Higher Serum Phosphate Levels Research Articles

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.

Phosphate level predicts mortality in acute kidney injury patients undergoing continuous kidney replacement therapy and has a U-shaped association with mortality in patients with high disease severity: a multicenter retrospective study.

This study investigated the association between serum phosphate level and mortality in acute kidney injury (AKI) patients undergoing continuous kidney replacement therapy (CKRT) and evaluated whether this association differed according to disease severity. Data from eight tertiary hospitals in Korea were retrospectively analyzed. The patients were classified into four groups (low, normal, high, and very high) based on their serum phosphate level at baseline. The association between serum phosphate level and mortality was then analyzed, with further subgroup analysis being conducted according to disease severity. Among the 3,290 patients identified, 166, 955, 1,307, and 862 were in the low, normal, high, and very high phosphate groups, respectively. The 90-day mortality rate was 63.9% and was highest in the very high group (76.3%). Both the high and very high groups showed a significantly higher 90-day mortality rate than did the normal phosphate group (high: hazard ratio [HR], 1.35, 95% confidence interval [CI], 1.21-1.51, p < 0.001; very high: HR, 2.01, 95% CI, 1.78-2.27, p < 0.001). The low group also exhibited a higher 90-day mortality rate than did the normal group among those with high disease severity (HR, 1.47; 95% CI, 1.09-1.99; p = 0.01) but not among those with low disease severity. High serum phosphate level predicted increased mortality in AKI patients undergoing CKRT, and low phosphate level was associated with increased mortality in patients with high disease severity. Therefore, serum phosphate levels should be carefully considered in critically ill patients with AKI.

Renal hyperparathyroidism- a risk factor in the development of encapsulating peritoneal sclerosis.

Encapsulating peritoneal sclerosis (EPS) is a rare complication of prolonged peritoneal dialysis (PD) exposure, characterised by peritoneal thickening, calcification, and fibrosis ultimately presenting with life-threatening bowel obstruction. The presence or role of peritoneal calcification in the pathogenesis of EPS is poorly characterised. We hypothesise that significantly aberrant bone mineral metabolism in patients on PD can cause peritoneal calcification which may trigger the development of EPS. We compared the temporal evolution of bone mineral markers during PD in EPS patients with non-EPS long-term PD controls. Linear mixed model and logistic regression analysis were used to compare four-monthly serum levels of calcium, phosphate, parathyroid hormone, and alkaline phosphatase (ALP) over the duration of PD exposure in 46 EPS and 46 controls (PD, non-EPS) patients. EPS patients had higher mean calcium (2.51 vs. 2.41 mmol/L) and ALP (248.00 vs. 111.13 IU/L) levels compared with controls (p=0.01 and p<0.001 respectively, maximum likelihood estimation). Logistic regression analysis demonstrated that high serum calcium and phosphate levels during PD were associated with a 4.5 and 2.9 fold increase in the risk of developing EPS respectively. High levels of calcium and phosphate in patients on PD were identified to be risk factors for EPS development. Possible reasons for this may be an imbalance of pro-calcifying factors and calcification inhibitors promoting peritoneal calcification which increases peritoneal stiffness. Mechanical alterations may trigger, unregulated fibrosis and subsequent development of EPS. Improved management of secondary hyperparathyroidism during PD may ultimately diminish the EPS risk.

Diagnostic pitfalls and therapeutic challenges of hypercalcaemia in chronic kidney disease: a case report and a narrative review

