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Dietary phosphate binds strongly to sucroferric oxyhydroxide in the gastrointestinal (GI) tract. The bound phosphate is eliminated in the faeces and thereby prevented from absorption into the blood. As a consequence of the decreased dietary phosphate absorption, serum phosphorus concentrations are reduced.
Phosphate-binding medications include sevelamer, lanthanum carbonate, calcium carbonate, and calcium acetate. [7] Previously aluminum hydroxide was the medication of choice, but its use has been largely abandoned due to the increased risk of aluminum toxicity .
Conventional therapy consisted of medications including human growth hormone, calcitriol, and oral phosphate, [37] [38] and calcitriol; [37] [38] Unwanted effects of this therapy have included secondary hyperparathyroidism, nephrocalcinosis, kidney stones, and cardiovascular abnormalities. [citation needed]
Hypophosphatemia is an electrolyte disorder in which there is a low level of phosphate in the blood. [1] Symptoms may include weakness, trouble breathing, and loss of appetite. [1]
Phosphate nephropathy or nephrocalcinosis [1] is an adverse renal condition that arises with a formation of phosphate crystals within the kidney's tubules. This renal insufficiency is associated with the use of oral sodium phosphate (OSP) such as C.B. Fleet's Phospho soda and Salix's Visocol, for bowel cleansing prior to a colonoscopy.
The levels of chloride in the blood can help determine if there are underlying metabolic disorders. [20] Generally, chloride has an inverse relationship with bicarbonate, an electrolyte that indicates acid-base status. [20] Overall, treatment of chloride imbalances involve addressing the underlying cause rather than supplementing or avoiding ...
Fanconi syndrome or Fanconi's syndrome (English: / f ɑː n ˈ k oʊ n i /, / f æ n-/) is a syndrome of inadequate reabsorption in the proximal renal tubules [1] of the kidney.The syndrome can be caused by various underlying congenital or acquired diseases, by toxicity (for example, from toxic heavy metals), or by adverse drug reactions. [2]
It represents a systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of the following: [1] [2] Abnormalities of calcium, phosphorus , parathyroid hormone, or vitamin D metabolism; Abnormalities in bone turnover, mineralization, volume, linear growth, or strength