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Antacids
Published in Charles Theisler, Adjuvant Medical Care, 2023
Antacids are medications that neutralize acid in the stomach. They are frequently used to treat heartburn or indigestion. Antacids such as Tums, Di-Gel, Dulcolax, Mylanta, etc., are different from acid reducers or block ers. Aluminum hydroxide gel in antacids (e.g., Equate) can combine with phosphorus to form a complex that is excreted in the feces. This is a valuable feature for reducing phosphate levels in hyperphosphatemia. However, aluminum-containing antacids can precipitate, leading to decreased absorption of vitamin A.1
Diabetic Nephropathy
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
There may be abnormalities of calcium, parathyroid hormone (PTH), phosphate, and vitamin D metabolism. Renal osteodystrophy is also possible. Reduced renal production of the active vitamin D hormone calcitriol adds to hypocalcemia. Reduced renal excretion of phosphate causes hyperphosphatemia. Secondary hyperparathyroidism is often seen, developing in kidney failure prior to abnormal calcium or phosphate concentrations manifesting. Therefore, it is important to monitor PTH in patients with moderate CKS prior to hyperphosphatemia occurring. Renal osteodystrophy is abnormal bone mineralization. It occurs because of a deficiency of calcitriol, hyperparathyroidism, excessive serum phosphate, or low to normal serum calcium. There is usually increased bone turnover because of osteitis fibrosa, a hyperparathyroid bone disease. There may be decreased bone turnover, however, caused by an adynamic disease from increased suppression of the parathyroid glands, or osteomalacia. If there is a calcitriol deficiency, this may result in osteomalacia or osteopenia.
PerformLyte—A Prodosomed PL425 PEC Phytoceutical-Enriched Electrolyte Supplement—Supports Nutrient Repletion, Healthy Blood pH, Neuromuscular Synergy, Cellular and Metabolic Homeostasis
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Bernard W. Downs, Manashi Bagchi, Bruce S. Morrison, Jeffrey Galvin, Steve Kushner, Debasis Bagchi
Hyperphosphatemia results from (a) excessive phosphate intake, (b) reduced phosphate excretion, or (c) a disorder that shifts intracellular phosphate to extracellular space. In addition, an overdose of oral phosphate administration, or random use of phosphate-containing enemas, can cause hyperphosphatemia.116,138 Also, hypocalcemia, diabetic ketoacidosis, crush injuries, nontraumatic rhabdomyolysis, systemic infections, and tumor lysis syndrome cause hyperphosphatemia.140–142,145,146 Nonetheless, hyperphosphatemia can be spurious in cases of hyperproteinemia, dyslipidemia, hemolysis, or hyperbilirubinemia. Extreme cases of hyperphosphatemia could be fatal.119,128
Influence of dietary protein on serum phosphorous levels in peritoneal dialysis patients with different initial transport function
Published in Renal Failure, 2022
Xiao-Pei Wang, Ying Ma, Jing Lv, Yu Liang, Li Jin, Wan-Hong Lu, Chang-Na Liang, Bao Qian, Zhao Li
Hyperphosphatemia is a common complication in individuals undergoing dialysis, which is associated with a high incidence of cardiovascular events and poor outcomes [1]. Phosphate control interventions include dietary phosphorus restriction, the use of phosphorus binders, and adequate dialysis. The Kidney Disease Improving Global Outcomes and Kidney Disease Outcomes Quality Initiative guidelines recommend a daily protein intake of 1.2 g/kg of body weight [2]. High dietary protein intake (DPI) increases the risk for hyperphosphatemia and accelerates the loss of residual kidney function [3]. Dietary protein restriction is considered to be effective for controlling serum phosphorus levels [4]. However, low dietary protein worsens nutritional status and increases mortality in peritoneal dialysis (PD) patients [5]. The role of peritoneal phosphate clearance rate, an important indicator of phosphate balance, has been under appreciated in PD patients [6]. The peritoneal phosphate clearance rate is lower and serum phosphorus levels are higher in patients with low and average low peritoneal membrane function characteristics (slow peritoneal transporters) than in those with high and high average peritoneal membrane function characteristics (fast peritoneal transporters) [7]. Very few studies have investigated the effects of DPI on serum phosphate levels in PD patients with different peritoneal transport types.
Pemigatinib in cholangiocarcinoma with a FGFR2 rearrangement or fusion
Published in Expert Review of Anticancer Therapy, 2022
Michael H. Storandt, Zhaohui Jin, Amit Mahipal
Due to its relatively unique conglomeration of toxicities including hyperphosphatemia, nail toxicity, and eye toxicity, there is much interest in management of these adverse effects to ensure medication adherence. With regards to hyperphosphatemia, close monitoring of serum phosphorus levels is recommended, with evaluation at baseline, one week after initiating therapy, and after the first cycle of therapy [39,87]. Although hyperphosphatemia is commonly reported, clinical complications from hyperphosphatemia are exceedingly rare. Dose reduction for hyperphosphatemia should be avoided unless serum phosphorus levels cannot be maintained with phosphate lowering drugs. Patients should be encouraged to adhere to a low phosphorus diet and phosphorus lowering therapy via phosphorus binders, such as sevelamer, or phosphaturic agents, such as acetazolamide, may be initiated if phosphorus levels rise above 7 mg/dL [39,87]. Dose reduction may be considering if serum phosphorus is greater than 7 mg/dL in spite of optimal phosphorus lowering therapy [39,87]. Reassuringly, although hyperphosphatemia is relatively common, discontinuation of FGFR inhibitors due to this AE is uncommon, likely due to aggressive measures to prevent and manage it [39].
An update on phosphate binders for the treatment of hyperphosphatemia in chronic kidney disease patients on dialysis: a review of safety profiles
Published in Expert Opinion on Drug Safety, 2022
Hiroaki Ogata, Akiko Takeshima, Hidetoshi Ito
Currently, various phosphate binders are clinically available for the management of hyperphosphatemia in patients with advanced CKD. As mentioned above, each phosphate binder has off-target actions, including lowering cholesterol or FGF-23, anti-inflammatory effects, supplementation of calcium or iron for their deficient states, and reduction of intravenous iron or ESA dosing. While various phosphate binders used in clinical practice facilitate the management of hyperphosphatemia, they worsen the pill burden and increase treatment costs. This increased pill burden may compromise or complicate drug safety. For a decade, it has been debated whether non-calcium-based phosphate binders are superior to calcium-based phosphate binders in improving hard outcomes [7,14,35,59]. Although this remains inconclusive, we should examine whether it is worth discussing in clinical practice. In clinical practice, concomitant treatment with multiple phosphate binders is more widely used for refractory hyperphosphatemia than single phosphate binders. Rather than comparing classes of binders, it would be more beneficial to establish novel therapies with higher effectiveness and safety.