BackgroundEvaluation of hypercalcaemia in a patient with chronic kidney disease (CKD) is challenging, especially in low-resource settings. Hormone assays should be interpreted with caution as CKD affects both parathyroid hormone (PTH) and vitamin D. Therapies such as bisphosphonates are contraindicated in CKD, while fluid resuscitation can lead to volume overload. We report the diagnostic workup of a patient with stage V CKD who presented with symptomatic hypercalcaemia and discuss the diagnostic pitfalls and therapeutic challenges.Case presentationA 72-year-old Sri Lankan woman with stage V, non-oliguric CKD presented with a 2-week history of worsening lassitude, increased thirst and constipation. She was clinically euvolemic and did not have signs of uraemia. Bilateral lung fields had occasional coarse crepitations. The rest of the physical examination was normal. Her serum creatinine level was similar to her baseline (4.7 mg/dl, eGFR 9 ml/min). She was found to have a high serum calcium (14.3 mg/dl) and phosphate (5.0 mg/dl) levels. Her PTH level was 24.1 pg/ml (15–68), and she was deficient in 25-hydroxycholecalciferol (9 mg/ml (30–100)). She was not on calcium or vitamin D supplementation. Disseminated tuberculosis was diagnosed after detecting granulomata in the lungs and abdomen in the contrast-enhanced computed tomography (CECT) and mycobacterial DNA in sputum. She was hydrated with 0.9% NaCl with meticulous use of frusemide. The effect of frusemide waned off by the 10th day, requiring haemodialysis to control the hypercalcaemia. Vitamin D was replaced intramuscularly with 200,000 IU, after which the calcium levels increased. She was treated with IV pamidronate 30 mg, and the calcium levels started reducing drastically. Antituberculous therapy (ATT) was initiated 7 days after pamidronate treatment. The calcium levels normalised 2 days after ATT and sustained beyond 2 months.ConclusionInterpretation of PTH and phosphate levels should be done with caution when evaluating hypercalcaemia in patients with advanced chronic kidney disease. First- and second-generation assays detect PTH fragments which accumulate in CKD, leading to false positives. Hypophosphataemic effects of PTH/PTHrP can be masked by accumulation of phosphate in CKD. Bisphosphonates might have a role in treating calcitriol-induced hypercalcaemia, although this needs further evaluation.

Assessing the predictive value of serum phosphate for short-term mortality in acute-on-chronic liver failure patients: An observational study at a non-transplant tertiary care centre.

The gradual clinical worsening of acute-on-chronic liver failure (ACLF) leads to a high 28-day mortality rate. There are several prognostication scores for predicting early mortality in ACLF. Serum phosphate, which is the main component of adenosine tri-phosphate (ATP) synthesis, is utilized for liver synthetic functions, leading to subnormal or decreased serum phosphate levels. Hence more than normal levels of serum phosphate can be used as a marker of decreased liver cell reserve. Hence, we aimed to compare serum phosphate levels with available prognostic scores to assess mortality among ACLF patients. 100 consecutive ACLF patients according to the Asia Pacific Association for Study of the Liver (APASL) definition were studied. The baseline blood workups and determination of viral bio-markers, serum phosphate, and lactate levels on days 1, 3, and 7 were carried out and prospectively followed up, and the baseline serum phosphate levels were compared with the usual scores to predict the 28-day mortality. CLIF-SOFA (accuracy 76-91%) followed by CLIF-C score (accuracy 73-84%) and AARC score (accuracy 70-85%) had the statistically significantly highest accuracy as compared with CTP, MELD, and MELD-Na on all three days. Serum phosphate values (accuracy 69-86%) on all three days were not better than the CLIF-SOFA score but better than all other prognostic scores on days 3 and 7. The high serum phosphate levels on day 3 with a value of more than 6.4 mg/dl showed almost comparable accuracy with CLIF-SOFA for screening short-term mortality. Hence serum phosphate measurement can be used as a simple bedside laboratory investigation to predict mortality in ACLF patients and early interventions in low-resource settings.

Higher serum phosphate within the normal range is associated with the development of calcified aortic valve disease.

Despite the essential role of ectopic osteogenic calcium-phosphate metabolism in the development of calcific aortic valve disease (CAVD), the implications of high serum phosphate levels in CAVD development are not fully understood. Asymptomatic individuals who underwent health screening using serial cardiac computed tomography (CT) and echocardiography were selected from a multicenter registry. CAVD was identified and quantified on CT images using the aortic valve calcification (AVC) score. The associations between initial serum phosphate levels and the presence of baseline CAVD, development of new CAVD, and the AVC score progression rate were investigated using multivariable regression models. A total of 736 individuals were selected for analysis, and the median interscan duration was 36.4 months. On initial CT, 83 (13.7%) participants had baseline CAVD, while 52 (7.0%) individuals developed new CAVD during follow-up. Serum phosphate levels were not associated with a higher probability of baseline CAVD but were predictive of newly developed CAVD (odds ratio per 1 mg/dl, 1.05; 95% confidence interval, 1.01-1.10; p = 0.02). Higher phosphate levels were also associated with a faster AVC score progression in those with baseline CAVD (regression coefficient per 1 mg/dl, 15.55 Agatston units/year; 95% confidence interval, 6.02-25.07; p < 0.01), an association which remained significant when the analysis was extended to include newly developed CAVD. Even slight elevations in serum phosphate are associated with accelerated CAVD progression from an early stage. Further studies are needed to investigate whether the regulation of phosphate metabolism can slow the progression of CAVD to aortic stenosis.

