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UNASSIGNED: Sarcopenia, commonly observed in patients treated with hemodialysis, correlates with low serum phosphate levels. Although normophosphatemia is desired, dietary phosphate restriction is difficult to achieve and may result in undesirable protein restriction.
UNASSIGNED: We aimed to evaluate whether hyperphosphatemia is associated with higher muscle strength in patients receiving hemodialysis treatment.
UNASSIGNED: A single-center prospective observational study.
UNASSIGNED: Ambulatory prevalent patients undergoing hemodialysis treatments in a dialysis unit of a tertiary hospital.
UNASSIGNED: Participants included prevalent patients treated with hemodialysis. All patients were above 18 years. Only patients with residual kidney function below 200 mL/24 hours were included to avoid bias.
UNASSIGNED: Muscle strength was measured by handgrip strength (HGS). Each patient repeated 3 measurements, and the highest value was recorded. Handgrip strength cutoffs for low muscle strength were defined as <27 kg in men and <16 kg in women. Biochemical parameters, including serum phosphate level, were driven from routine monthly blood tests. Hyperphosphatemia was defined as serum phosphate above 4.5 mg/dL.
UNASSIGNED: Handgrip strength results were compared to nutritional, anthropometric, and biochemical parameters-in particular phosphate level. Long-term mortality was recorded.
UNASSIGNED: Seventy-four patients were included in the final analysis. Handgrip strength was abnormally low in 33 patients (44.5%). Patients with abnormal HGS were older and more likely to have diabetes mellitus and lower albumin and creatinine levels. There was no correlation between HGS and phosphate level (r = 0.008, P = .945). On multivariable analysis, predictors of higher HGS were body mass index and creatinine. Diabetes mellitus and female sex predicted lower HGS. Hyperphosphatemia correlated with protein catabolic rate, blood urea nitrogen, and creatinine. On multivariable analysis, predictors of hyperphosphatemia were higher creatinine level, normal albumin level, and heart failure. During mean follow-up time of 7.66 ± 3.9 months, 11 patients died. Mortality was significantly higher in patients with abnormally low HGS compared with normal HGS (odds ratio = 9.32, P = .02).
UNASSIGNED: A single-center study. All measurements were performed at one time point without repeated assessments. Direct dietary intake, degree of physical activity, and medication compliance were not assessed.
UNASSIGNED: Hyperphosphatemia correlated with increased protein intake as assessed by protein catabolic rate in patients treated with hemodialysis; however, neither correlated with higher muscle strength as measured by HGS.Trial registration: MOH 202125213.
UNASSIGNED: La sarcopénie, qui est fréquemment observée chez les patients traités par hémodialyse, est corrélée à de faibles taux sériques de phosphate. Dans ce contexte, la normophosphatémie est souhaitée, mais la restriction alimentaire en phosphate est difficile à réaliser et peut entraîner une restriction indésirable en protéines.
UNASSIGNED: Notre objectif était de déterminer si l’hyperphosphatémie est associée à une plus grande force musculaire chez les patients qui reçoivent un traitement par hémodialyse.
UNASSIGNED: Étude observationnelle prospective monocentrique.
UNASSIGNED: Le service de dialyse d’un hôpital de soins tertiaires.
UNASSIGNED: Des patients prévalents âgés de plus de 18 ans qui recevaient des traitements d’hémodialyse en ambulatoire dans le service de dialyse de l’hôpital. Afin de limiter les biais, seuls les patients avec une fonction rénale résiduelle inférieure à 200 ml/24 heures ont été inclus.
UNASSIGNED: La force musculaire a été mesurée par le test de force de préhension (HGS - handgrip strength). Trois mesures ont été faites pour chaque patient et la valeur la plus élevée a été enregistrée. Les seuils de faible force musculaire à l’HGS ont été établis à < 27 kg pour les hommes et à < 16 kg pour les femmes. Les paramètres biochimiques, notamment le taux de phosphate sérique, ont été déterminés à partir des analyses sanguines mensuelles des patients. L’hyperphosphatémie a été définie par une concentration sérique en phosphate supérieure à 4,5 mg/dl.
UNASSIGNED: Les résultats de l’HGS ont été comparés aux paramètres nutritionnels, anthropométriques et biochimiques — plus particulièrement au taux de phosphate. La mortalité à long terme a été enregistrée.
UNASSIGNED: Soixante-quatorze patients ont été inclus dans l’analyse finale. Les résultats de l’HGS étaient anormalement faibles chez 33 patients (44,5 % des sujets). Les patients qui avaient obtenu un résultat anormal à l’HGS étaient plus âgés, plus susceptibles de souffrir de diabète, et présentaient des taux d’albumine et de créatinine plus faibles. Aucune corrélation n’a été observée entre le résultat à l’HGS et le taux sérique de phosphate (r=0.008; p=0.945). Dans l’analyse multivariée, l’indice de masse corporelle et le taux de créatinine étaient des prédicteurs d’un résultat plus élevé à l’HGS, alors que le diabète et le fait d’être une femme étaient prédictifs d’un résultat inférieur à l’HGS. L’hyperphosphatémie a été corrélée au taux de catabolisme des protéines, à l’urée et au taux de créatinine. Dans l’analyse multivariée, un taux de créatinine plus élevé, un taux d’albumine normal et une insuffisance cardiaque étaient des facteurs prédictifs d’une hyperphosphatémie. Au cours de la période moyenne de suivi (7,66 ± 3,9 mois), 11 patients sont décédés. La mortalité était significativement plus élevée chez les patients qui présentaient un résultat anormalement faible à l’HGS par rapport à la normale (RC: 9,32; p = 0,02).
UNASSIGNED: L’étude a été menée dans un seul centre. Toutes les mesures ont été effectuées à un moment donné sans évaluations répétées. L’apport alimentaire direct, le degré d’activité physique et l’observance des médicaments n’ont pas été évalués.
UNASSIGNED: Chez des patients traités par hémodialyse, l’hyperphosphatémie est corrélée à une augmentation de l’apport en protéines évalué par le taux de catabolisme des protéines, mais ni l’une ni l’autre n’est corrélée à une plus grande force musculaire mesurée par HGS.

