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Thai Journal of Gastroenterology

Thai Journal of Gastroenterology

2009 Vol.10 No.2

Article :
Biochemical and Physiologic Changes Following Sodium Phosphate Preparation for Colonoscopy


Author :
Yooyongwatana W
Sobhonslidsuk A
Domrongkitchaiporn S
Stitchantrakul W


Abstract :

Background:

 

 

Sodium phosphate (NaP) is widely used for endoscopic bowel preparation. Acute phosphate nephropathy associated with nephrocalcinosis and a reduced glomerular filtration has been increasingly reported after NaP bowel preparation. The aim of this study was to evaluate biochemical and physiologic changes following NaP bowel preparation.

Methods:

Results:

Patients with normal renal function (creatinine level <1.5 mg/dl) who were scheduled for colonoscopy were enrolled in the study. Two doses of 45 ml NaP (phosphate 373.5 mEq/45 ml) followed by 2 liters of water were taken with 12 hours interval apart. Clinical data and blood chemistry were collected at baseline, 24 hours after taking NaP, and 3 days later. Twelve hour urine was collected prior to NaP taking, and after each dose of NaP. Patients with acute elevation of serum creatinine  >0.3 mg/dl was defined as having acute kidney injury (AKI), and their data were compared with those of the entire group.There were 30 patients with age (mean ±SD) of 58.9 ±12.6 years. Twenty-four hours after NaP taking, serum phosphate level increased sharply, contrasting with reducing serum calcium, sodium, potassium, chloride and magnesium levels. Urine acidosis and increased urine excretion of phosphate occurred nearly at the same time. Elevated serum phosphate level returned to baseline 3 days later. There was no change in serum creatinine and parathyroid hormone levels. Two patients developed transient AKI without any other biochemical changes far from the whole group.

Conclusions:

After NaP taking, transient hyperphosphatemia, hypocalcemia, phosphaturia with urine acidosis occurred. Urine acid excretion may be the physiologic response to acute phosphate loading in order to enhance renal phosphate excretion and prevent phosphate nephropathy. Hypocalcemia without increased urine calcium loss may be the effect of calcium-phosphate binding product following hyperphosphatemia. No significantly different parameters were identified in patients who developed AKI. Further study is needed to confirm our observation in this study.


Keyword :


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