Prognostic value of serum phosphate levels in sepsis: a systematic review and meta-analysis.

There remain controversies over the conclusion of different serum phosphate levels as prognostic predictors of sepsis patients. As such, this study investigated the association between different serum phosphate and the prognosis of sepsis. Data from PubMed, Embase, Cochrane Library, and Web of Science were systematically retrieved from the inception of databases to June 1, 2023 and independently screened and extracted by two authors. Binary variables in the study were estimated as relative risk ratio (RR) and 95% confidence interval (CI), and continuous variables were estimated as mean and standard deviation. The Newcastle-Ottawa Scale (NOS) was employed to evaluate the quality of the included studies, and subgroup analysis and sensitivity analysis were performed for all outcomes to explore the sources of heterogeneity. Ten studies were included in this study including 38,320 patients with sepsis or septic shock. Against normal serum phosphate levels, a high serum phosphate level was associated with an elevated all-cause mortality risk (RR = 1.46; 95% CI [1.22-1.74]; P = 0.000) and prolonged Intensive Care Unit (ICU) length of stay (LOS) (WMD = 0.63; 95% CI [0.27-0.98]; P = 0.001). However, there was no significant difference in the in-hospital LOS (WMD = 0.22; 95% CI [-0.61-1.05]; P = 0.609). A low serum phosphate level was not significantly associated with the all-cause mortality risk (RR = 0.97; 95% CI [0.86-1.09]; P = 0.588), ICU LOS (WMD = -0.23; 95% CI [-0.75-0.29]; P = 0.394) and in-hospital LOS (WMD = -0.62; 95% CI [-1.72-0.49]; P = 0.274). Sepsis patients with high serum phosphate levels before therapeutic interventions were associated with a significant increase in the all-cause mortality risk, prolonged ICU LOS, and no significant difference in in-hospital LOS. Sepsis patients with low serum phosphate levels before interventions may have a reduced risk of all-cause mortality, shorter ICU LOS, and in-hospital LOS, but the results were not statistically significant.

Association between serum phosphate and in-hospital mortality of patients with AECOPD: A retrospective analysis on eICU database

Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is an important adverse event in the development of chronic obstructive pulmonary disease (COPD). Hyperphosphatemia is associated with higher mortality in patients with multiple diseases. In this study, we aimed to determine the relationship between serum phosphate and the risk of in-hospital mortality in patients with AECOPD. Methods: In the present study, patients with AECOPD were enrolled in the electronic Intensive Care Unit Collaborative Research Database (eICU-CRD), and divided into three groups according to the tertiles of serum phosphate level. The primary outcome measure was all-cause in-hospital mortality. The association between serum phosphate level and in-hospital mortality was investigated using multivariate logistic regression analysis. Moreover, subgroup analysis was performed to explore whether the relationship was consistent among different subgroups. Results: A total of 1199 AECOPD patients were included in this study. Non-survivors had higher serum phosphate levels than survivors. All patients were classified into lowest tertile, median tertile, and highest tertile, respectively. Multivariate logistic regression analysis indicated that serum phosphate was positively associated with in-hospital mortality after adjusting for confounders. Moreover, there was a significant trend across tertiles when serum phosphate level was diverted as a categorical variable. In addition, subgroup analysis demonstrated that serum phosphate was consistently associated with a higher risk of in-hospital mortality in different subgroups. Conclusion: Higher serum phosphate was positively associated with the increased in-hospital mortality in patients with AECOPD. Hyperphosphatemia may be an underlying high-risk factor for in-hospital mortality owing to AECOPD.

