Withdrawal Of Non-steroidal Anti-inflammatory Drugs Research Articles

Raised plasma renin and prorenin in rheumatoid vasculitis.

The value of plasma renin and its inactive precursor, prorenin, were examined as a marker for vasculitis in rheumatoid arthritis (RA). Plasma renin and prorenin rise when the renin-angiotensin system is activated; an isolated increase of prorenin may be a marker for microvascular complications in diabetes mellitus. Renin concentrations in plasma obtained from 34 patients with RA (seven with vasculitis, 27 controls) were measured under standard conditions, before and five days after stopping non-steroidal anti-inflammatory drugs; creatinine clearance was also measured. At first the median renin concentration in the patients with vasculitis was 19 (range 12-63) mU/l (normal less than 61 mU/l) and in the controls 9 (3-43) mU/l. The median prorenin concentration in patients with vasculitis was 233 (144-428) mU/l (normal less than 358 mU/l) and in the controls 144 (25-364) mU/l. Renin and prorenin concentrations increased significantly in both groups after withdrawal of nonsteroidal anti-inflammatory drugs. The creatinine clearance was similar in both groups and did not correlate with renin concentrations. In conclusion, it was found that, unlike patients with diabetes mellitus, patients with RA with vasculitis had slightly raised concentrations of both renin and prorenin. These findings signal activation of the renin-angiotensin system and might indicate early cardiac or renal involvement by vasculitis.

NON-STEROIDAL ANTI-INFLAMMATORY DRUGS AND RENAL FAILURE

In 3 years seventeen patients presented to one unit with renal failure associated with the use of non-steroidal anti-inflammatory drugs (NSAID). Seven patients presented with acute renal failure, in four due to acute tubular necrosis and in three to acute interstitial nephritis; all recovered when NSAID treatment was stopped. Four patients presented with symptomless renal impairment discovered during routine follow-up in a rheumatology clinic; again all improved on withdrawal of NSAID. The remaining six patients presented with chronic renal failure, a disorder not previously associated with NSAID treatment. The pattern of renal disease associated with NSAID may be more extensive than has previously been recognised. A history of NSAID use should be sought in all patients presenting with unexplained renal failure.

Small Bowel Ulceration in Patients Receiving Non-Steroidal Anti-inflammatory Drugs for Rheumatoid Arthritis

Evidence is presented for a non-specific ulcerative process in the small bowel of patients with rheumatoid arthritis. All three cases presented with lower gastrointestinal bleeding; on withdrawal of non-steroidal anti-inflammatory drugs no further bleeding occurred. Non-steroidal anti-inflammatory drugs may lead to small bowel ulceration in inhibiting mucosal glycoprotein synthesis and increasing intestinal permeability.

Renal Changes in Systemic Lupus Erythematosus

To the Editor.— Dr Cunningham and associates, in theArchives(138:1560-1561, 1978), reported an interesting case of systemic lupus erythematosus (SLE) and transient changes in renal function, which they attribute to lupus interstitial nephritis. While this interpretation is intriguing in view of the emerging recognition of lupus interstitial renal disease,1an alternative explanation of the patient's deteriorating condition and response to is possible. Aspirin and other nonsteroidal antiinflammatory drugs (NSAID) may cause acute elevations of serum creatinine value and BUN level with decreased glomerular filtration rate,2.3which may occasionally mimic incipient acute renal failure.4These changes are rapidly reversible when the drug therapy is discontinued, but the recovery of renal function may be confused with a therapeutic effect of corticosteroids initiated at the time of NSAID withdrawal.2Patients with SLE appear to be more susceptible to this effect than normal subjects, especially if there is