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 18 January 2018

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News

Renal tubular injury in IBD patients receiving 5-aminosalicylic acid

Renal tubular injury is present in acute inflammatory bowel disease prior to the introduction of 5-aminosalicylic acid therapy, claims a team from Canterbury and Carshalton, England.

News image

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The researchers investigated whether markers of early renal disease can assess renal function in inflammatory bowel disease (IBD) patients, who are receiving 5-aminosalicylic acid (5-ASA).

They will report their findings in August's Alimentary Pharmacology & Therapeutics.

The markers measured were urinary albumin, alpha-1-microglobulin (alpha-1-M) and N-acetyl-beta-D-glucosaminidase (NAG), serum cystatin-C, and serum creatinine.

Renal function is typically monitored using serum creatinine. However, significant disease may predate increases in creatinine.

Samples were taken from 21 IBD patients at diagnosis, and at 3-monthly intervals after the commencement of 5-ASA treatment, for 1 year.

Tubular proteinuria is an extra-intestinal manifestation of IBD, irrespective of 5-ASA treatment.
Dr J. S. Fraser

The researchers found that mean creatinine clearance was 100 mL/min and did not change following treatment. IBD was found not to be associated with albuminuria.

Urinary NAD and alpha-1-M at diagnosis were increased in 10 (48%) and 11 (52%) patients, respectively.

5-ASA treatment was not associated with consistent changes in urinary protein excretion.

There was a significant correlation between cystatin C and creatinine clearance both at diagnosis, and combining the initial and follow-up data. However, there was no correlation between creatinine and creatinine clearance.

Dr J. S. Fraser, of the Kent and Canterbury Hospital, Canterbury, said on behalf of the authors, "Tubular proteinuria is an extra-intestinal manifestation of IBD, irrespective of 5-ASA treatment."

"Tubular proteins are not useful predictors of an adverse renal response to 5-ASA.

"Serum cystatin C may be an improved marker of glomerular filtration rate in this setting," it was concluded.

Aliment Pharmacol Ther 2001; 15 (8): 1131-1138
14 June 2001

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