Association between serum phosphate levels and anemia in non-dialysis patients with chronic kidney disease: a retrospective cross-sectional study from the Fuji City CKD Network

BackgroundPatients with chronic kidney disease (CKD) present high mortality and morbidity rates despite the availability of various therapies. Although CKD-mineral and bone disorder (MBD) and renal anemia are important factors in patients with CKD, only few studies have analyzed the relationship between them. Therefore, this study aimed to evaluate the relationship between CKD-MBD and anemia in patients with CKD who did not receive erythropoiesis-stimulating agent or iron therapies.MethodsThis retrospective cross-sectional study included patients with CKD aged ≥ 20 years with estimated glomerular filtration rate (eGFR) categories G2a to G5 who were referred to the Fuji City General Hospital between April 2018 and July 2019. The exclusion criterion was ongoing treatment for CKD-MBD and/or anemia.ResultsThe data of 300 patients with CKD were analyzed in this study. The median age of patients was 71 (range, 56.5–79) years. The median eGFR was 34 (range, 20–48) mL/min/1.73 m2, and the mean hemoglobin (Hb) level was 12.7 g/dL (standard deviation, 2.3), which decreased as the CKD stage increased. In a multivariate linear regression analysis of anemia-related factors, including age, renal function (eGFR), nutritional status, inflammation, and iron dynamics (serum iron level, total iron-binding capacity, ferritin levels), the serum phosphate levels were significantly associated with the Hb levels (coefficient [95% confidence interval], -0.73 [-1.1, -0.35]; P < 0.001). Subgroup analysis revealed a robust association between serum phosphate levels and Hb levels in the low-ferritin (coefficient [95% confidence interval], -0.94 [-1.53, -0.35]; P = 0.002) and advanced CKD groups (coefficient [95% confidence interval], -0.89 [-1.37, -0.41]; P < 0.001).ConclusionsWe found an association between high serum phosphate levels and low Hb levels in patients with CKD not receiving treatment for anemia. These results underscore the possibility of a mechanistic overlap between CKD-MBD and anemia.

#5566 DIETARY MAGNESIUM SUPPLEMENTATION REDUCES RENAL AND CARDIAC FIBROSIS IN AN EXPERIMENTAL MODEL OF TYPE 4 CARDIORENAL SYNDROME

Abstract Background and Aims In chronic kidney disease (CKD) patients, high serum phosphate (HP) levels are associated with the development of a cardiorenal renal syndrome type 4 (CRS4). In this syndrome, the heart is damaged by oxidative stress, inflammation, and fibrosis in renal tissue. In this study we have evaluated if dietary Mg supplementation could reduce CRS4. Method The in vivo studies were performed in 5/6Nx rats fed a high (0.9%) phosphate diet with high or low dietary content of Mg to evaluate: 1) The effect of dietary Mg supplementation (0.3%) on oxidative stress, inflammation and fibrosis of kidney and heart. 2) The contribution of hypomagnesemia (using a low Mg diet (0,03%) to the progression of CRS4 in Nx rats and normal rats as controls. 3) Whether dietary Mg supplementation (8 weeks) reduces renal and cardiac fibrosis in Nx rats with established CRS4. In vitro, we evaluated the effects of Mg (Mg2Cl) on mesangial and tubular cells and also cardiomyocytes cells expose to TGF-β. Results Dietary Mg supplementation (0,3%) improved renal function, decreased oxidative stress, FGF23 levels, hypertension, renal and cardiac fibrosis and recovered renal expression of Klotho. A low Mg diet increased FGF23 and renal fibrosis but a subsequent switch to dietary Mg supplementation did not significantly improve CRS4 parameters although it reduced the values of blood pressure. In HK2 and rat mesangial cells treated with TGFβ (100 ng/ml), high Mg levels (1,4- and 2,8-times basal levels in the medium) reduced the amount of pro-fibrotic proteins such as α-smooth muscle actin, fibronectin, or renin, recovering Klotho expression and decreasing Smad3 phosphorylation. Conclusion Dietary Mg supplementation is a useful tool to improve renal function and prevent CRS4, by reduction the progression of renal and cardiac fibrosis.

