The four reported cases were diagnosed at a children's hospital. None of the children had pre‐existing renal disease and all four had documented normal renal function during the preceding 24–48 h. NSAID treatment in therapeutic doses preceded the ARF in each patient. The drug, highest serum urea and creatinine, and time to normalisation of the renal parameters are given in table 1. The patients were treated by stopping the relevant NSAID and intravenous rehydration which led to rapid normalisation of renal function in three of the four patients.
Table 1Patient details
Patient 1 was a 13 year old girl with Crohn's disease of 1 year's duration. She presented to her local hospital with a relapse of Crohn's disease. She was mildly dehydrated clinically. She was treated with intravenous hydrocortisone, mesalazine, cefotaxime and metronidazole. She received four doses of 50 mg diclofenac sodium per rectum for analgesia following which she became anuric. Within 36 h of presentation to her local hospital, her serum creatinine had risen from 87 to 360 μmol/l. Her serum potassium had risen to 5.6 mmol/l. Her haemoglobin was 10.2 g/dl and platelet count was 200×109/l. Her blood film was normal. Her serum urea was 22 mmol/l and creatinine rose further to 629 μmol/l over the next 24 h. An ultrasound scan of her kidneys was normal.
An autoimmune screen including ANA, dsDNA, p and c ANCA, anti Sm, anti GBM and anti‐mitochondrial antibodies was negative. Immunoglobulins were normal. Renal biopsy demonstrated acute cortical haemorrhagic infarction with medullary sparing and acute tubular necrosis. There were no histopathological features of interstitial nephritis (fig 1).
Figure 1Extensive necrosis of the renal cortex of patient 1 (haematoxylin and eosin, original magnification ×40). Inset shows necrotic tubules (haematoxylin and eosin, original magnification ×400).
The patient was treated with haemodialysis for 26 days and her renal function remains mildly impaired 3 years later with a predicted GFR of 75 ml/min/1.73 m2 and persistent proteinuria with an albumin:creatinine ratio of 26.6 mg/mmol creatinine.
Patient 2 was a 7 year old boy with recently diagnosed systemic juvenile idiopathic arthritis (JIA). He had been symptomatic for 4 weeks and had fasted for the insertion of a Broviac line. He was on ibuprofen (10 mg/kg/dose 8 hourly) and indomethacin (25 mg 12 hourly) for 48 h preceding the surgery. He had never been treated with methotrexate. He received per rectal diclofenac sodium post‐operatively. He became clinically mildly dehydrated as a result of vomiting post‐operatively. He was treated with intravenous rehydration after which his serum urea and creatinine normalised over the next 3 days.
Patient 3 had undifferentiated JIA for 5 years and had been on methotrexate (15 mg/m2) for 6 months, prednisolone forte and diclofenac sodium (75 mg 12 hourly). He developed shingles with vomiting and was treated with intravenous acyclovir. Clinically, he was slightly dehydrated. He was treated with intravenous rehydration and his renal profile normalised over 4 days in spite of continuing treatment with intravenous acyclovir.
Patient 4 was a 13 year old boy who had a craniopharyngioma resected. He was given regular oral diclofenac sodium as post‐operative analgesia (50 mg 8 hourly). He developed diabetes insipidus 48 h after surgery. He was given 250 μg of intravenous desmopressin 12 hourly for 24 h prior to the onset of his renal impairment. The maximum negative balance while on diclofenac sodium was 570 ml. He was treated with intravenous rehydration after which his serum urea and creatinine normalised over the next 5 days.