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ACS Omega Nov 2023Polyphosphate polymers are chains of phosphate monomers chemically bonded together via phosphoanhydride bonds. They are found in all prokaryotic and eukaryotic organisms...
Polyphosphate polymers are chains of phosphate monomers chemically bonded together via phosphoanhydride bonds. They are found in all prokaryotic and eukaryotic organisms and are among the earliest, most anionic, and most mysterious molecules known. They are everywhere, from small cellular components to additives in our food. There is a strong association between hyperphosphatemia and mortality. That is why it is crucial to assess how polyphosphates, as food additives, affect the quality of edible proteins. This study investigated the effect of inexpensive and widely used food additives (hexametaphosphate labeled as E452) on bakery items, meat products, fish, and soft drinks. Using various spectroscopic and microscopic techniques, we examined how hexametaphosphate affected the aggregation propensity, structure, and stability of a commonly used food protein: hen egg white lysozyme (HEWL). The solubility of HEWL is affected in a bimodal fashion by the concentration of hexametaphosphate. The bimodal concentration-dependent effect was also observed in the tertiary and secondary structural changes. Hexametaphosphate-induced HEWL aggregates were amorphous, as evidenced by ThT fluorescence, far-UV CD, and TEM imaging. This study showed that the food additive (hexametaphosphate) may denature and aggregate proteins and may lead to undesirable health issues.
PubMed: 38027328
DOI: 10.1021/acsomega.3c06210 -
Kidney International Reports Nov 2023
PubMed: 38025212
DOI: 10.1016/j.ekir.2023.10.001 -
Kidney International Reports Nov 2023Serum phosphorus management is important for patients with chronic kidney disease on dialysis to reduce the risk of hyperparathyroidism and ectopic vascular...
INTRODUCTION
Serum phosphorus management is important for patients with chronic kidney disease on dialysis to reduce the risk of hyperparathyroidism and ectopic vascular calcification. Phosphate binders (PBs) control serum phosphorus levels; however, some patients do not achieve adequate control with existing PBs. The similar mechanisms of action of each PB may limit their ability to lower serum phosphorus levels. Therefore, drugs with novel mechanisms of action that can be added to existing PBs to further lower serum phosphorus levels are desired. Tenapanor, a novel selective inhibitor of intestinal sodium/hydrogen exchanger 3 transporters, decreases passive phosphate absorption in the intestine, thereby decreasing serum phosphorus levels.
METHODS
This study evaluated the efficacy and safety of tenapanor treatment with up-titration when added to PBs among Japanese hemodialysis patients with hyperphosphatemia poorly controlled by PBs alone. In total, 169 patients taking PBs whose serum phosphorus level was ≥6.1 and <10.0 mg/dl initiated the 8-week treatment (placebo + PB, = 85; tenapanor + PB, = 84).
RESULTS
The least squares mean change from baseline to week 8 in serum phosphorus level was -0.24 and -2.00 mg/dl in the placebo and tenapanor groups, respectively, with a statistically significant difference between groups (-1.76 mg/dl; < 0.0001). Diarrhea as a treatment-emergent adverse event (TEAE) occurred in 14.1% and 63.1% of patients in the placebo and tenapanor groups, respectively. All diarrhea events were mild or moderate.
CONCLUSION
Tenapanor added to PBs improved serum phosphorus levels that could not previously be controlled by PBs alone, and no new safety concerns were raised.
PubMed: 38025211
DOI: 10.1016/j.ekir.2023.08.003 -
Caspian Journal of Internal Medicine 2023The increase in serum phosphorus level is an independent risk factor for mortality in patients with chronic renal failure or undergoing dialysis due to end-stage renal...
BACKGROUND
The increase in serum phosphorus level is an independent risk factor for mortality in patients with chronic renal failure or undergoing dialysis due to end-stage renal disease. Proton pump inhibitors (PPI) are the general name given to agents used to suppress stomach acid. In this study, the clinical benefit of using PPIs in addition to drugs used for phosphorus control was investigated.
METHODS
153 patients with end-stage renal disease were included in the study. The data of the patients who had been on hemodialysis for at least 6 months and using calcium acetate for at least 1 month were recorded in the SPSS 21 program. The patients were analyzed in two groups according to whether they used PPI or not. Anamnesis, patient follow-up, laboratory, and treatment forms collected from hemodialysis centers were used.
RESULTS
Of the 153 patients in the study, 49% were males and the mean age was 65.11±11.23. The mean duration of patients on dialysis was 48.5 months. Hypertension was found to be the most common comorbidity with 75.8% prevalence among the patients. The mean phosphorus levels of the patients using calcium acetate together with PPI were found to be approximately 1.2 mg/dl lower (p= 0.000).
CONCLUSION
It should be taken into account that the use of PPI together with calcium acetate, which is still common as a phosphorus binder in developing countries, can contribute to controlling phosphorus levels.
PubMed: 38024165
DOI: 10.22088/cjim.14.4.737 -
The Journal of International Medical... Nov 2023We report a 15-year-old Chinese girl who presented with intermittent seizure episodes and had been misdiagnosed as having idiopathic epilepsy 5 years previously....
