Hyperphosphatemia after sodium phosphate laxatives inlow risk patients: Prospective study

Abstract

AIM:To establish the frequency of hyperphosphatemia following the administration of sodium phosphate laxatives in low-risk patients. METHODS:One hundred consecutive ASA Ⅰ-Ⅱ individuals aged 35-74 years, who were undergoing colonic cleansing with oral sodium phosphate (OSP) before colonoscopy were recruited for this prospective study. Exclusion criteria: congestive heart failure, chronic kidney disease, diabetes, liver cirrhosis, intestinal obstruction, decreased bowel motility, increased bowel permeability, and hyperparathyroidism. The day before colonoscopy, all the participants entered a 24-h period of diet that consisted of 4 L of clear fluids with sugar or honey and 90 mL (60 g) of OSP in two 45-mL doses, 5 h apart. Serum phosphate was measured before and after the administration of the laxative. RESULTS:The main demographic data (mean ± SD) were: age, 58.9 ± 8.4 years; height, 163.8 ± 8.6 cm; weight, 71 ± 13 kg; body mass index, 26 ± 4; women, 66%. Serum phosphate increased from 3.74 ± 0.56 to 5.58 ± 1.1 mg/dL, which surpassed the normal value (2.5-4.5 mg/dL) in 87% of the patients. The highest serum phosphate was 9.6 mg/dL. Urea and creatinine remained within normal limits. Post-treatment OSP serum phosphate concentration correlated inversely with glomerular filtration rate (P < 0.007, R 2 = 0.0755), total body water (P < 0.001, R 2 = 0.156) and weight (P < 0.013, R 2 = 0.0635). CONCLUSION:In low-risk, well-hydrated patients, the standard dose of OSP-laxative-induced hyperphosphatemia is related to body weight.

Renal risk associated with sodium phosphate medication: safe in healthy individuals, potentially dangerous in others

“…A possible explanation for the asymmetric sex distribution is that women have lower BMIs than do men, but the OSP dose is usually the same [61,104]. However, dosage alone is not completely responsible for this phenomenon.…”

“…Patients with impaired renal function have been found to have lower phosphaturic capability and may thus develop prolonged hyperphosphatemia after OSP. It has also been documented that the elevation of serum phosphate after OSP positively correlates with a decrease in GFR [2,59,61,62]. Even before APhN had been defined as a nosological unit, case reports had been published describing worsening renal function after OSP in patients with preexisting renal insufficiency [47,48].…”

“…OSP-induced hyperphosphatemia is a consequence of both high phosphate intestinal absorption and decreased renal excretion [6]. Several studies documented an increase in serum phosphate after OSP intake, even in patients with normal renal function, were the average phosphate levels ranged between 1.19 and 2.6 mmol/l [59][60][61][62][63], with the highest phosphate concentrations seen in older subjects [59,61,62].…”

“…Commonly reported risk factors for development of considerable hyperphosphatemia after OSP administration are multiple doses, impaired colon motility, impaired renal function, advanced age, and use of ACEI, ARBs, and diuretics [8,61,62,[68][69][70][71].…”

Preparing for Colonoscopy

“…A prospective study by Casais et al found that hyperphosphatemia in low-risk individuals was related to low weight and can be minimized with adequate hydration. It was their recommendation to prescribe an appropriate NaP dose according to the individual's weight (Casais, M., Guillermo, R-D., Perez, S, et al, 2009). In December 2008, the Federal Drug Administration (FDA) has recommended NaP preparations be removed as an over-the-counter bowel prep to avoid inappropriate use or overdosing, and a black box warning be included in the labels of prescription products warning consumers of the risk of acute phosphate nephropathy.…”