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(BQ) Part 2 book Fluid, electrolyte and acid base disorders has contents: Disorders of magnesium, disorders of phosphate, disorders of phosphate, evaluation of an acid–base disorder, high anion gap metabolic acidosis, hyperchloremic metabolic acidosis,... and other contents.
Disorders of Phosphate: Hyperphosphatemia 22 Hyperphosphatemia is defined as serum [Pi] >4.5 mg/dL. Spurious increase in serum [Pi] is called pseudohyperphosphatemia It is rather rare but has been described in conditions of hyperglobulinemia, hypertriglyceridemia, and hyperbilirubinemia This spurious increase has been attributed to the interference of proteins and triglycerides in the colorimetric assay of phosphate The causes of true hyperphosphatemia can be discussed under three major categories: (1) addition of phosphate from the intracellular fluid (ICF) to extracellular fluid (ECF) compartment, (2) a decrease in renal excretion of phosphate, and (3) drugs (Table 22.1) In clinical practice, acute and chronic kidney diseases are probably the most significant causes of hyperphosphatemia Table 22.1 Major causes of hyperphosphatemia Cause Mechanism Addition of phosphate to ECF compartment Endogenous Hemolysis Release from hemolyzed red blood cells Rhabdomyolysis Release from muscle cells Tumor lysis syndrome Release from tumor cells due to chemotherapy or cell turnover High catabolic state Release from cells Exogenous Oral intake or through IV route Ingestion of sodium phosphate solution for bowl preparation or IV Na/K phosphate in hospitalized patients Phosphate-containing enemas Phosphate absorption from enemas (fleet enema) Respiratory acidosis Release from cells Lactic acidosis Phosphate utilization during glycolysis, leading to its depletion and subsequent release from cells Diabetic ketoacidosis Shift of phosphate from ICF to ECF due to insulin deficiency and metabolic acidosis (continued) © Springer Science+Business Media LLC 2018 A.S Reddi, Fluid, Electrolyte and Acid-Base Disorders, DOI 10.1007/978-3-319-60167-0_22 273 274 22 Disorders of Phosphate: Hyperphosphatemia Table 22.1 (continued) Cause Decreased renal excretion Chronic kidney disease stages and Acute kidney injury Hypoparathyroidism Pseudohypoparathyroidism Familial tumor calcinosis Drugs Excess vitamin D Bisphosphonates Growth hormone Liposomal amphotericin B Sodium phosphate (oral) Mechanism Inability of the kidneys to excrete phosphate load Inability to excrete phosphate and release from muscle during rhabdomyolysis Increased renal phosphate reabsorption Renal and skeletal resistance to PTH Mutations in GALNT3, FGF-23, and KLOTHO genes Increased gastrointestinal (GI) absorption of phosphate Decreased phosphate excretion, cellular shift Increased proximal tubule reabsorption Contains phosphatidyl choline and phosphatidyl serine GI absorption of phosphate Some Specific Causes of Hyperphosphatemia Acute Kidney Injury (AKI) Serum phosphate levels between and 10 mg/dL are common in patients with AKI. However, when AKI is caused by rhabdomyolysis, tumor lysis syndrome, hemolysis, or severe burns, serum levels may be as high as 20 mg/dL. The mechanisms for hyperphosphatemia in AKI include (1) decreased 1,25(OH)2D3 production, (2) skeletal resistance to parathyroid hormone (PTH) action, and (3) metastatic deposition as calcium phosphate in soft tissues Chronic Kidney Disease (CKD) In early stages of CKD (glomerular filteration rate (GFR) 30–60 mL/min), phosphate homeostasis is maintained by progressive increase in phosphate excretion by the surviving nephrons As a result, FEPO4 increases to >35% (normal 5–7%) This increased phosphate excretion is due to elevated FGF-23 levels, which subsequently inhibit 1,25(OH)2D3 production The low production of 1,25(OH)2D3 stimulates the secretion of PTH causing secondary hyperparathyroidism Both FGF-23 and PTH inhibit reabsorption of phosphate in the proximal tubule and enhance its urinary excretion Thus, FEPO4 increases by >35% to maintain normal serum phosphate level at the cost of high FGF-23 and PTH Some Specific Causes of Hyperphosphatemia 275 In CKD stages and 5, the GFR is