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Perioperative Care
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
Sodium phosphate (NaP) was introduced in 1990. This hyperosmotic preparation is ingested with 250 mL of water, and every 45 mL of preparation draws 1–1.8 L of water into the colon to produce its cleansing effect. This low-volume preparation is better tolerated by patients and has comparable effectiveness compared with PEG solutions; NaP, however, causes significant fluid and electrolyte change such as hyperphosphataemia, hypocalcaemia, hypernatraemia and hypokalaemia.36 Electrolyte changes are usually transient and tolerated by healthy patients. It can, however, cause severe detrimental effects in patients with kidney disease, heart failure and liver disease and patients on angiotensin converting enzyme inhibitors or angiotensin receptor blockers. NaP is no longer recommended as routine use for bowel preparation unless the benefit of its use outweighs the risk of phosphate nephropathy and long-term renal impairment.
Ferric carboxymaltose–induced hypophosphatemia in the Axenfeld-Reiger syndrome
Published in Baylor University Medical Center Proceedings, 2022
Jasmeet Gill, Sebastian Melo, Ankit Mehta
Ten weeks after discharge, she presented again to the emergency department with a 4-day history of fever, upper respiratory tract infection, and poor oral intake. The blood urea nitrogen was 42 mg/dL; creatinine, 6.78 mg/dL; and serum phosphorus, 8.6 mg/dL. Serum phosphorus on the day of last infusion (72 h earlier) was 2.2 mg/dL with a creatinine of 0.69 mg/dL. A renal biopsy confirmed acute phosphate nephropathy (Figure 1). Her renal function did not improve with intravenous fluids, and she was discharged after 4 days with a normal phosphorus level. Intravenous phosphorus replacement was discontinued and 3 weeks later her creatinine was 4.05 mg/dL and her phosphorus was 4.0 mg/dL. The patient was diagnosed with chronic kidney disease stage 4 and received a cadaveric kidney transplant within 6 months. Table 2 and Figure 2 show the creatinine and phosphorus trends over the 15-week course.
Elevated admission serum calcium phosphate product as an independent risk factor for acute kidney injury in hospitalized patients
Published in Hospital Practice, 2019
Charat Thongprayoon, Wisit Cheungpasitporn, Michael A. Mao, Andrew M. Harrison, Stephen B. Erickson
In the setting of acute phosphate nephropathy, previously termed acute nephrocalcinosis, injuries to the distal tubules and collecting ducts due to calcium phosphate deposits have been demonstrated [12,35,36]. As CaP levels increase, precipitation of calcium phosphate crystals may occur [22,23]. Acute phosphate nephropathy has not only been described after phosphate containing bowel preparation [37–39], but also been reported in patients who received oral or intravenous phosphate replacement [40,41]. Elevated serum calcium levels are associated with an increase in urinary calcium excretion due to compensatory increase in the filtered load and a decrease in the tubular reabsorption of calcium [42,43]. Consequently, hyperphosphatemia in patients with elevated calcium level may result in increased phosphate and calcium load in the distal tubules, resulting in acute phosphate nephropathy. AKI can also occur, or be exacerbated, by elevated serum calcium levels, which can cause renal vasoconstriction, leading to renal ischemia and tubular injury [44–46]. Based on the findings of our study, we demonstrate a linear trend of higher AKI incidence with increasing CaP levels.