Renal tubular injury is present in acute inflammatory bowel disease prior to the introduction of drug therapy

Background: 5-aminosalicylic acid (5-ASA) has been associated with renal complications in inflammatory bowel disease. Renal function is typically monitored using serum creatinine; however, significant disease may predate increases in creatinine. Aims: To identify whether markers of early renal disease (urinary albumin, alpha -1-microglobulin [alpha -1-M] and N-acetyl-beta -D-glucosaminidase [NAG], and serum cystatin C) are useful in the assessment of renal function in inflammatory bowel disease patients receiving 5-ASA. Methods: Twenty-one patients with a new diagnosis of inflammatory bowel disease were investigated. Samples were taken at diagnosis, and at 3-monthly intervals after the commencement of 5-ASA, for 1 year. Results: Mean creatinine clearance was 100 mL/min and did not change following treatment. Inflammatory bowel disease was not associated with albuminuria. Urinary N-acetyl-beta -D-glucosaminidase and alpha -1-microglobulin at diagnosis were increased in 10 (48%) and 11 (52%) patients, respectively: 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 (r=-0.533, P=0.0275) and combining the initial and follow-up data (r=-0.601, P < 0.01), but not between creatinine and creatinine clearance (P > 0.05). Conclusions: Tubular proteinuria is an extra-intestinal manifestation of inflammatory bowel disease 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.