Nephrotoxicity from Medical Treatment

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Renal toxicity is unusual with the drugs commonly utilised to treat IBD [91-95], buthappens more frequently during treatment with cyclosporine, with reported incidence of up to 19% [96-98]. However, the risk of irreversible damage is very low if cyclosporine dosage does not exceed 5 mg/kg/day and if the creatinine level does not increase over 30% of the normal level [99]. Results from a review showed that a >30% increase in serum creatinine was present in 6% of patients treated with oral or intravenous cyclosporine, but the value returned within the normal range after suspension of the therapy in all of the patients except one [100]. Nephrotoxicity of cyclosporine is not related to duration of treatment but rather to its concentration [99, 101], so this drug should always be started at a low dosage and then adjusted on the basis of close monitoring of the serum creatinine level. Its use is not indicated in patients with impaired renal func

Fig. 4. Left-side ureteral obstruction secondary to Crohn's colitis. a Preoperative intravenous pyelography showing a dilated ureter with smooth cone-shaped restriction at the pelvic brim. b Intraoperative identification of the ureter after mobilization of descending and sigmoid colon. c iv pyelogram 6 months after resection of the affected bowel demonstrating a resolution of ureteral obstruction tion and in association with other potential nephrotoxic drugs [100].

Glomerulonephritis and interstitial nephritis have also been described, although with a very low incidence, after long-term administration of aminosalicylates (ASA) [102-105]. In a series of 2 940 patients on mesalamine, only 0.3% developed mild signs of nephrotoxicity [106]. Another prospective survey among 27 European centres found that only 13 (0.8%) of 1529 patients on 5-ASA therapy, only 13 (0.8%) had renal impairment [107]. Sulphasalazine is even safer and it has been successfully given in patients who developed interstitial nephritis with mesalamine [108]. The mechanism of ASA toxicity is unknown. The fact that its occurrence is so uncommon and that it is not related to dosage or duration of treatment, has suggested that the reported cases might have been rather secondary to a hypersensitivity reaction [103, 106]. Permanent damages can be avoided with early recognition of nephropathy and prompt discontinuation of the responsible drug [103, 104].

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