Acute kidney injury

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Acute kidney injury
Other namesAcute renal failure (ARF), acute kidney failure (AKF)
Kidney - acute cortical necrosis.jpg
Pathologic kidney specimen showing marked pallor of the cortex, contrasting to the darker areas of surviving medullary tissue. The patient died with acute kidney injury.
Specialty Nephrology, Urology

Acute kidney injury (AKI), previously called acute renal failure (ARF), [1] [2] is a sudden decrease in kidney function that develops within 7 days, [3] as shown by an increase in serum creatinine or a decrease in urine output, or both. [4]

Contents

Causes of AKI are classified as either prerenal (due to decreased blood flow to the kidney), intrinsic renal (due to damage to the kidney itself), or postrenal (due to blockage of urine flow). [5] Prerenal causes of AKI include sepsis, dehydration, excessive blood loss, cardiogenic shock, heart failure, cirrhosis, and certain medications like ACE inhibitors or NSAIDs. [5] Intrinsic renal causes of AKI include glomerulonephritis, lupus nephritis, acute tubular necrosis, certain antibiotics, and chemotherapeutic agents. [5] Postrenal causes of AKI include kidney stones, bladder cancer, neurogenic bladder, enlargement of the prostate, narrowing of the urethra, and certain medications like anticholinergics. [5]

The diagnosis of AKI is made based on a person's signs and symptoms, along with lab tests for serum creatinine and measurement of urine output. Other tests include urine microscopy and urine electrolytes. Renal ultrasound can be obtained when a postrenal cause is suspected. A kidney biopsy may be obtained when intrinsic renal AKI is suspected and the cause is unclear. [5]

AKI is seen in 10-15% of people admitted to the hospital and in more than 50% of people admitted to the intensive care unit (ICU). [4] AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, effects on other organ systems, and death. People who have experienced AKI are at increased risk of developing chronic kidney disease in the future. [4] Management includes treatment of the underlying cause and supportive care, such as renal replacement therapy.

Signs and symptoms

The clinical presentation is often dominated by the underlying cause. The various symptoms of acute kidney injury result from the various disturbances of 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. [6] Marked increases in the potassium level can lead to abnormal heart rhythms, which can be severe and life-threatening. [7] Fluid balance is frequently affected, though blood pressure can be high, low, or normal. [8]

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. [9] If the kidney injury is the result of dehydration, there may be thirst as well as evidence of fluid depletion on physical examination. [9] 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. [9]

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 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. [10] : 26-27 

Intrinsic or Intrarenal

Intrinsic AKI refers to disease processes which 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. [11] 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. [12]

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, [13] specific criteria exist for the diagnosis of AKI.

AKI can be diagnosed if any one of the following is present:

Staging

The RIFLE criteria, proposed by the Acute Dialysis Quality Initiative (ADQI) group, aid in assessment of the severity of a person's acute kidney injury. The acronym RIFLE is used to define the spectrum of progressive kidney injury seen in AKI: [14] [15]

Pathophysiology of acute kidney injury in the proximal renal tubule Acute Renal Failure.svg
Pathophysiology of acute kidney injury in the proximal renal tubule

Evaluation

The deterioration of kidney function may be signaled by a measurable decrease in urine output. Often, it is diagnosed on the basis of blood tests for substances normally eliminated by the kidney: urea and creatinine. Additionally, the ratio of BUN to creatinine is used to evaluate kidney injury. Both tests have their disadvantages. For instance, it takes about 24 hours for the creatinine level to rise, even if both kidneys have ceased to function. A number of alternative markers have been proposed (such as NGAL, HAVCR1, IL18 and cystatin C), but none of them are established enough as of 2018 to replace creatinine as a marker of kidney function. [16]

These may include urine sediment analysis, renal ultrasound and/or kidney biopsy. Indications for kidney biopsy in the setting of AKI include the following: [17]

  1. Unexplained AKI, in a patient with two non-obstructed normal sized kidneys.
  2. AKI in the presence of the nephritic syndrome.
  3. Systemic disease associated with AKI.
  4. Kidney transplant dysfunction.

