A systematic review of the literature in 2008 demonstrated no difference in outcomes between the use of intermittent hemodialysis and continuous venovenous hemofiltration (CVVH) (a type of continuous hemodialysis). Among critically ill patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis. However, other clinical and health economic studies demonstrated that, initiation of CRRT is associated with a lower likelihood of chronic dialysis and was cost-effective compared with IRRT in patients with acute kidney injury. Complications
Metabolic acidosis, hyperkalemia, and pulmonary edema may require medical treatment with sodium bicarbonate, antihyperkalemic measures, and diuretics. Lack of improvement with fluid resuscitation, therapy-resistant hyperkalemia, metabolic acidosis, or fluid overload may necessitate artificial support in the form of dialysis or hemofiltration. However, oliguria during anesthesia may predict AKI, but the effect of a fluid load is highly variable. Striving toward a predefined urine output  target to prevent AKI is futile. Early recovery of AKI
AKI recovery can be classified into three stages 1–3 on the basis of the inverse of the AKI KDIGO serum creatinine criteria. Prognosis
Mortality
Mortality after AKI remains high. AKI has a death rate as high as 20%, which may reach up to 50% in the intensive care unit (ICU). Each year, around two million people die of AKI worldwide.AKI develops in 5% to 30% of patients who undergo cardiothoracic surgery, depending on the definition used for AKI.
Both kidneys need to be affected as one kidney is still more than adequate for normal kidney function. Notable causes of prerenal AKI include low blood volume (e.g., dehydration), low blood pressure, heart failure (leading to cardiorenal syndrome), hepatorenal syndrome in the context of liver cirrhosis, and local changes to the blood vessels supplying the kidney. The latter include renal artery stenosis, or the narrowing of the renal artery which supplies the kidney with blood, and renal vein thrombosis, which is the formation of a blood clot in the renal vein that drains blood from the kidney. Intrinsic or renal
Intrinsic AKI refers to disease processes which directly damage the kidney itself. Intrinsic AKI can be due to one or more of the kidneys structures including the glomeruli, kidney tubules, or the interstitium. Common causes of each are glomerulonephritis, acute tubular necrosis (ATN), and acute interstitial nephritis (AIN), respectively. Other causes of intrinsic AKI are rhabdomyolysis and tumor lysis syndrome. Certain medication classes such as calcineurin inhibitors (e.g., tacrolimus) can also directly damage the tubular cells of the kidney and result in a form of intrinsic AKI. Postrenal
Postrenal AKI refers to acute kidney injury caused by disease states downstream of the kidney and most often occurs as a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasia, kidney stones, obstructed urinary catheter, bladder stones, or cancer of the bladder, ureters, or prostate. Diagnosis
Definition
Introduced by the KDIGO in 2012, specific criteria exist for the diagnosis of AKI.