Acute kidney injury

The underlying cause often dominates the clinical presentation. The symptoms of acute kidney injury result from various disturbances in kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue, loss of appetite, headache, nausea, and vomiting. Marked increases in the potassium level can lead to abnormal heart rhythms, which can be severe and life-threatening. Fluid balance is frequently affected, though blood pressure can be high, low, or normal. Pain in the flanks may be encountered in some conditions (such as clotting of the kidneys' blood vessels or inflammation of the kidney). This is the result of stretching of the fibrous tissue capsule surrounding the kidney. If the kidney injury is the result of dehydration, there may be thirst as well as evidence of fluid depletion on physical examination. Physical examination may also provide other clues as to the underlying cause of the kidney problem, such as a rash in interstitial nephritis (or vasculitis) and a palpable bladder in obstructive nephropathy. ==Causes==

Prerenal Prerenal causes of AKI ("pre-renal azotemia") are those that decrease effective blood flow to the kidney and cause a decrease in the glomerular filtration rate (GFR). 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 (e.g. NSAID induced vasoconstriction of afferent arteriole). The latter includes 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 intrarenal Intrinsic AKI refers to disease processes that directly damage the kidney itself. Intrinsic AKI can be due to one or more of the kidney's 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 antibiotics (e.g. amoxicillin/clavulanic acid) and 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 • Cancer of the bladder, ureters, or prostate • Damage to the nerves controlling urine flow and bladder function. ==Diagnosis==

Definition Introduced by the KDIGO in 2012, specific criteria exist for the diagnosis of AKI. AKI can be diagnosed if any one of the following is present: • Increase in SCr by ≥0.3 mg/dl (≥26.5 μmol/L) within 48 hours; or • Increase in SCr to ≥1.5 times baseline, which has occurred within the prior 7 days; or • Urine volume File:Ultrasonography of acute pyelonephritis.jpg|Renal ultrasonograph of acute pyelonephritis with increased cortical echogenicity and blurred delineation of the upper pole AKI can be caused by systemic disease, e.g., autoimmune conditions, like lupus nephritis), as well as other conditions, such as crush injury, contrast agents, some antibiotics, and more. AKI is often due to multiple factors. The causes of acute kidney injury are commonly categorized into prerenal, intrinsic, and postrenal. Acute kidney injury occurs in up to 30% of patients following cardiac surgery. Mortality increases by 60-80% in post-cardiopulmonary bypass patients who go on to require renal replacement therapy. Preoperative creatinine greater than 1.2 mg/dL, combined valve and bypass procedures, emergency surgery, and preoperative intra-aortic balloon pump are risk factors most strongly correlated with post-cardiopulmonary bypass acute kidney injury. Other well-known minor risk factors include female gender, congestive heart failure, chronic obstructive pulmonary disease, insulin-requiring diabetes, and depressed left ventricular ejection fraction. Postoperative acute kidney injury is defined as an AKI based on the KDIGO criteria occurring within 7 days of an operative intervention. Pediatric AKI is defined using the KDIGO definition and the modified neonatal KDIGO criteria for neonates. ==Treatment==

The management of AKI hinges on identifying the underlying cause and treating it. The main objectives of initial management are to prevent cardiovascular collapse and death and to call for specialist advice from a nephrologist. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen or naproxen, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances. Intrinsic The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to vasculitis or glomerulonephritis may respond to steroid medication, cyclophosphamide, and (in some cases) plasma exchange. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as ACE inhibitors, ARB antagonists, aminoglycosides, penicillins, NSAIDs, or paracetamol. nor with any reduced mortality or length of intensive care unit or hospital stay. Postrenal If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary. Renal replacement therapy Renal replacement therapy, such as with hemodialysis, may be instituted in some cases of AKI. Renal replacement therapy can be applied intermittently (IRRT) and continuously (CRRT). Study results regarding differences in outcomes between IRRT and CRRT are inconsistent. 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. 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 based on 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. If AKI develops after major abdominal surgery (13.4% of all people who have undergone major abdominal surgery) the risk of death is markedly increased (over 12-fold). Kidney function Depending on the cause, a proportion of patients (5–10%) will never regain full kidney function, thus entering end-stage kidney failure and requiring lifelong dialysis or a kidney transplant. Patients with AKI are more likely to die prematurely after being discharged from the hospital, even if their kidney function has recovered. ==Epidemiology==

New cases of AKI are unusual but not rare, affecting approximately 0.1% of the UK population per year (2000 ppm/year), 20x incidence of new ESKD (end-stage kidney disease). AKI requiring dialysis (10% of these) is rare (200 ppm/year), 2x incidence of new ESKD. Hot weather can increase the risk of AKI. For example, there is an increased incidence of AKI in agricultural workers because of occupational hazards such as dehydration and heat illness. No other traditional risk factors, including age, BMI, diabetes, or hypertension, were associated with incident AKI. Acute kidney injury is common among hospitalized patients. It affects some 3–7% of patients admitted to the hospital and approximately 25–30% of patients in the intensive care unit. Acute kidney injury was one of the most expensive conditions seen in U.S. hospitals in 2011, with an aggregated cost of nearly $4.7 billion for approximately 498,000 hospital stays. This was a 346% increase in hospitalizations from 1997, when there were 98,000 acute kidney injury stays. According to a review article of 2015, there has been an increase in cases of acute kidney injury in the last 20 years which cannot be explained solely by changes to the manner of reporting. Clinical investigations have revealed a higher incidence of AKI and associated mortality in males compared to premenopausal women. ==History==

Before the advancement of modern medicine, acute kidney injury was referred to as uremic poisoning while uremia was contamination of the blood with urine. Starting around 1847, uremia came to be used for reduced urine output, a condition now called oliguria, which was thought to be caused by the urine's mixing with the blood instead of being voided through the urethra. Acute kidney injury due to acute tubular necrosis (ATN) was recognized in the 1940s in the United Kingdom, where crush injury victims during the London Blitz developed patchy necrosis of kidney tubules, leading to a sudden decrease in kidney function. During the Korean and Vietnam wars, the incidence of AKI decreased due to better acute management and administration of intravenous fluids. == See also ==