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NDT Advance Access originally published online on June 25, 2007
Nephrology Dialysis Transplantation 2007 22(10):2757-2762; doi:10.1093/ndt/gfm404
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


Acute renal failure in HIV patients

Hassane Izzedine, Alain Baumelou and Gilbert Deray

Department of Nephrology, Pitie-Salpetriere Hospital, Paris, France

Correspondence and offprint requests to: Dr Hassane Izzedine, Department of Nephrology, La Pitié-Salpetrière Hospital, 47-80 Boulevard de I'Hopital, Assistance Publique-Hopitaux de Paris, Pierre et Marie Curie University, 75013 Paris-France; or Email: hassan.izzedine@psl.aphp.fr

Keywords: acute tubular necrosis; HAART; HIV

The first 150 words of the full text of this article appear below.



   Introduction
 
Acute Kidney Injury (AKI) is the generic term for an abrupt and sustained decrease in renal function, resulting in retention of nitrogenous (urea and creatinine) and non-nitrogenous waste products [1]. As renal failure is often asymptomatic, it must be detected by carefully tracking the serum creatinine level. Early recognition is critical. The earliest manifestations of AKI may be subtle. Losing the function of one half of the nephron mass will cause creatinine to rise from about 0.7 mg/dl only up to ~1.4 mg/dl. In general, the threshold used to identify AKI is a rise in the serum creatinine level ≥1.0 mg/dl, but smaller elevations should be taken as early signs of trouble [2]. The major cause of intrinsic renal azotaemia is acute tubular necrosis (ATN). Pre-renal azotaemia and ischaemic ATN occur on a continuum of the same pathophysiological process and together account for 75% of the . . . [Full Text of this Article]



   Epidemiology
 
Underlying mechanisms


   Conclusion
 

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