Acute kidney injury causes

Crystal deposition Particularly important with acyclovir and indinavir, but also noted with sulfonamides, methotrexate and triamterene. This mechanism is becoming more recognized due to the rise in the incidence of tumor-lysis syndrome with AKI. Acute kidney injury caused by tubular obstruction can also occur with a number of drugs (Table 2), due to intratubular precipitation of the... 

Fujita Y, Hasegawa M, Nabeshima K, Tomita M, Murakami K, Nakai S, Yamakita T, Matsunaga K. Acute kidney injury caused by zonisamide-induced hypersensitivity syndrome. Intern Med 2010 49(5) 409-13. 

Traditionally, when searching for the etiology of AKI, the clinician s will subdivides the potential causes of a sudden decline of GFR into one of three general pathophysiologic processes pre renal failure, intrarenal failure or post renal failure [1]. Recently, Miet et al [ 52] in discussing drug-induce acute kidney injury detailed two additional mechanisms that need to be considered in addition to those outlined in Table 2. 

AIN is a relatively uncommon cause of kidney disease, accounting for only 2-3% of all renal biopsies [33-35]. However, in patients with acute kidney injury (AKl) who have normal sized kidneys on ultrasound, AIN is much more common, accounting for up to 27% of biopsies [36]. Omeprazole was fhe first PPl described to cause AIN. In this case, a 74 year old female on omeprazole therapy for 6 months developed fatigue, malaise and was noted to have hematuria, proteinuria and eosinophiluiia [17]. Over the next 12 years, 29 cases of AIN associated with omeprazole were published, 23 of which were biopsy proven [18-23]. In 2004 other PPls were implicated in two large case series that included omeprazole, lansoprazole and pantoprazole [24, 25]. 

Ecstacy (MDMA methylenedioxymethamphetamine) use has been a fast growing new form of drug abuse in the USA and has been implicated as a cause of rhabdomyolysis and acute kidney injury [2]. Ironically, efforts to pre-empt overheating and dehydration... 

Ingestion of large doses of soluble mercuric salts causes acute kidney injury with tubular necrosis and possibly coexisting renal vasospasm [60]. In the 1950 s, when acute treatment with dialysis was not available, the lethal dose of mercuric bichloride, was estimated to range from 2 to 3.5 g [101]. Long-term ingestion of a laxative containing mercurous chloride by two demented patients resulted in renal impairment with... 

Toxin-induced acute kidney injury (AKI) is a common cause of morbidity and mortality in Africa. However reports in the medical literature are limited because in the majority of cases, identification of the precise toxin is missing [1]. 

Seedat, in 1978 [14], concluded that the commonest medical causes of acute kidney injury in the east of South Africa were toxins. The toxins were mainly herbal in nature and the composition of the majority was unknown. However the best studied toxin from this area is the impila [15]. 

ATN associated with the administration of radiographic contrast agents is the third leading cause of hospital-acquired acute kidney injury (Waybill and Waybill 2001 Barrett and Parfrey 2006). The incidence rises from < 2% in patients with low risk to 40-50% in high-risk patients such as those with CKD or diabetes meUitus (Waybill and Waybill 2001 Rudnick et al. 2006 Maeder et al. 2004). The risk of contrast-induced nephrotoxicity increases as the number of risk factors increases, and diabetic patients with CKD have the greatest risk (Rudnick et al. 2006 Murphy et al. 2000). 

More recently referred to as contrast-induced acute kidney injury (CIAKI), contrast medium-induced nephrotoxicity can occur after intravascular administration of iodinated contrast media. It is the third leading cause of acute kidney failure in hospitalized patients in the USA and Europe [11 ]. It leads to prolonged hospital stay and is associated with increased long-term morbidity and mortality. Traditionally it has been defined as an acute rise in serum creatinine by at least 44 pmoUl (0.5 mg/dl) or at least 25% above baseline within 48-72 hours of administration. The incidence is 5-50% [125], depending on the... 

Viral infection The authors report a case in which a child became infected with Epstein-Barr virus developed immune thrombocytopenic purpura, and treatment with anti-D Ig caused intravascular haemolysis as well as acute kidney injury [118 ]. Although some degree of extravascular haemolysis is expected, this case is tmusual because of tile severity and intravascular nature. The authors speculate that the use of intravenous anti-D triggered an xmusual virus-induced immune response that resulted in the pattern of haemolysis seen, which has been reported previously. 

The prevalence of GIN has been found to be as high as the third most common cause of acute kidney injury (AKl) in hospital acquired AKI [20 ]. Yet other studies which included noncontrast enhanced CT patients foxmd that the rate of post-CT AKI was similar between patients who were administered with contrast agents and those who were not [21,22 ]. There is some controversy for the real prevalence of CIN. 

L. Patzer, Nephrotoxicity as a cause of acute kidney injury in children, Pediatr. Nephrol, 2008, 23, 2159-2173. 

Renal ischemia-reperfusion has been shown to induce polyamine catabolism through SSAT and SMOX in both the kidney and liver, resulting in oxidative stress and apoptosis that do not occur in SSAT-deticient animals (Zahedi et al. 2009 Zahedi and Soleimani 2011). Furthermore, endotoxin, or EPS, is a major cause of sepsis-related acute kidney injury, and injection of mice with EPS resulted in inductions of renal SSAT and SMOX. Pharmacological inhibition of polyamine oxidation or ablation of SSAT decreased renal cell damage, implicating the catalysis of... 

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