Snapshot A 56-year-old man presents with lower abdominal pain. His symptoms have progressively worsened over the course of the day. Medical history is significant for benign prostatic hyperplasia on tamsulosin. His blood pressure is 144/106 mmHg (normally, his blood pressure is 120/80 mmHg). On physical examination he has bladder distension. Laboratory testing is significant for a creatinine of 2.4 mg/dL (last serum creatinine was 0.7 mg/dL.) Introduction Clinical definition acute reduction in glomerular filtration rate (GFR) recall that GFR represents the sum of the filtration rates of nephrons therefore, GFR reflects functioning renal mass Epidemiology risk factors hypertension chronic kidney disease dehydration and volume depletion diabetes chronic liver or lung disease Etiology prerenal causes decreased renal perfusion (e.g., hemorrhage, congestive heart failure, and diuretic use) intrarenal causes acute tubular necrosis ischemia and toxic causes interstitial nephritis glomerulonephritis vasculitis hemolytic uremic syndrome postrenal causes urinary flow obstruction (e.g., benign prostatic hyperplasia and nephrolithiasis) Pathogenesis based upcome etiology (look at etiology) Prognosis lower rates of recovery in patients > 65 years of age increased risk of end-stage renal disease, chronic kidney disease, and mortality Presentation Symptoms may be asymptomatic oliguria anuria polyuria confusion Physical exam hypertension edema decreased urine output Imaging Renal ultrasound indication initial imaging study for assessing acute kidney injury can assess for renal size and hydronephrosis to assess for postrenal obstruction Studies Labs increase in serum creatinine by ≥ 0.3 mg/dL within 48 hours blood urea nitrogen (BUN):creatinine ratio urinalysis dipstick to assess for protein, glucose, leukocyte esterase, hemoglobin and myoglobin, and specific gravity microscopy for example red dysmorphic cells suggests a glomerular etiology (e.g., glomerulonephritis) muddy brown casts suggests tubular necrosis white blood cell casts suggest pyelonephritis or acute interstitial nephritis fractional excretion of Na+ (FeNa+) if patient is on diuretics use FeUrea urine osmolality and Na+ Studies To Assess For Prerenal, Intrarenal, and Postrenal Acute Kidney Injury (AKI) Studies Prerenal AKI Intrarenal AKI Postrenal AKI Urine osmolality (mOsm/kg) > 500 < 350 < 350 FeNa+ < 1% > 2% < 1% in mild cases> 2% in severe cases Urine Na+ (mEq/L) < 20 > 40 > 40 Serum BUN/Cr > 20:1 < 15:1 Variable Differential Acute gastrointestinal bleeding Rhabdomyolysis Medication-induced impairment of creatinine secretion cimetidine trimethoprim pyrimethamine Treatment Treatment is dependent on the etiology of AKI and its consequences for example a patient who is hyperkalemic and not responding to medical treatment should be dialyzed a patient with a history of excessive fluid loss (e.g., diarrhea and vomiting) should be given intravenous fluid Complications Hyperkalemia Metabolic acidosis Uremic encephalopathy and platelet dysfunction Anemia Chronic kidney disease