BACKGROUND: Aberrations in blood phosphate (Pi) levels, whether presenting as hypo- or hyperphosphatemia, appear to be associated with clinical complications and adverse outcomes in patients admitted to an intensive care unit (ICU). However, the prevalence of Pi disorders and the association with subsequent factors and organ failures leading to death in ICU patients are poorly described. Despite endeavors to understand the etiology and treatment of low Pi levels from systematic reviews and meta-analyses, the literature lacks comprehensive guidance for managing hypophosphatemia. Hyperphosphatemia, on the other hand, appears to be associated with higher mortality among critically ill patients, yet its prevalence among ICU patients, particularly following phosphate repletion, remains unknown. The present study aims to investigate the prevalence of Pi abnormalities upon ICU admission and their incidence during the first week of ICU stay, the factors associated with Pi alterations, and the effect of phosphate repletion on the normalization of Pi levels, and its associations with clinical outcomes.
METHODS: This multicentre, prospective, non-interventional cohort study will include at least 1000 consecutive adult ICU patients (≥18 years) as part B of the GUTPHOS study. Sites are eligible if an anticipated minimal inclusion of 50 eligible patients during eight weeks from January 2024 until June 2024 and daily phosphate measurements during the first seven days of ICU stay are expected. All consecutive adult patients admitted to a participating ICU during the recruitment period, lasting up to eight weeks, or up to 120 patients if enrollment reaches that limit earlier, will be included. Study parameters include study site characteristics, patient demographics, daily assessment of Pi levels, Pi-related treatment, feeding details, renal replacement therapy details, the incidence of refeeding-associated hypophosphatemia and administered medication (during the first seven calendar days of ICU stay). There will be a follow-up period of a maximum of 90 days to document 28- and 90-day all-cause mortality as the primary outcome. Multiple logistic regression will be used to assess independent associations with mortality in addition to Receiver Operating Characteristics curves to identify cut-off Pi values associated with mortality and overcorrection. Linear mixed models will be conducted to assess Pi treatment effects. Subgroup analyses will be performed based on Pi abnormalities observed during ICU admission, categorized as normo-, hypo-, hyper-, or mixed, along with its severity (mild, moderate, or severe).
CONCLUSIONS: The GUTPHOS study will be the first multicentre, prospective observational cohort study to investigate the prevalence, management practices, and consequent outcomes associated with Pi abnormalities during the first week of ICU admission. Its results may bridge the current evidence gap in repletion protocols while establishing the groundwork for a subsequent randomized controlled trial.
BACKGROUND: NCT05909722.

UNASSIGNED: COPD patients frequently have abnormal serum phosphorus levels. The objective of this study was to examine the correlation between serum phosphorus levels with hospital and 90-day mortality in critically ill patients with COPD.
UNASSIGNED: The MIMIC IV database was used for this retrospective cohort analysis. We extracted demographics, vital signs, laboratory tests, comorbidity, antibiotic usage, ventilation and scoring systems within the first 24 hours of ICU admission. Restricted cubic splines and multivariate cox regression analysis models were used to evaluate the connection between serum phosphorus with hospital and 90-day mortality. We assessed and classified various factors including gender, age, renal disease, severe liver disease, the utilization of antibiotics and congestive heart failure.
UNASSIGNED: We included a total of 3611 patients with COPD, with a median age of 70.7 years. After adjusting for all other factors, we observed a significant positive association between serum phosphate levels with both hospital mortality (HR 1.19, 95% CI: 1.07-1.31, p<0.001) and 90-day mortality (HR 1.15, 95% CI: 1.06-1.24, p<0.001). Compared to the medium group (Q2 ≥3.15, <4.0), the adjusted hazard ratios for hospital mortality were 1.47 (95% CI: 1.08-2, p=0.013), and 1.31 (95% CI: 1.06-1.61, p=0.013) for 90-day mortality in the high group (Q3≥4.0). Hospital mortality decreased at serum phosphate levels below 3.8 mg/dl (HR 0.664, 95% CI: 0.468-0.943, p=0.022), but increased for both hospital (HR 1.312, 95% CI: 1.141-1.509, p<0.001) and 90-day mortality (HR 1.236, 95% CI: 1.102-1.386, p<0.001) when levels were above 3.8 mg/dl. Subgroup and sensitivity analyses yielded consistent results.
UNASSIGNED: In critical ill COPD patients, this study demonstrated a non-linear association between serum phosphate levels and both hospital and 90-day mortality. Notably, there was an inflection point at 3.8 mg/dl, indicating a significant shift in outcomes. Future prospective research is necessary to validate this correlation.

