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, α‐1‐microglobulin [α‐1‐M] and N‐acetyl‐β‐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‐β‐D‐glucosaminidase and α‐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.

SUMMARYAim: To establish whether bone disease is present at diagnosis in inflammatory bowel disease and to identify contributory metabolic abnormalities. Methods: Newly diagnosed patients with inflammatory bowel disease (19 males, 15 females; mean age, 44 years; range, 17-79 years; 23 ulcerative colitis, 11 Crohn's disease) were compared against standard reference ranges and a control group with irritable bowel syndrome (eight males, 10 females; mean age, 40 years; range, 19-64 years). Bone mineral density (g ⁄ cm 2 , dual-energy X-ray absorptiometry: lumbar spine and femoral neck) and biochemical bone markers were measured. Results: Femoral neck bone mineral density, T-and Z-scores (mean ± s.d., respectively) were lower in inflammatory bowel disease patients than in irritable bowel syndrome controls (0.78 ± 0.12 vs. 0.90 ± 0.16, P ¼ 0.0046; ) 0.88 ± 0.92 vs. 0.12 ± 1.17, P ¼ 0.0018; ) 0.30 ± 0.89 vs. 0.61 ± 1.10, P ¼ 0.0030). Lumbar spine bone mineral density and T-scores were also significantly lower in patients than controls (0.98 ± 0.15 vs. 1.08 ± 0.13, P ¼ 0.0342; ) 1.05 ± 1.39 vs. ) 0.14 ± 1.19, P ¼ 0.0304). Compared with controls, the urinary deoxypyridinoline : creatinine ratio was increased (7.66 vs. 5.70 nmol ⁄ mmol, P ¼ 0.0163) and serum 25-hydroxy vitamin D was decreased (18.7 vs. 28.5 lg ⁄ L, P ¼ 0.0016); plasma osteocalcin and serum parathyroid hormone did not differ (P > 0.05). Conclusions: The bone mineral density is reduced at diagnosis, prior to corticosteroid treatment, in both Crohn's disease and ulcerative colitis. Our data suggest that this is attributable to increased resorption rather than decreased bone formation.

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