Prevalence and characteristics of paediatric X-linked hypophosphataemia in Australia and New Zealand: Results from the Australian and the New Zealand Paediatric Surveillance Units survey

BackgroundX-linked hypophosphataemia (XLH) is the most common heritable form of rickets. Prevalence data varies across the literature between 1 in 20,000 and 1 in 200,000 per population. MethodsAustralian and New Zealand Paediatric Surveillance Units collected cross-sectional data from paediatricians on existing cases to estimate prevalence and characteristics of paediatric XLH in Australia and New Zealand. ResultsSeventy-five cases in Australia and 18 cases in New Zealand were identified. Estimated minimum prevalence based on these cases was 1.33 (1.04–1.66) per 100,000 and 1.60 per 100,000 (95%CI 0.97–2.58) in Australia and New Zealand respectively, with actual prevalence likely higher due to incomplete ascertainment. Despite a family history in most cases, delayed diagnosis was common, with 49 % diagnosed after 2 years of age. Delayed diagnosis was more common in sporadic versus familial cases. Most common clinical characteristics included leg bowing (89 %), bone and joint pain (68 %), abnormal gait (57 %) and short stature (49 %). There was a significant burden of orthopaedic disease and surgeries and a high rate of complications of nephrocalcinosis and hyperparathyroidism (32 % and 20 % respectively). Additionally, while guidelines stress the importance of multidisciplinary care, many did not have access to recommended health professionals, with only 3 % seeing a psychologist and 68 % seeing a dentist. This is despite the high psychological burden of XLH and a significant proportion (41 %) of this cohort having dental issues (tooth abscess, dental capping, tooth extraction).There were two cases from NZ without data available. Of the 91 cases with data collected, 46 % were on burosumab therapy. Consistent with clinical trials, those on burosumab had a higher serum phosphate levels (p < 0.001) at most recent follow-up. Three cases reported cancellation of orthopaedic surgery due to improvement in lower limb deformity after commencement of burosumab. ConclusionThese data describe the multisystem burden of disease for children with XLH with care impacted by delayed diagnosis and a lack of access to many health professionals, especially psychological support.

Variability of Serum Phosphate in Incident Hemodialysis Patients: Association with All-Cause Mortality.

Key Points An increase in serum phosphate variability is an independent risk factor of mortality.The effects of a positive directional range (DR) is most pronounced in patients with high serum phosphate levels whereas the effects of a negative DR is most pronounced in patients with low serum phosphate and/or serum albumin. Background In maintenance hemodialysis (HD) patients, previous studies have shown that serum phosphate levels have a bidirectional relation to outcome. Less is known about the relation between temporal dynamics of serum phosphate in relation to outcome. We aimed to further explore the relation between serum phosphate variability and all-cause mortality. Methods All adult incident HD patients treated in US Fresenius Kidney Care clinics between January 2010 and October 2018 were included. Baseline period was defined as 6 months after initiation of HD and months 7–18 as follow-up period. All-cause mortality was recorded during the follow-up period. The primary metric of variability used was directional range (DR) that is the difference between the largest and smallest values within a time period; DR was positive when the smallest value preceded the largest and negative otherwise. Cox proportional hazards models with spline terms were applied to explore the association between phosphate, DR, and all-cause mortality. In addition, tensor product smoothing splines were computed to further elucidate the interactions of phosphate, DR, and all-cause mortality. Results We included 302,613 patients. Baseline phosphate was 5.1±1.2 mg/dl, and mean DR was +0.6±3.3 mg/dl. Across different levels of phosphate, higher levels of DR of phosphate were associated with higher risk of all-cause mortality. In patients with lower levels of phosphate and serum albumin, the effect of a negative DR was most pronounced, whereas in patients with higher phosphate levels, a positive DR was related to increased mortality. Conclusions Higher variability of serum phosphate is related to mortality at all levels of phosphate, especially in lower levels with a negative DR and in low serum albumin levels. This could possibly reflect dietary intake in patients who are already inflamed or malnourished, where a further reduction in serum phosphate should prompt for nutritional evaluation.

Role of the gut microbiota and their metabolites in hemodialysis patients.

High serum phosphate levels in chronic kidney disease (CKD) are linked to adverse health outcomes, including cardiovascular disease, kidney disease progression, and all-cause mortality. This study is aimed to find out which microorganisms or microbial functions have a significant impact on higher calcium-phosphorus product (Ca x P) after they undergo hemodialysis (HD) treatment. Feces samples from 30 healthy controls, 15 dialysis patients with controlled Ca xP (HD), and 16 dialysis patients with higher Ca xP (HDHCP) were collected to perform in 16S amplicon sequencing. We found gut microbial composition was significantly different between hemodialysis patients and healthy controls. Three phyla including Firmicutes, Actinobacteria, and Proteobacteria were significantly enriched in hemodialysis patients. Although only one genus, Lachnospiraceae_FCS020_group, was significantly increased in higher Ca xP group, there were four metabolic pathways predicted by PICRUSt significantly increased in higher Ca xP group and associated with causing VC, including the pentose phosphate pathway, steroid biosynthesis, terpenoid backbone biosynthesis, and fatty acid elongation pathway. Characterizing dysbiosis of gut microbiome played the important role in hemodialysis patients.