What is this summary about?This is a summary of an article that was published in the medical journal Kidney360 describing results from the NORMALIZE study. The NORMALIZE study looked at how well tenapanor tablets reduced higher-than-normal levels of phosphate in the blood of persons with kidney disease who are on maintenance dialysis. These persons are unable to keep their blood phosphate levels in a normal range, and high levels of phosphate can contribute to several serious health consequences.Tenapanor is approved as an add-on treatment for high levels of phosphate in the blood of adults with chronic kidney disease who are on maintenance dialysis and whose disease does not respond adequately to treatment with phosphate binders or who are not able to take phosphate binders. In earlier clinical studies, tenapanor was studied alone or studied together with phosphate binders. In a 1-year clinical study called PHREEDOM, researchers learned that when tenapanor was used alone, it lowered blood phosphate levels, and treated patients experienced acceptable safety and tolerability as determined by the doctors running the study. In the NORMALIZE study, adult patients took a 30-mg tenapanor tablet twice a day, either alone or with sevelamer, for up to 18 months after they completed the PHREEDOM study.What were the main conclusions reported by the researchers?The researchers found that one-third of patients taking tenapanor, either alone or with sevelamer, achieved normal blood phosphate levels. This is an improvement from the current standard of care with sevelamer alone to reduce blood phosphate levels. As seen in the earlier studies of tenapanor, the most common adverse event experienced by patients was softer or loose stools. No new safety concerns were reported in the NORMALIZE study.What are the key takeaways?The researchers concluded that tenapanor, used alone or combined with sevelamer, can be used long-term by adult patients receiving maintenance dialysis to reduce the phosphate levels in their blood to within the normal range. Patients who take tenapanor may experience softer or loose stools.This summary was developed by the authors to help adult patients with chronic kidney disease receiving dialysis, and their family members and/or caregivers, better understand the effects of taking tenapanor.[Box: see text]Link to original article here.

What is this summary about?This summary provides a review of the OPTIMIZE study, the results of which were published in Kidney360 in February 2024. The OPTIMIZE study looked at how well tenapanor tablets work to treat patients receiving dialysis who have high levels of phosphate in their blood, a condition called hyperphosphatemia. In the OPTIMIZE study, researchers wanted to understand if tenapanor would decrease phosphate levels in the blood to the target range. They also tested different ways of starting tenapanor treatment in patients.In the human body, kidneys are organs that filter blood and remove waste products. In chronic kidney disease, sometimes referred to as CKD, a patient’s kidneys do not work as well at filtering their blood and removing waste products. This can allow phosphate to build up in the blood. Phosphate levels may remain high despite patients receiving treatment such as dialysis, using pills that keep phosphate in the intestines (called phosphate binders) to prevent phosphate from being absorbed into the blood, and eating a low-phosphate diet. Phosphate levels may remain high despite these treatments because they can be difficult to follow. Most people receiving dialysis take 7–8 phosphate binder pills every day, and over half of those people have reported skipping at least one dose in the past month. Additionally, low-phosphate diets can be difficult to follow and people often struggle to meet their other nutritional needs.What are the key takeaways?Tenapanor used in combination with phosphate binders led to lower phosphate levels in the blood with the use of fewer phosphate-lowering pills. Tenapanor also lowered phosphate levels in patients who were not previously on phosphate binders but needed phosphate-lowering treatment.What were the main conclusions reported by the researchers?Tenapanor can help patients receiving dialysis better control their hyperphosphatemia.[Box: see text]Link to original article here.

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BACKGROUND: Data 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.
METHODS: This 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.
RESULTS: A 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.
CONCLUSIONS: Hypophosphatemia, 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.

Because of increased risks of cardiovascular disease and death, patients with hyperphosphatemia receiving maintenance dialysis are advised to limit phosphorus consumption and are prescribed phosphate binders in an effort to better control serum phosphate concentrations. Because of large pill size, pill burden, and tolerability issues, phosphate binder adherence is relatively poor. On ingestion, phosphate is absorbed from the intestine via transcellular or paracellular transport. Data show that inhibiting sodium-hydrogen exchanger 3 modulates paracellular phosphate absorption (the predominant pathway in humans). Tenapanor is a first-in-class, minimally absorbed, phosphate absorption inhibitor that selectively inhibits sodium-hydrogen exchanger 3, with a mechanism distinct from, and complementary to, that of phosphate binders. In phase 3 and postregistrational studies, tenapanor conferred statistically significant and clinically meaningful reductions in serum phosphate in patients receiving maintenance dialysis with hyperphosphatemia. Here, we review the available preclinical and clinical data on the effects of tenapanor on controlling intestinal phosphate absorption.