In medical imaging, the acute changes in the kidney are often examined with renal ultrasonography as the first-line modality, where CT scan and magnetic resonance imaging (MRI) are used for the follow-up examinations and when US fails to demonstrate abnormalities. In evaluation of the acute changes in the kidney, the echogenicity of the renal structures, the delineation of the kidney, the renal vascularity, kidney size and focal abnormalities are observed. [18] CT is preferred in renal traumas, but US is used for follow-up, especially in the patients suspected for the formation of urinomas. A CT scan of the abdomen will also demonstrate bladder distension or hydronephrosis. [19]

Classification

Acute kidney injury is diagnosed on the basis of clinical history and laboratory data. A diagnosis is made when there is a rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria (less than 0.5 mL/kg/h for at least 6 hours). [20]

Classic laboratory findings in AKI
TypeUOsmUNaFeNa BUN/Cr
Prerenal>500<10<1%>20 [21]
Intrinsic<350>20>2%<10-15 [21]
Postrenal<350>40>4%>20 [21]

AKI can be caused by systemic disease (such as a manifestation of an autoimmune disease, e.g., lupus nephritis), crush injury, contrast agents, some antibiotics, and more. AKI often occurs due to multiple processes. [10] : 31-32 

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. [22] 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. [22] Volatile anesthetic agents have been shown to increase renal sympathetic nerve activity (RSNA), which causes retention of salts and water, diminished renal blood flow (RBF) and an increase in serum renin levels, but not in antidiuretic hormone (ADH). [23]

Treatment

The management of AKI hinges on identification and treatment of the underlying cause. 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. [24]

Monitoring of kidney function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate. [10] : 39 

Prerenal

In prerenal AKI without fluid overload, administration of intravenous fluids is typically the first step to improving kidney function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid. [10] : 29 

If low blood pressure persists despite providing a person with adequate amounts of intravenous fluid, medications that increase blood pressure (vasopressors) such as norepinephrine, and in certain circumstances medications that improve the heart's ability to pump (known as inotropes) such as dobutamine may be given to improve blood flow to the kidney. While a useful vasopressor, there is no evidence to suggest that dopamine is of any specific benefit and may in fact be harmful. [25]

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. [9]

The use of diuretics such as furosemide, is widespread and sometimes convenient in improving fluid overload. It is not associated with higher mortality (risk of death), [26] nor with any reduced mortality or length of intensive care unit or hospital stay. [27]

Postrenal

If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary. [10]

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). [28] Among critically ill patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis. [24] [29] 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. [30] [31] [32]

Complications

Metabolic acidosis, hyperkalemia, and pulmonary edema may require medical treatment with sodium bicarbonate, antihyperkalemic measures, and diuretics. [33]

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. [7] However, oliguria during anesthesia may predict AKI, [34] [35] but the effect of a fluid load is highly variable. Striving toward a predefined urine output target to prevent AKI is futile. [23] [36] [37]

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. [38]

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. [39]

AKI develops in 5% to 30% of patients who undergo cardiothoracic surgery, depending on the definition used for AKI. [40] 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). [41]

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 hospital, even if their kidney function has recovered. [2]

The risk of developing chronic kidney disease is increased (8.8-fold). [42]

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. [43]

Hot weather can increase the risk of AKI. [44] [45] For example, there is an increased incidence of AKI in agricultural workers because of occupational hazards such as dehydration and heat illness. [46] 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. [47]

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. [48] This was a 346% increase in hospitalizations from 1997, when there were 98,000 acute kidney injury stays. [49] 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. [50]

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. [51]

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. [52] During the Korean and Vietnam wars, the incidence of AKI decreased due to better acute management and administration of intravenous fluids. [53]

See also

Related Research Articles

Nephrology is a specialty for both adult internal medicine and pediatric medicine that concerns the study of the kidneys, specifically normal kidney function and kidney disease, the preservation of kidney health, and the treatment of kidney disease, from diet and medication to renal replacement therapy. The word "renal" is an adjective meaning "relating to the kidneys", and its roots are French or late Latin. Whereas according to some opinions, "renal" and "nephro" should be replaced with "kidney" in scientific writings such as "kidney medicine" or "kidney replacement therapy", other experts have advocated preserving the use of renal and nephro as appropriate including in "nephrology" and "renal replacement therapy", respectively.

