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HWN Suggests

Hyperphosphatemia

Acute hyperphosphatemia is often a result of intracellular -> extracellular shift (tumor lysis syndrome, rhabdomyolisis, among other causes). In patients with normal kidney function, the treatment should be focused on promoting phosphaturia with the administration of normal saline as well as acetazolamide and sodium bicarbonate if needed...

Chronic hyperphosphatemia, which occurs often in patients with chronic kidney disease, should be treated with low phosphate diet to a maximum dietary intake of 900mg/day (avoid dairy products, sodas, processed foods) and phosphate binders (e.g. Sevelamer 800-1600mg TID, lanthanum carbonate 1500-4500mg daily, calcium acetate or calcium carbonate).

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 Why there is great need for additional treatments to manage hyperphosphatemia in patients with CKD on dialysis

Current phosphate management options, including dietary restrictions and phosphate binders, decrease overall QoL for dialysis patients. The difficulty of maintaining a low phosphate diet is exacerbated by the large amounts of “hidden” phosphate additives in modern processed foods (e.g., frozen food, dry food mixes, packaged meat, cheese, and soft drinks) that are not required to be listed on labels.

Articles of Interest

Differential Diagnosis: Hyperphosphatemia

Differential diagnoses, listed in order of likelihood, for patients presented with hyperphosphatemia...

Hyperphosphatemia - Be Aware!

Phosphorus is a mineral which helps keep your bones strong and healthy. As kidney function declines, your blood phosphate level may rise, causing itchy skin or painful joints, and loss of calcium from your bones. Excess phosphorus can crystalize with calcium and be deposited in the artery walls. This can lead to blockage of the arteries and other problems. This Webinar will examine the issue of high phosphate and explain the various treatments available to control or prevent it.

Hyperphosphatemia and Cardiovascular Disease

Hyperphosphatemia or even serum phosphate levels within the “normal laboratory range” are highly associated with increased cardiovascular disease risk and mortality in the general population and patients suffering from chronic kidney disease (CKD). As the kidney function declines, serum phosphate levels rise and subsequently induce the development of hypertension, vascular calcification, cardiac valvular calcification, atherosclerosis, left ventricular hypertrophy and myocardial fibrosis by distinct mechanisms. Therefore, phosphate is considered as a promising therapeutic target to improve the cardiovascular outcome in CKD patients.

Hyperphosphatemia from Fosphenytoin?

Despite the phosphate load from fosphenytoin administration, hyperphosphatemia is very rare and probably associated with renal insufficiency and dosing errors.

Internal Medicine Residency Handbook

Symptoms are usually secondary to coexistent hypocalcemia (psychosis, seizure, perioral paresthesia’s, muscle weakness),

New Pharmacotherapy Options for Hyperphosphatemia

The management of hyperphosphatemia has included dietary phosphate restriction and use of phosphate binders. The first phosphate binders were aluminum- and magnesium-based antacids. Adverse effects and toxicity limited the use of these agents, and therapy evolved with calcium carbonate, calcium acetate, sevelamer, and lanthanum carbonate. Recently, two iron-based phosphate binders have been approved.

Spurious Hyperphosphatemia: A Diagnostic and Therapeutic Challenge

In the setting of hyperglobulinemia, hyperbilirubinemia, and hyperlipidemia, PHP secondary to interference with the assay has been described. In multiple myeloma, hyperphosphatemia is frequently a manifestation of renal failure.1,2 We report here a case of multiple myeloma with normal renal function and P-HP.

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EMCrit Project

Hyperphosphatemia itself is generally asymptomatic. However, hyperphosphatemia may indirectly cause symptoms in two ways. more common: symptomatic hypocalcemia, rare: calciphylaxis.

Life in the Fastlane

CLINICAL FEATURES (related to hypocalcaemia)...

StatPearls

Renal failure is the most common cause of hyperphosphatemia. A glomerular filtration rate of less than 30 mL/min significantly reduces the filtration of inorganic phosphate, increasing its serum level. Other less common causes include a high intake of phosphorus or increased renal reabsorption.