Tuesday, July 6, 2010

Does Bowel Prep Before Colonoscopy Put Kidney at Risk?

Tags: Colonoscopy Risk Kidney from Use of Oral Sodium Phosphate? 1.4% Risk, Age Related

Any medical procedure involves risk with surgery being one percent risk of death, mostly from anesthesia. Even patients who have normal kidney function are susceptible to oral sodium phosphate damage. Family incidence of colon cancer, your diet over a significant amount of years, and check of your vitals are necessary before deciding whether to take the test or not.

Whether I take my third test will depend on whether there is a safer alternative means to efficiently clean out my intestines for the test.

My guess is that your kidneys health should be checked with a calculated efficiency of the kidneys with a blood test of critical indicators such as creatinine. I recommend a Comprehensive Blood Test and a Metabolic Comprehensive Test. A check for uric acid, blood lipids, vitamin D (Ideally at least 50 nanograms/ml well above the usual 30 before the introduction of UVB sunscreens which stop your skin from producing vitamin D from UVB. 15-30 minutes exposure a few times a week during the summer and fall may be adequate as determined by your concentration of 25-hydroxy-vitamin D.

Family colon cancer history, diet, and other health considerations need to be considered.

Good Luck!

jim kawakami, July 6, 2010, http://jimboguy.blogspot.com

From Nature Clinical Practice Nephrology

Is Bowel Preparation Before Colonoscopy a Risky Business for The Kidney?

Yeong-Hau H. Lien, MD http://cme.medscape.com/viewarticle/580522 Nov 2008

  1. Summary and Introduction
  1. Patterns of Acute Kidney Injury Induced by Oral Sodium Phosphate
  2. Acute Phosphate Nephropathy After Standard Dose of Oral Sodium Phosphate
  3. Incidence of and Risk Factors For Acute Phosphate Nephropathy
  4. Electrolyte Abnormalities After Use of Oral Sodium Phosphate
  5. Pathogenesis of Acute Phosphate Nephropathy
  6. Recommendations to Minimize the Renal Risks of Oral Sodium Phosphate
  7. Conclusions
  8. Key Points
  1. References

Summary and Introduction


Acute phosphate nephropathy after bowel preparation with oral sodium phosphate (OSP) for colonoscopy has emerged as an important clinical entity. In 2004, five cases of nephrocalcinosis and irreversible renal failure after bowel preparation with OSP were reported. More recently, several retrospective studies have shown that the incidence of acute kidney injury after OSP use is in the range of 1-4%, similar to the incidence of contrast nephropathy in the general population. The degree of renal failure is not generally as severe as in the first reported cases, but irreversible damage can still occur.

Millions of people worldwide undergo screening colonoscopies for colon and rectal cancer after the age of 50, so careful patient selection and monitoring for possible complications is essential when OSP is used. In addition to educating patients about the possibility of renal damage, physicians should routinely watch for considerable weight loss during bowel preparation and correct the fluid deficit as needed. Carrying out a renal function panel, which includes serum phosphorus level, is prudent after colonoscopy. Alternative bowel cleansing agents are needed because calcium phosphate precipitation is inevitable after OSP use even in the normal kidney.


Routine screening for colon and rectal cancer after the age of 50 by use of colonoscopy has been one of the most successful public health projects worldwide. As a result of improvements in colonoscopy technology, bowel preparation is now the least tolerable part of the procedure, so gastroenterologists have been searching for more tolerable, efficient, and economic ways to cleanse the bowel.

At present, oral sodium phosphate (OSP) solution is favored.[1] The initially reported adverse effects of this agent were unremarkable, particularly in patients with normal kidney and gastrointestinal function.[2] However, the attractive safety profile of OSP has been questioned recently following a series of cases of OSP-induced acute and irreversible renal failure.[3]

This disease has been named acute phosphate nephropathy (APN)[3,4] because renal biopsy uniformly revealed nephrocalcinosis. These and subsequently reported cases of APN[5,6] raised such concern that the FDA issued a warning about the use of OSP in patients with chronic kidney disease (CKD) or major cardiovascular comorbidities.

Several retrospective studies have been performed in order to facilitate a better understanding of APN. Unfortunately, the results of these studies are quite differing, adding to the controversy over the safety of OSP. This uncertainty about the toxicity of OSP clearly increases the anxiety of those who are scheduled to undergo elective colonoscopy and their physicians, and the lack of clear instructions regarding the use of OSP for bowel preparation further increases the level of uneasiness. The purpose of this Review is to provide a nephrologist’s perspective on the pathogenesis, risk factors, and prevention of APN, based on the current literature.

Patterns of Acute Kidney Injury Induced by Oral Sodium Phosphate

Two patterns of OSP-induced acute kidney injury (AKI) can be distinguished: early symptomatic, and late insidious ( Table 1 ).[5] The former presents as an acute illness that manifests as changes in mental status, tetany, or cardiovascular collapse, usually within hours of bowel preparation. Patients have marked hyperphosphatemia (4.5-19.4 mmol/l) and hypocalcemia (1.0-1.7 mmol/l) and require urgent fluid resuscitation, rapid correction of electrolyte abnormalities, and even hemodialysis.

Outcomes vary—some patients show excellent recovery of renal function, while others develop CKD or die soon after the onset of symptoms. The second pattern of AKI is insidious onset of renal failure days or months after colonoscopy.[3] At the time of diagnosis, serum phosphorus and calcium levels are normal or near normal unless APN is detected within 3 days of bowel preparation.[7]

None of these patients recover their renal function completely and some even progress to end-stage renal disease. The major difference in bowel preparation between these two groups of patients is that those with early symptomatic AKI received a much higher phosphate load than the standard dose.[2,5,8] Their symptoms are mainly related to hypocalcemia, and, if managed promptly and aggressively, recovery of renal function is possible. In patients whose presentation is insidious, the opportunity to remove renal calcium phosphate precipitates is often missed, and CKD develops. ... http://cme.medscape.com/viewarticle/580522

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