Impact of X-Linked Hypophosphatemia on Muscle Symptoms

X-linked hypophosphatemia (XLH) is the most common hereditary form of rickets and deficiency of renal tubular phosphate transport in humans. XLH is caused by the inactivation of mutations within the phosphate-regulating endopeptidase homolog X-linked (PHEX) gene and follows an X-dominant transmission. It has an estimated frequency of 1 case per 20,000, and over 300 distinct pathogenic variations have been reported that result in an excess of fibroblast growth factor 23 (FGF23) in the serum. Increased levels of FGF23 lead to renal phosphate loss, decreased serum 1,25-dihydroxyvitamin D, and increased metabolism of 1,25-dihydoxyvitamin D, resulting in hypophosphatemia. Major clinical manifestations include rickets, bone deformities, and growth retardation that develop during childhood, and osteomalacia-related fractures or pseudo-fractures, degenerative osteoarthritis, enthesopathy, dental anomalies, and hearing loss during adulthood, which can affect quality of life. In addition, fatigue is also a common symptom in patients with XLH, who experience decreased motion, muscle weakness, and pain, contributing to altered quality of life. The clinical and biomedical characteristics of XLH are extensively defined in bone tissue since skeletal deformations and mineralization defects are the most evident effects of high FGF23 and low serum phosphate levels. However, despite the muscular symptoms that XLH causes, very few reports are available on the effects of FGF23 and phosphate in muscle tissue. Given the close relationship between bones and skeletal muscles, studying the effects of FGF23 and phosphate on muscle could provide additional opportunities to understand the interactions between these two important compartments of the body. By describing the current literature on XLH and skeletal muscle dysfunctions, the purpose of this review is to highlight future areas of research that could contribute to a better understanding of XLH muscular disability and its management.

A case of tumor-induced osteomalacia masked by acute kidney injury

Introduction: Hypophosphatemia in patients with tumor-induced osteomalacia (TIO) is due to abnormal excess production of fibroblast growth factor 23 (FGF-23) causing urinary phosphate wasting. However, in patients with coexisting acute kidney injury (AKI), hypophosphatemia may not be apparent as AKI reduces filtration and excretion of phosphate. Case report: We describe a case of 36-year-old woman who presented with right-sided abdominal pain. Initial laboratory testing revealed non oliguric AKI with creatinine (Cr) of 2.0 mg/dL (baseline 1.2 mg/dL), low phosphate (1.8 mg/dL), and normal parathyroid (PTH) levels. Hypophosphatemia in the setting of AKI and normal PTH raised suspicion for renal phosphate wasting disorder independent of PTH, triggering an order for FGF-23 level. Further into hospital stay, the AKI worsened (Cr rose to 7.2 mg/dL) and phosphate levels increased to 6.7 mg/dL casting doubt on the initial suspicion. However, FGF-23 level resulted at 12,715 RU/mL, strongly suggesting TIO. Random liver biopsy was obtained as part of TIO work up due to liver ultrasound findings of hepatomegaly, diffuse parenchymal heterogenicity mimicking steatosis and potential ill-defined mass. Liver specimen showed tumor cells positive for CD56 and Ki-67, indicating high-grade metastatic neuro endocrine tumor which was the likely source of FGF-23. Patient rapidly deteriorated and opted for comfort measures. Conclusion: TIO typically manifests with overt hypophosphatemia. This case highlights the fact that decreased glomerular filtration rate may mask the degree of urinary phosphate wasting resulting in normal to high serum phosphate level. This warrants high index of suspicion to diagnose an underlying phosphate wasting disorder in the setting of normal to high serum phosphate levels and reduced kidney function.

