Drug-Induced acute interstitial nephritis: prospective randomized trial comparing oral steroids and high-dose intravenous pulse steroid therapy in guiding the treatment of this condition

الملخص EN

The most important aspect of treating drug-induced acute interstitial nephritis (AIN) is timely discontinuation of the offending drug.

Steroids, oral as well as intravenous (IV), are used in the treatment of drug-induced AIN.

The present study was undertaken to compare the efficacy of oral prednisolone versus IV suprapharmacological doses of corticosteroids in the treatment of drug-induced AIN.

This prospective randomized controlled study included druginduced AIN diagnosed on histopathology over a period of two years.

Patients were randomized to oral prednisolone (Group A) 1 mg/kg for two weeks or pulse methylprednisolone (Group B) 30 mg/kg for three days (maximum 1 g) followed by oral prednisolone 1 mg/kg for two weeks, tapered over two weeks.

Response was reported as complete remission (CR) [improvement in estimated glomerular filtration rate (eGFR) to ≥60 mL/min/1.73 m2], partial remission (PR) (improvement but eGFR <60 mL/min/1.73 m2), or nonresponders to steroids (no CR/PR).

Steroid therapy was instituted to 31 biopsy-proven AIN cases (Group A – 16 and Group B – 15).

Drugs implicated in the causation of AIN included pantoprazole, diclofenac, rifampicin, naproxen, aspirin, imipenem, piroxicam, cefixime, lornoxicam, Chinese herbs, etoricoxib, ciprofloxacin, and phenytoin.

There was no difference in the baseline parameters between the two groups.

At the end of follow-up, 58.06% achieved CR and 41.93% achieved PR.

In Group A, nine (56.2%) achieved CR and seven (43.7%) achieved PR.

In Group B, nine (60%) achieved CR and six (40%) achieved PR.

There was no significant difference between the two groups.

Pulses of high doses of corticosteroids have a significant but transient anti-inflammatory effect.

Both oral and IV suprapharmacological doses of corticosteroids are equally effective in the treatment of drug-induced AIN, if used early.