidney injury (AKI) and mortality, hypothesizing a dose-dependent relationship between serum CaPO4 concentrations and the likelihood of developing AKI. This large retrospective cohort study analyzed hospitalized adult patients who had serum calcium, phosphate, and albumin levels measured within 24 hours of admission between January 2014 and December 2018. Piecewise regression was employed to identify the optimal CaPO4 cutoff values for predicting in-hospital AKI and mortality. Subsequently, the odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to assess the risks of in-hospital AKI and mortality associated with these cutoff values. A total of 2,116 patients were included in the study. The incidence rates of AKI for patients with CaPO4 levels ≤27 and >27 mg2/dL2 were 9.6% and 10.9%, respectively. The bilinear association pattern revealed the lowest risk of AKI at a CaPO4 level of 27 mg2/dL2. Piecewise regression analysis showed that each 1 mg2/dL2 increase in CaPO4 level above the 27 mg2/dL2 cutoff was associated with increased risks of in-hospital AKI and mortality, with OR of 1.048 (95% CI: 1.030-1.065) and 1.048 (95% CI: 1.032-1.065), respectively. Our findings indicate a critical relationship between elevated serum CaPO4 levels and increased risks of in-hospital AKI and mortality, with a notable cutoff at CaPO4 >27 mg2/dL2.