## Basic introduction:
- AKI is defined as an acute or subacute decline in the glomerular filtration rate and/or tubular function that is characterized by azotemia
- It is an abrupt loss of renal function that develops within a period of about 7 days
## Causes of AKI:
- Pre-renal AKI (is responsible for more than 90% of AKI): diuretic therapy; burns; diarrhea; vomiting; heart failure; pancreatitis; liver disease with ascites; and peritonitis
- Diseases of renal arteries and veins: dissecting aortic aneurysm; and trauma to renal vessels
- Intrinsic renal causes -
_Glomerulonephritis: nephritogenic strain of β-hemolytic streptococci; drug toxicity such as gentamycin, methicillin, and NSAIDS among other
_Acute interstitial nephritis: Drugs such as NSAIDs, infections; autoimmune diseases.
_Acute tubular necrosis: prolonged ischemia; volume depletion; toxins
_Intratubular obstruction: rhabdomyolysis; uric acid neuropathy
- Post renal (mainly obstruction of collection system): bladder outlet obstruction (mainly by tumors); bilateral ureteral obstruction; ureteral obstruction in single kidney; calculus; pelvic malignancy; retroperitoneal fibrosis; urethral stricture, prostatic hypertrophy or malignancy; papillary necrosis and radiation fibrosis.
## Risk factors for AKI:
- Co-morbidity with chronic kidney disease (CKD), heart failure, diabetes, liver disease etc.
- Past history of AKI
- Old age (65yrs and above)
- Use of renal toxic drugs such as aminoglycosides, ACE inhibitors, ARB, diuretics and NSAIDS
- Peri-operative period
- Recent use of iodinated contrast agents