We report a 15-year-old Chinese girl who presented with intermittent seizure episodes and had been misdiagnosed as having idiopathic epilepsy 5 years previously. Laboratory testing revealed hypocalcemia, hyperphosphatemia, and a high parathyroid hormone (PTH) concentration. She was subsequently shown to have pseudohypoparathyroidism type Ib (PHPIb) based on the results of methylation analysis of the gene, which showed a loss of methylation of the differentially methylated regions (DMR) of , , and ; and a gain of methylation of the DMR of the GNAS-NESP55 region. We adjusted the patient's medication by prescribing calcium and calcitriol supplements, and gradually reduced the doses of antiepileptic drugs, until they had been completely discontinued. As a result, the patient did not experience any further seizures or epileptiform symptoms; and had normal plasma calcium, phosphorus, and 25-hydroxyvitamin D concentrations and 24-hour urinary calcium excretion. In addition, her PTH concentration gradually normalized over 12 months, and no urinary stones were found on ultrasonographic examination. In conclusion, the clinical presentation of PHP is complex, and the condition is often misdiagnosed. The diagnosis and follow-up of the present patient have provide valuable insights that should contribute to informed clinical decision-making and the implementation of appropriate treatment strategies.
Topics: Humans; Female; Adolescent; GTP-Binding Protein alpha Subunits, Gs; DNA Methylation; Calcium; Follow-Up Studies; Chromogranins; Pseudohypoparathyroidism; Parathyroid Hormone; Epilepsy; Diagnostic Errors
PubMed: 38017366
DOI: 10.1177/03000605231215202 -
Journal of Nephrology Mar 2024Ultraprocessed food (UPF) is defined as industrialized, packaged and ready-to-eat food produced on a large scale, using sophisticated industrial machinery. Examples of...
Ultraprocessed food (UPF) is defined as industrialized, packaged and ready-to-eat food produced on a large scale, using sophisticated industrial machinery. Examples of UPFs include salty and sweet snacks, industrialized biscuits and packaged meals, processed meats and sugary drinks. Ultraprocessed food has a long-shelf life, is highly palatable, microbiologically safe, affordable and most of all, easy to consume. For these reasons, its consumption has been increasing worldwide, and is replacing healthy homemade meals. The main concern of this dietary shift is that UPFs come with the addition of salt, sugar, unhealthy fats, and several additives and taste enhancers that contain, among other substances, relevant quantities of potassium, phosphate and sodium. A large proportion of UPF in the diet may carry risks for patients with chronic kidney disease (CKD) since it can worsen blood pressure and glycemic control, and lead to constipation, hyperkalemia and hyperphosphatemia. Acknowledging the importance of UPF in kidney health implies integrating nutritional counseling with information on UPFs, and specific educational material can be helpful for patients, caregivers, and also for health care providers. We developed a set of 3 infographics dedicated to CKD patients, with information on how to identify UPFs, reasons for decreasing consumption, how to compose a healthy CKD plate and tips for reading food labels in supermarkets and grocery shops. We hope that this material can be useful in CKD outpatient clinics and dialysis centers as well as in general practitioners' offices, caring for early stage CKD.
Topics: Humans; Renal Insufficiency, Chronic; Diet, Healthy; Fast Foods; Food Handling; Patient Education as Topic; Nutritive Value; Food, Processed
PubMed: 37995043
DOI: 10.1007/s40620-023-01817-3 -
The American Journal of Case Reports Nov 2023BACKGROUND Hyperphosphatemia is a complication of chronic renal failure (CRF) due to reduction in the glomerular filtration rate. Lanthanum carbonate is a commonly used...
BACKGROUND Hyperphosphatemia is a complication of chronic renal failure (CRF) due to reduction in the glomerular filtration rate. Lanthanum carbonate is a commonly used phosphate binder for patients with CRF and hyperphosphatemia, but has adverse effects if patients are not monitored. This report is of a 47-year-old man with hyperphosphatemia due to CRF treated with lanthanum carbonate tablets who presented acutely with partial large bowel obstruction. The incidence of lanthanum carbonate causing intestinal obstruction is rare, and few cases in the literature have described the course of the disease in detail. CASE REPORT A 47-year-old man diagnosed with diabetic nephropathy underwent hemodialysis treatment and was prescribed 0.5 g/day of chewable lanthanum carbonate tablets. After taking lanthanum carbonate for 5 months, the patient experienced symptoms of decreased bowel movements and exhaustion, which progressively worsened. Abdominal computed tomography (CT) revealed multiple hyperdensities in the large bowel, indicating the presence of lanthanum deposition. Lanthanum carbonate was promptly discontinued. After undergoing enema and catharsis treatment, the large bowel obstruction was relieved, and the hyperdensities in the abdominal CT disappeared. The colonoscopy and histologic examination revealed ulcerations and inflammatory changes in the large bowel mucosa. CONCLUSIONS This report highlights the rare association between the use of lanthanum carbonate tablets and intestinal obstruction. Healthcare providers should enhance their vigilance regarding lanthanum carbonate-induced serious gastrointestinal adverse reactions and actively seek to detect lanthanum deposition by abdominal CT or radiography (X-ray). After the occurrence of lanthanum deposition, drug withdrawal and promotion of defecation are primary treatment methods.
