SUMMARY BackgroundPatients attending for endoscopy are generally anxious and worried.

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 study 5-aminosalicylate nephrotoxicity in patients with inflammatory bowel disease in the UK.

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Proton pump inhibitors are an important iatrogenic cause of acute kidney injury

Background-In patients with chronic heart failure there is no relation between

1. The regional haemodynamic effects of intravenous bolus doses of captopril, enalaprilat and lisinopril were assessed in conscious Brattleboro (i.e. vasopressin-deficient) rats, chronically instrumented with miniaturized pulsed Doppler probes and intravascular catheters. 2. Responses to incremental doses of each drug (spanning the median effective dose for the inhibition of the pressor response to angiotensin I) were examined in both water-replete and water-deprived states. 3. In the water-replete state, the haemodynamic profiles of captopril, enalaprilat and lisinopril were generally similar, with incremental doses causing rises in mesenteric and renal flow and, to a lesser extent, hindquarters flow. There were small tachycardias and only slight falls in mean blood pressure. 4. In the water-deprived state, the effects of all three drugs were greatly enhanced; tachycardic and hypotensive effects occurred together with increases in mesenteric, renal and hindquarters flows. However, for renal flow and renal vascular conductance the effectiveness of the drugs decreased in the order enalaprilat greater than captopril greater than lisinopril, whereas for mesenteric flow and mesenteric vascular conductance the order was captopril greater than enalaprilat greater than lisinopril. 5. Since marked haemodynamic actions were seen with doses one-tenth of the median effective dose for the inhibition of the pressor effect of angiotensin I, it is likely these effects were due to inhibition of angiotensin-converting enzyme, although not necessarily to inhibition of angiotensin II production.(ABSTRACT TRUNCATED AT 250 WORDS)