Azotemia is a medical condition characterized by abnormally high levels of nitrogen-containing compounds in the blood. It is largely related to insufficient or dysfunctional filtering of blood by the kidneys. It can lead to uremia and acute kidney injury if not controlled.

<span class="mw-page-title-main">Kidney dialysis</span> Removal of nitrogenous waste and toxins from the body in place of or to augment the kidney

Kidney dialysis is the process of removing excess water, solutes, and toxins from the blood in people whose kidneys can no longer perform these functions naturally. This is referred to as renal replacement therapy. The first successful dialysis was performed in 1943.

<span class="mw-page-title-main">Creatinine</span> Breakdown product of creatine phosphate

Creatinine is a breakdown product of creatine phosphate from muscle and protein metabolism. It is released at a constant rate by the body.

<span class="mw-page-title-main">Rhabdomyolysis</span> Human disease (condition) in which damaged skeletal muscle breaks down rapidly

Rhabdomyolysis is a condition in which damaged skeletal muscle breaks down rapidly, often due to high intensity exercise over a short period of time. Symptoms may include muscle pains, weakness, vomiting, and confusion. There may be tea-colored urine or an irregular heartbeat. Some of the muscle breakdown products, such as the protein myoglobin, are harmful to the kidneys and can cause acute kidney injury.

<span class="mw-page-title-main">Kidney failure</span> Disease where the kidneys fail to adequately filter waste products from the blood

Kidney failure, also known as end-stage renal disease (ESRD), is a medical condition in which the kidneys can no longer adequately filter waste products from the blood, functioning at less than 15% of normal levels. Kidney failure is classified as either acute kidney failure, which develops rapidly and may resolve; and chronic kidney failure, which develops slowly and can often be irreversible. Symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications of acute and chronic failure include uremia, hyperkalemia, and volume overload. Complications of chronic failure also include heart disease, high blood pressure, and anaemia.

<span class="mw-page-title-main">Fluid replacement</span> Medical practice of replenishing bodily fluid

Fluid replacement or fluid resuscitation is the medical practice of replenishing bodily fluid lost through sweating, bleeding, fluid shifts or other pathologic processes. Fluids can be replaced with oral rehydration therapy (drinking), intravenous therapy, rectally such as with a Murphy drip, or by hypodermoclysis, the direct injection of fluid into the subcutaneous tissue. Fluids administered by the oral and hypodermic routes are absorbed more slowly than those given intravenously.

<span class="mw-page-title-main">Uremia</span> Excess urea in the blood due to kidney dysfunction

Uremia is the term for high levels of urea in the blood. Urea is one of the primary components of urine. It can be defined as an excess in the blood of amino acid and protein metabolism end products, such as urea and creatinine, which would be normally excreted in the urine. Uremic syndrome can be defined as the terminal clinical manifestation of kidney failure. It is the signs, symptoms and results from laboratory tests which result from inadequate excretory, regulatory, and endocrine function of the kidneys. Both uremia and uremic syndrome have been used interchangeably to denote a very high plasma urea concentration that is the result of renal failure. The former denotation will be used for the rest of the article.

<span class="mw-page-title-main">Chronic kidney disease</span> Abnormal kidney structure or gradual loss of kidney function

Chronic kidney disease (CKD) is a type of long-term kidney disease, in which either there is a gradual loss of kidney function occurs over a period of months to years, or abnormal kidney structure. Initially generally no symptoms are seen, but later symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications can relate to hormonal dysfunction of the kidneys and include high blood pressure, bone disease, and anemia. Additionally CKD patients have markedly increased cardiovascular complications with increased risks of death and hospitalization.

<span class="mw-page-title-main">Hepatorenal syndrome</span> Human disease

Hepatorenal syndrome (HRS) is a life-threatening medical condition that consists of rapid deterioration in kidney function in individuals with cirrhosis or fulminant liver failure. HRS is usually fatal unless a liver transplant is performed, although various treatments, such as dialysis, can prevent advancement of the condition.

<span class="mw-page-title-main">Nephritic syndrome</span> Symptoms resulting from kidney inflammation

Nephritic syndrome is a syndrome comprising signs of nephritis, which is kidney disease involving inflammation. It often occurs in the glomerulus, where it is called glomerulonephritis. Glomerulonephritis is characterized by inflammation and thinning of the glomerular basement membrane and the occurrence of small pores in the podocytes of the glomerulus. These pores become large enough to permit both proteins and red blood cells to pass into the urine. By contrast, nephrotic syndrome is characterized by proteinuria and a constellation of other symptoms that specifically do not include hematuria. Nephritic syndrome, like nephrotic syndrome, may involve low level of albumin in the blood due to the protein albumin moving from the blood to the urine.

