The Journal of rheumatology · 1994
Subclinical renal toxicity in rheumatic patients receiving longterm treatment with nonsteroidal antiinflammatory drugs.
Сравнительное исследованиеСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Calvo-Alén J, De Cos M A, Rodríguez-Valverde V, Escallada R, Florez J, Arias M
Аннотация
OBJECTIVE: To study the possible renal toxicity of longterm treatment with nonsteroidal antiinflammatory drugs (NSAID), in a population of patients with rheumatic diseases.
METHODS: Comparative study of 104 patients treated for more than 2 years with NSAID and 123 healthy controls, nonusers of these drugs. After fasting during 12 h the following tests were performed in both groups: urinalysis, creatinine clearance, osmolar clearance, negative free water clearance, and urinary excretion of sodium.
RESULTS: In the patient group the urinary pH was higher than in the controls (5.9 +/- 0.7 versus 5.2 +/- 0.6 p < 0.05) and in addition, they had an impaired renal concentration capacity, as it is shown by a significant decreased urinary density (1018.6 +/- 4.7 vs 1026.3 +/- 5.4 in the controls p < 0.05), a decreased urinary osmolality (502.1 +/- 150.7 vs 661.6 +/- 157.6 mOsm/ml p < 0.001), a lower osmolar clearance (1.26 +/- 0.25 ml/min vs 1.83 +/- 0.4 ml/min p < 0.001) and an increased free water clearance (-0.21 +/- 0.40 ml/min vs -0.98 +/- 0.41 ml/min, p < 0.001). This renal impairment was related to the cumulative intake of NSAID:
CONCLUSION: The longterm treatment with NSAID is able to produce a subclinical renal dysfunction, consistent with the early stages of analgesic nephropathy.
METHODS: Comparative study of 104 patients treated for more than 2 years with NSAID and 123 healthy controls, nonusers of these drugs. After fasting during 12 h the following tests were performed in both groups: urinalysis, creatinine clearance, osmolar clearance, negative free water clearance, and urinary excretion of sodium.
RESULTS: In the patient group the urinary pH was higher than in the controls (5.9 +/- 0.7 versus 5.2 +/- 0.6 p < 0.05) and in addition, they had an impaired renal concentration capacity, as it is shown by a significant decreased urinary density (1018.6 +/- 4.7 vs 1026.3 +/- 5.4 in the controls p < 0.05), a decreased urinary osmolality (502.1 +/- 150.7 vs 661.6 +/- 157.6 mOsm/ml p < 0.001), a lower osmolar clearance (1.26 +/- 0.25 ml/min vs 1.83 +/- 0.4 ml/min p < 0.001) and an increased free water clearance (-0.21 +/- 0.40 ml/min vs -0.98 +/- 0.41 ml/min, p < 0.001). This renal impairment was related to the cumulative intake of NSAID:
CONCLUSION: The longterm treatment with NSAID is able to produce a subclinical renal dysfunction, consistent with the early stages of analgesic nephropathy.