The relationship between good collateral development and magnesium/phosphate ratio in chronic total occlusion

Objective: Coronary collateral formation can be triggered by many acquired factors such as ischemia and growth factors, which ultimately manifests as differences in the quality of the coronary collateral circulation (CCC) in patients. Low magnesium (Mg) levels can increase endothelial cell dysfunction and potentially increase the risk of thrombosis and atherosclerosis. However, it has been reported that high serum phosphate (P) levels are correlated with the development of atherosclerosis and mortality. In this article, we aimed to reveal the relationship between CCC quality and Mg/P ratio in chronic total occlusion (CTO).&#x0D; Methods: A total of 269 patients with detected CTO in coronary angiography between March 2014 and June 2018 were included in the study. The patients were divided into two groups as group I (127 patients) and group II (142 patients) according to the Rentrop classification. The study is a retrospective, observational study.&#x0D; Results: In the multivariable regression analysis; smoking (p=0.004), triglyceride (p

Modifiable Risk Factors Are Important Predictors of COVID-19-Related Mortality in Patients on Hemodialysis.

Patients with end-stage kidney disease face a higher risk of severe outcomes from SARS-CoV-2 infection. Moreover, it is not well known to what extent potentially modifiable risk factors contribute to mortality risk. In this historical cohort study, we investigated the incidence and risk factors for 30-day mortality among hemodialysis patients with SARS-CoV-2 infection treated in the European Fresenius Medical Care NephroCare network using conventional and machine learning techniques. We included adult hemodialysis patients with the first documented SARS-CoV-2 infection between February 1, 2020, and March 31, 2021, registered in the clinical database. The index date for the analysis was the first SARS-CoV-2 suspicion date. Patients were followed for up to 30 days until April 30, 2021. Demographics, comorbidities, and various modifiable risk factors, expressed as continuous parameters and as key performance indicators (KPIs), were considered to tap multiple dimensions including hemodynamic control, nutritional state, and mineral metabolism in the 6 months before the index date. We used logistic regression (LR) and XGBoost models to assess risk factors for 30-day mortality. We included 9,211 patients (age 65.4 ± 13.7 years, dialysis vintage 4.2 ± 3.7 years) eligible for the study. The 30-day mortality rate was 20.8%. In LR models, several potentially modifiable factors were associated with higher mortality: body mass index (BMI) 30-40 kg/m2 (OR: 1.28, CI: 1.10-1.50), single-pool Kt/V (OR off-target vs on-target: 1.19, CI: 1.02-1.38), overhydration (OR: 1.15, CI: 1.01-1.32), and both low (<2.5 mg/dl) and high (≥5.5 mg/dl) serum phosphate levels (OR: 1.52, CI: 1.07-2.16 and OR: 1.17, CI: 1.01-1.35). On-line hemodiafiltration was protective in the model using KPIs (OR: 0.86, CI: 0.76-0.97). SHapley Additive exPlanations analysis in XGBoost models shows a high influence on prediction for several modifiable factors as well, including inflammatory parameters, high BMI, and fluid overload. In both LR and XGBoost models, age, gender, and comorbidities were strongly associated with mortality. Both conventional and machine learning techniques showed that KPIs and modifiable risk factors in different dimensions ascertained 6 months before the COVID-19 suspicion date were associated with 30-day COVID-19-related mortality. Our results suggest that adequate dialysis and achieving KPI targets remain of major importance during the COVID-19 pandemic as well.

Hypo- and Hyperphosphatemia at Admission as Independent Factors of Mortality of COVID-19 Patients: Findings from a Retrospective Cohort Study.

Electrolyte imbalances are common in COVID-19 infection and are associated with poor outcomes in hospitalized patients. This study examined whether serum phosphate imbalances at admission are associated with mortality in hospitalized COVID-19 patients. In this registry-based single-center retrospective cohort study, 1349 inpatients with COVID-19 were included from March 2020 to March 2021 in an academic hospital in Ilam (southwest Iran). The Cox proportional hazard (PH) regression model was applied to the data set of COVID-19. The in-hospital median survival time for patients with low, normal, and high serum phosphate levels was 14, 25, and 8 days, respectively. In a multivariate model, adjusted for the other variables, patients with hypophosphatemia (adjusted hazard ratio [HR], 2.53; 95% CI, 1.15 - 5.58; P = 0.02) and hyperphosphatemia (adjusted HR, 1.77; 95% CI, 1.00 - 3.14; P = 0.05) had an increased mortality hazard compared with those who had normal levels of serum phosphate. Our results demonstrate associations of hypophosphatemia and hyperphosphatemia with increased in-hospital mortality in COVID-19 patients. Intensive medical care and more attention must be paid to COVID-19 patients with serum phosphate imbalances at admission.

