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Portuguese Journal of Nephrology & Hypertension

versão impressa ISSN 0872-0169

Resumo

JABUR, Wael Lateef. NSAID-related renal tubular dysfunction, an old new conundrum. Port J Nephrol Hypert [online]. 2012, vol.26, n.4, pp.285-289. ISSN 0872-0169.

Aim.To report on ten patients who presented withacute kidney injury secondary to nonsteroidal anti-inflammatory drug administration. Renal tubular function test was consistent with acute tubular necrosis; however kidney biopsy in two of them revealed a normal ultrastructural finding, which along with the atypical clinical course refuted the suggested diagnosis. The constellation of features pointed to a clear reversible tubular dysfunction in the absence of tubular necrosis, highlighting a peculiar mechanism that might provoke acute kidney injury, involving the inhibition of the prostaglandin, the integral mediator of the tubular function, in addition to its role in maintaining the perfusion of the glomeruli and supporting the function of the macula densa. Conclusively a potential mechanism, apart from acute tubular necrosis and haemodynamic renal failure, was considered in this cohort of patients to explain nonsteroidal anti-inflammatory drug-related AKI, with an elaborate discussion of the particular findings of renal tubular function test, focusing on the probable physiological aberration that might culminate in nonsteroidal anti-inflammatory drug-related nephropathy. Patients and Methods. Ten patients attended the NMC specialty hospital in Dubai from 2006 through 2011 with acute kidney injury secondary to nonsteroidal anti-inflammatory drug use, which developed within 2-5 days. The main complaints were abdominal pain, nausea and vomiting. Blood pressure was elevated in all of them. Renal tubular function test revealed characteristic findings in all of them. Kidney biopsy was performed in two patients. Results. Investigations revealed prominent renal tubular dysfunction suggestive of acute tubular necrosis, with high sodium fractional excretion of 3-5 %, high uric acid fractional excretion of 12-13 %, urine osmolality to plasma osmolality ratio of 1, urine creatinin to plasma creatinin ratio of 16, and urine specific gravity of 1.010-1.020. However kidney biopsy in two of them showed normal renal tubular architecture, which in combination with the short-term, reversible course of the kidney injury in the rest of the patients coincided with nonstructural acute renal tubular dysfunction. Management was supportive. Most of them improved within 5-7 days and two of them improved within 40-45 days. Conclusion. This report highlights that renal tubular dysfunction might be the consistent primary lesion in some of the cases of nonsteroidal anti-inflammatory drug-related acute kidney injury, notwithstanding that acute tubular necrosis and interstitial involvement were evidently excluded. This might be a new explanation for the mechanism of renal failure in patients with otherwise normal renal function

Palavras-chave : Acute kidney injury (AKI); acute renal tubular dysfunction; nonsteroidal anti-inflammatory drugs (NSAID).

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