Topics: Male; Humans; Middle Aged; Hyperphosphatemia; Lanthanum; Kidney Failure, Chronic; Renal Insufficiency, Chronic; Renal Dialysis; Intestinal Obstruction; Tablets
PubMed: 37994013
DOI: 10.12659/AJCR.942113 -
Annals of Translational Medicine Oct 2023Vascular calcification (VC) is common in chronic kidney disease (CKD) patients and is associated with poor cardiovascular outcomes. This study aims to review nutritive... (Review)
Review
BACKGROUND AND OBJECTIVE
Vascular calcification (VC) is common in chronic kidney disease (CKD) patients and is associated with poor cardiovascular outcomes. This study aims to review nutritive pro-calcifying factors of CKD.
METHODS
Electronic databases (PubMed, Embase, and the Cochrane Central Register of Controlled Trials) were searched from 2001 as at July 26, 2022, to select and summarize the basic and clinical studies reporting the effects of malnutrition or metabolic disorders on VC in CKD and the evolving treatments for these nutrient metabolic disorders.
KEY CONTENT AND FINDINGS
Hyperphosphatemia, calcium load, hypomagnesemia, iron deficiency, lipoprotein(a) abnormalities, protein malnutrition, and vitamin K deficiency secondary to CKD were closely associated with the occurrence and development of VC. Elevated phosphate and calcium levels were essential contributors to VC, yet current phosphate binders with good phosphate-lowering effects had not been shown to delay VC progression in CKD, and it remained challenging on how to identify and prevent calcium overload. Magnesium supplementation was the most promising treatment for mitigating VC, as supported by and studies and clinical trials. Correction of iron and vitamin K deficiency might contribute to VC attenuation, yet there was a lack of clinical evidence on CKD patients.
CONCLUSIONS
This review highlighted the effects of nutrient metabolism disorders on CKD-VC, and additional studies are needed to further address optimal nutrition strategies for mitigating VC in CKD.
PubMed: 37970595
DOI: 10.21037/atm-22-5358 -
Journal of Clinical Biochemistry and... Nov 2023Disorder of phosphate metabolism is a common pathological condition in chronic kidney disease patients. Excessive intake of dietary phosphate deteriorates chronic kidney...
Disorder of phosphate metabolism is a common pathological condition in chronic kidney disease patients. Excessive intake of dietary phosphate deteriorates chronic kidney disease and various complications including cardiovascular and infectious diseases. Recent reports have demonstrated that gut microbiome disturbance is associated with both the etiology and progression of chronic kidney disease. However, the relationship between dietary phosphate and gut microbiome remains unknown. Here, we examined the effects of excessive intake of phosphate on gut microbiome. Five-week-old male C57BL/6J mice were fed either control diet or high phosphate diet for eight weeks. Analysis of the gut microbiota was carried out using MiSeq next generation sequencer, and short-chain fatty acids were determined with GC-MS. In analysis of gut microbiota, significantly increased in and decreased in were observed in high phosphate diet group. Furthermore, high phosphate diet induced reduction of microbial diversity and decreased mRNA levels of colonic tight junction markers. These results suggest that the excessive intake of dietary phosphate disturbs gut microbiota and affects intestinal barrier function.
PubMed: 37970557
DOI: 10.3164/jcbn.23-9 -
Journal of Clinical Biochemistry and... Nov 2023Hyperphosphatemia is an independent and non-classical risk factor of cardiovascular disease and mortality in patients with chronic kidney disease (CKD). Increased levels...
Hyperphosphatemia is an independent and non-classical risk factor of cardiovascular disease and mortality in patients with chronic kidney disease (CKD). Increased levels of extracellular inorganic phosphate (Pi) are known to directly induce vascular calcification, but the detailed underlying mechanism has not been clarified. Although serum Pi levels during the growth period are as high as those observed in hyperphosphatemia in adult CKD, vascular calcification does not usually occur during growth. Here, we have examined whether the defence system against Pi-induced vascular calcification can exist during the growth period using mice model. We found that calcification propensity of young serum (aged 3 weeks) was significantly lower than that of adult serum (10 months), possibly due to high fetuin-A levels. In addition, when the aorta was cultured in high Pi medium , obvious calcification was observed in the adult aorta but not in the young aorta. Furthermore, culture in high Pi medium increased the mRNA level of tissue-nonspecific alkaline phosphatase (TNAP), which degrades pyrophosphate, only in the adult aorta. Collectively, our findings indicate that the aorta in growing mouse may be resistant to Pi-induced vascular calcification via a mechanism in which high serum fetuin-A levels and suppressed TNAP expression.
PubMed: 37970550
DOI: 10.3164/jcbn.23-11