MO938: Variability of Serum Phosphate in Incident Hemodialysis Patients: Association With All-Cause Mortality

Abstract BACKGROUND AND AIMS In maintenance hemodialysis, both low and high serum phosphate levels are related to patient outcomes. We aimed to further explore the relation between serum phosphate (P) variability and all-cause mortality. METHOD All adult incident hemodialysis patients treated in U.S. Fresenius Kidney Care clinics between January 2010 and October 2018 were included. The first 6 months on hemodialysis were defined as baseline, months 7–18 as the follow-up period. All-cause mortality was recorded during follow-up. We quantitated variability as directional range (DR), a metric that describes during baseline the difference between the largest and the smallest value; the DR is positive when the smallest value precedes the largest; otherwise, the DR is negative. Cox proportional hazards models with spline terms were applied to explore the association between DR and SD of serum P and all-cause mortality. Additionally, tensor product smoothing splines were computed to study the interactions of P with the DR and SD of P and their joint associations with outcomes. All analyses were adjusted for demographics, comorbidities and nutritional parameters. RESULTS A total of 281 356 patients were included, 258 741 patients were studied. The average age was 62.3 years, 58% were males, 68% were diabetic, 10% with COPD and 25% with CHF. Baseline mean serum P was 5.07 mg/dL, the median DR was + 1.7 mg/dL and the median SD was 0.97. Our results indicate that both higher and lower levels of DR are associated with a higher risk of mortality (Fig. 1). With higher levels of serum P, both lower (negative) and higher levels of DR of serum P were associated with a higher risk of mortality (Fig. 2). In patients with lower levels of serum P, a negative level of DR is associated with a high mortality risk, while the association is attenuated in patients with higher (positive) levels of DR (Fig. 2). On all levels of serum P, higher SD is associated with a higher risk of mortality. CONCLUSION Stable serum P levels between 4 and 6 mg/dL are associated with the best outcomes. Negative DR of serum P is associated with particularly high HR for all-cause mortality in the presence of serum P levels &amp;lt;3 mg/dL, possibly because patients are generally malnourished or inflamed, and a further reduction of serum P indicates nutritional deterioration. Serum P &amp;gt; 8 mg/dL is associated with increased all-cause mortality, irrespective of DR.

Prevalence, Characteristics, and Associated Risk Factors of Wrist Fractures in Americans Above 50: The Cross-Sectional NHANES Study.

SummaryBy analyzing data from NHANES, we aimed to evaluate the prevalence, characteristics, and associated factors of wrist fractures in Americans aged 50 and above.IntroductionWrist fractures, whose prevalence increases with age, are one of the most common fractures in the United States. However, epidemiological studies on the prevalence of wrist fractures of certain ages were limited.MethodsThe data of Americans aged 50 or above from 2013–2014 and 2017–2018 in NHANES were extracted and analyzed.ResultsThe prevalence of wrist fractures among Americans whose age was 50 or above was 12%, which was similar between men and women (men 12.8% vs. women 11.4%, p = 0.267). Among those who had experienced their first wrist fracture, 17.8% of the population experienced a second wrist fracture. The top two causes of the first wrist fracture were a fall from a standing height (56%) or a hard fall (34.8%). The prevalence of wrist fractures was higher in men than in women (13.7% versus 8.7%, p = 0.023) aged < 60, but higher in women than in men aged ≥ 60 (11.8% versus 14.3%, p = 0.007). Multivariate analysis showed that obesity, frequent drinking, current smoking, high serum phosphate level, non-Hispanic white women, and osteoporosis were independently associated with wrist fractures. Stratified by race, osteoporosis, frequent drinking, and high serum phosphate level were risk factors for wrist fractures in all races. As for Mexican Americans, non-Hispanic whites, and other races including multi-racial, current smoking was a risk factor of wrist factures. Furthermore, obesity was positively associated with wrist fractures in Mexican Americans, other Hispanics, and non-Hispanic whites.ConclusionThe prevalence of wrist fractures in Americans aged 50 and above was 12%. Falling from a standing height was the main cause of the first wrist fracture. Frequent drinking, current smoker, high serum phosphate level, osteoporosis, obesity, and non-Hispanic women were more likely to experience wrist fractures.