Contrast-induced nephropathy (CIN) is a purported form of kidney damage in which there has been recent exposure to medical imaging contrast material without another clear cause for the acute kidney injury.

Acute uric acid nephropathy is a rapidly worsening (decreasing) kidney function that is caused by high levels of uric acid in the urine (hyperuricosuria).

Phosphate nephropathy or nephrocalcinosis is an adverse renal condition that arises with a formation of phosphate crystals within the kidney's tubules. This renal insufficiency is associated with the use of oral sodium phosphate (OSP) such as C.B. Fleet's Phospho soda and Salix's Visocol, for bowel cleansing prior to a colonoscopy.   

The consumption of grapes and raisins presents a potential health threat to dogs. Their toxicity to dogs can cause the animal to develop acute kidney injury with anuria. The phenomenon was first identified by the Animal Poison Control Center (APCC), run by the American Society for the Prevention of Cruelty to Animals (ASPCA). Approximately 140 cases were seen by the APCC in the one year from April 2003 to April 2004, with 50 developing symptoms and seven dying.

<span class="mw-page-title-main">Lipocalin-2</span> Protein-coding gene in the species Homo sapiens

Lipocalin-2 (LCN2), also known as oncogene 24p3 or neutrophil gelatinase-associated lipocalin (NGAL), is a protein that in humans is encoded by the LCN2 gene. NGAL is involved in innate immunity by sequestering iron and preventing its use by bacteria, thus limiting their growth. It is expressed in neutrophils and in low levels in the kidney, prostate, and epithelia of the respiratory and alimentary tracts. NGAL is used as a biomarker of kidney injury.

Onconephrology is a specialty in nephrology that deals with the study of kidney diseases in cancer patients. A nephrologist who takes care of patients with cancer and kidney disease is called an onconephrologist. This branch of nephrology encompasses nephrotoxicity associated with existing and novel chemotherapeutics, kidney disease as it pertains to stem cell transplant, paraneoplastic kidney disorders, paraproteinemias, electrolyte disorders associated with cancer, and more as discussed below.

Renal angina is a clinical methodology to risk stratify patients for the development of persistent and severe acute kidney injury (AKI). The composite of risk factors and early signs of injury for AKI, renal angina is used as a clinical adjunct to help optimize the use of novel AKI biomarker testing. The term angina from Latin and from the Greek ankhone ("strangling") are utilized in the context of AKI to denote the development of injury and the choking off of kidney function. Unlike angina pectoris, commonly caused due to ischemia of the heart muscle secondary to coronary artery occlusion or vasospasm, renal angina carries no obvious physical symptomatology. Renal angina was derived as a conceptual framework to identify evolving AKI. Like acute coronary syndrome which precedes or is a sign of a heart attack, renal angina is used as a herald sign for a kidney attack. Detection of renal angina is performed by calculating the renal angina index.

In pharmacology, augmented renal clearance (ARC) is a phenomenon where certain critically ill patients may display increased clearance of a medication through the kidneys. In many cases, it is observed as a measured creatinine clearance above that which is expected given the patient's age, gender, and other factors. The phenomenon is most commonly observed in patients with neurologic damage, sepsis, major trauma, or burns.

Kidney ischemia is a disease with a high morbidity and mortality rate. Blood vessels shrink and undergo apoptosis which results in poor blood flow in the kidneys. More complications happen when failure of the kidney functions result in toxicity in various parts of the body which may cause septic shock, hypovolemia, and a need for surgery. What causes kidney ischemia is not entirely known, but several pathophysiology relating to this disease have been elucidated. Possible causes of kidney ischemia include the activation of IL-17C and hypoxia due to surgery or transplant. Several signs and symptoms include injury to the microvascular endothelium, apoptosis of kidney cells due to overstress in the endoplasmic reticulum, dysfunctions of the mitochondria, autophagy, inflammation of the kidneys, and maladaptive repair.

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