Acute kidney injury

Figure 3. Improved renal function in rats with AKI after MSC treatment. Serum creatinine (mean + SD) at baseline and days 1, 2 and 3 after acute kidney injury (AKI) in control animals (/ =6, white bars) and in mesenchymal stem cell treated animals (n=7, black bars). Mesenchymal stem cell treatment led to a significant improvement in renal function on days two and three after AKI, as determined by ftest.

In a model of acute kidney injury we provide the clear evidence that therapy with MSC affords significant renoprotection in rats with I/R ARE. Animals infused with MSC after reperfusion had significantly better renal function, lower renal injury and apoptotic scores, and higher mitogenic indices than vehicle-treated animals ((Lange et al., 2005b Togel et al, 2005). 

Resolvin D series and Protectin D1 mitigate acute kidney injury. J. Immunol. 177 5902-5911. 

In 1982, we classified exercise-related acute renal failure into two types myoglobinuric acute renal failure, as had previously been reported, and non-myoglobin-related acute renal failure (exercise-induced acute renal failure). In 2002, the latter was named ALPE (Acute renal failure with severe Loin pain and Patchy renal ischemia after anaerobic Exercise) [4]. The term acute kidney injury (AKI) has recently been proposed as a patho-physiologically more correct alternative to the term acute renal failure. Therefore, exercise-induced acute renal failure in this book may be replaced by exercise-induced acute kidney injury. 

Stevens P (2007). Assessment of patients presenting with acute renal failure (acute kidney injury). Medicine 35 429-433... 

Mechanisms of drug induced acute kidney injury... 

Acute kidney injury (AKI) is easily defined as a syndrome characterized by a sudden decrease in GFR accompanied by azotemia [4]. However the reported incidence of AKI varies depending on a number of independent variables. For example, was the patient population surveyed derived from a community wide database or was it restricted to hospitalized patients What definition was adopted to designate acute kidney injury (AKI) The lack of a universally agreed upon definition of acute kidney injury (AKI), makes it difficult to compare clinical reports as to the incidence. 

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. 

Table 2. Classification of various drugs based on pathophysiologic categories of acute kidney injury.

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... 

Osmotic nephrosis When the proximal tubules are exposed to hyper osmotic, non-reabsorbable solutes such as mannitol, osmotic nephrosis can lead to AKI. [69]. More recently the use of hy-droxyethylstarch for resuscitation of hypotensive patients has been associated with increased incidence of AKI [70] The addition of sugar excipients to Intravenous immunoglobulin s, while reducing the constitutional symptoms associated with their administration have increased in the risk of acute kidney injury [71]. 

Zhang et al [79] recently reported the results of renal biopsies in 104 cases of acute kidney injury complicating CKD. Drug related acute tubulointerstitial neprhritis accounted for 31% of all cases, while an additional 5% had evidence of drug-related acute tubular necrosis by biopsy. NSAIDs were the most common drug responsible for the AKI. 

Acute kidney injury has been associated with the use of ACE inhibitors in patients with heart failure, renal artery stenosis and acute volume depletion... 

Warnock DG Toward a definition and classification of acute kidney injury. J Am Soc Nephrol 2005 16 3149-3150... 

All T, Khan I, Simpson W, Puscatt G, Townsend J, Smith W and MacLeod A. incidence and outcome in acute kidney injury a comprehensive population-based study. J Am Soc Nephrol 2007 18 1292-1298. 

ChertowGM, Burdick E, Flonour M, Bonventre JV, Bates DW Acute Kidney Injury, Mortality, EengthofStayand Costs in Elospital-ized Patients. J Am Soc Nephrol 2005 16 3365-70... 

Drug-associated acute kidney injury in the intensive care unit... 

Specific strategies to reduce the incidence of acute kidney injury References ... 

Acute kidney injury may be due to tissue parenchymal injury as manifested by direct tubule toxicity, acute interstitial nephritis, osmotic nephrosis and thrombotic microangiopathy. 

Despite the significant progress made in understanding the biology and mechanisms of acute kidney injury (AKI) in animal models, translation of this knowledge into improved management and outcomes for patients has been limited. In fact, with few exceptions pharmacological therapies to prevent AKI have not been successful. Thus, prevention of AKI must be a priority to avoid the morbidity and mortality associated with this event. 

Hoste EA, Ciermont G, Kersten A,Venkataraman R, Angus DC, De Bacquer D, and Keiium J.. 2006. RiFLE criteria for acute kidney injury are associated with hospitai mortaiity in criticaiiy iii patients a cohort anaiysis. Cnf Core 10 R73. 

Schetz M, Dasta J, Goidstein S, and GoiperT. 2005. Drug-induced acute kidney injury. CurrOpin Crit Care 11 555-565. 

Brewster UC, and Perazella MA. 2007. Acute kidney injury following proton pump inhibitor therapy. Kidney Int 71 589-593. 

Rosner MFI, and Okusa MD. 2006. Acute kidney injury associated with cardiac surgery. Clin. J. Am. Soc. Nephrol. 1 19-32. 

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