Background NSAID are the major pathogenic agents in the treatment of patients with inflammatory and degenerative arthropathies. Their use is associated with multiple side effects, such as: Gastrointestinal bleeding, worsening of accompanying Arterial hypertension, Heart Failure and Ishemic Heart disease and dysfunction of the liver and kidney. Types of nephrotoxicity caused by NSAID are: nephropathy, papillary necrosis and kidney insufficiency.
Objectives The aim of this study is to reveal the frequency of NSAID neuphrotoxicity at optimum therapy duration
Methods We studied 187 subjects with degenerative and inflammatory arthropathies (102 with degenerative disease at mean age of 45 and 85 with inflammatory arthropathy at mean age 67) at different NSAID therapy (Diclofenac sodium 150 mg/daily, Aceclofenac 200mg/daily and Naproxen 1000mg/daily) with mean duration of the therapeutic course as it shown:
Subjects with inflammatory arthropathy- 7 courses per year with mean duration of one course 23 days.
Subjects with degenerative arthropathies-6 courses per year with mean duration of one course 17 days.
Results Inthe group with inflammatory arthropathy, nephrotoxicity were established in 6patients. One patient at Aceclofenac therapy for 6 months presented with reversible nephritic syndrome, hypercholesterolemia (8.7mmol/L), low-grade hypoproteinaemia, creatine up to 147 mmol / l, creatine clearance up to 10 ml /sec and non-selective proteinuria (1.250 gr/24h). After exclusion of NSAID drugs regimen of the kidney function was achieved with persistence of low-grade proteinuria up to 0.560 g / 24h. Five of these patients were with non-selective proteinuria ( 0.650 to 0.520 g / 24 h) and normal glomerul filtration rate. Four patients from these group were with accompanying arterial hypertension, and two of the group were with tubulointerstitial nephritis.
In the group with degenerative arthropathy, nephrotoxicity were established in 29 patients and only four of them were without accompanying diseases. In 16 patients there were impairment of the kidney function: glomerul filtration (26 ml/sec), creatine (156-210 mmol/L), low-grade proteinuria (0.624g/24h) without fully regiment of the kidney function after exclusion of the NSAID drugs. Accompanying tubulointerstitial nephritis were established in 19 patients, and 16 of them were with arterial hypertension also and the rest three patients were with Chronic kidney insufficiency.
Conclusions The uncontrolled intake of COX-1 inhibitors from the NSAID group are associated with reduction of prostaglandin synthesis and consequent reduction of kidney blood flow which lead to renal dysfunction. The kidney impairment is reversible when the treatment discontinue but only in patients without accompanying disease and renal pathology. Nephrotoxicity is very common side effect in polymorbidic patients despite of the lasting of NSAID treatment course. Thus individual approach to each patient have to be found.
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Disclosure of Interest None Declared