Acute kidney injury

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Acute kidney disease
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Acute kidney injury
Other namesAcute renal failure (ARF), acute kidney failure (AKF)
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.
SpecialtyNephrology, Urology

Acute kidney injury (AKI), previously called acute renal failure (ARF),

serum creatinine or a decrease in urine output, or both.[4]

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).

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

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

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

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

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.[citation needed]

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 kidney's structures including the

calcineurin inhibitors (e.g., tacrolimus) can also directly damage the tubular cells of the kidney and result in a form of intrinsic AKI.[11]

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 catheter, bladder stones, or cancer of the bladder, ureters, or prostate
.

Diagnosis

Definition

Introduced by the KDIGO in 2012,[12] 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 < 0.5 mL/kg/h for 6 hours.

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:[13][14]

Pathophysiology of acute kidney injury in the proximal renal tubule
  • Risk: 1.5-fold increase in the serum creatinine, or glomerular filtration rate (GFR) decrease by 25 percent, or urine output <0.5 mL/kg per hour for six hours.
  • Injury: Two-fold increase in the serum creatinine, or GFR decrease by 50 percent, or urine output <0.5 mL/kg per hour for 12 hours.
  • Failure: Three-fold increase in the serum creatinine, or GFR decrease by 75 percent, or urine output of <0.3 mL/kg per hour for 24 hours, or no urine output (anuria) for 12 hours.
  • Loss: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than four weeks.
  • End-stage kidney disease
    : Complete loss of kidney function (e.g., need for renal replacement therapy) for more than three months.

Evaluation

The deterioration of kidney function may be signaled by a measurable decrease in urine output. Often, it is diagnosed on the basis of

NGAL, KIM-1, IL18 and cystatin C), but none of them are established enough as of 2018 to replace creatinine as a marker of kidney function.[15]

Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. It is useful to perform a bladder scan or a post void residual to rule out urinary retention. In post void residual, a catheter is inserted into the urinary tract immediately after urinating to measure fluid still in the bladder. 50–100 mL suggests neurogenic bladder dysfunction.[citation needed]

These may include urine sediment analysis,

kidney biopsy. Indications for kidney biopsy in the setting of AKI include the following:[16]

  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

urinomas. A CT scan of the abdomen will also demonstrate bladder distension or hydronephrosis.[18]

  • Renal ultrasonograph of acute pyelonephritis with increased cortical echogenicity and blurred delineation of the upper pole.[17]
    Renal ultrasonograph of acute pyelonephritis with increased cortical echogenicity and blurred delineation of the upper pole.[17]
  • Renal ultrasonograph in renal failure after surgery with increased cortical echogenicity and kidney size. Biopsy showed acute tubular necrosis.[17]
    Renal ultrasonograph in renal failure after surgery with increased cortical echogenicity and kidney size. Biopsy showed acute tubular necrosis.[17]
  • Renal ultrasonograph in renal trauma with laceration of the lower pole and subcapsular fluid collection below the kidney.[17]
    Renal ultrasonograph in renal trauma with laceration of the lower pole and subcapsular fluid collection below the kidney.[17]

Classification

Acute kidney injury is diagnosed on the basis of

kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria (less than 400 mLs of urine per 24 hours).[citation needed
]

Classic laboratory findings in AKI
Type UOsm UNa FeNa
BUN/Cr
Prerenal >500 <10 <1% >20[19]
Intrinsic <350 >20 >2% <10-15[19]
Postrenal <350 >40 >4% >20[19]

AKI can be caused by systemic disease (such as a manifestation of an autoimmune disease, e.g.,

contrast agents.[citation needed
]

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.[20] 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.[20] 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).[21]

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

antibiotics such as gentamicin, and a range of other substances.[22]

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.[citation needed]

Prerenal

In prerenal AKI without

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.[citation needed
]

If

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.[23]

Intrinsic

The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to vasculitis or glomerulonephritis may respond to

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),[24] nor with any reduced mortality or length of intensive care unit or hospital stay.[25]

Postrenal

If the cause is obstruction of the urinary tract, relief of the obstruction (with a

urinary catheter) may be necessary.[citation needed
]

Renal replacement therapy

continuous venovenous hemofiltration (CVVH) (a type of continuous hemodialysis).[26] Among critically ill patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis.[22][27] 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.[28][29][30]

Complications

Metabolic acidosis, hyperkalemia, and pulmonary edema may require medical treatment with sodium bicarbonate, antihyperkalemic measures, and diuretics.[31]

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,[32][33] but the effect of a fluid load is highly variable. Striving toward a predefined urine output target to prevent AKI is futile.[21][34][35]

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.[36]

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.[37]

AKI develops in 5% to 30% of patients who undergo cardiothoracic surgery, depending on the definition used for AKI.[38] 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).[39]

Kidney function

Depending on the cause, a proportion of patients (5–10%) will never regain full kidney function, thus entering

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).[40]

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.[41]

There is an increased incidence of AKI in agricultural workers because of occupational hazards such as dehydration and heat illness.[42] 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.[43]

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.[44] This was a 346% increase in hospitalizations from 1997, when there were 98,000 acute kidney injury stays.[45] 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.[46]

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.[47]

Acute kidney injury due to

intravenous fluids.[49]

See also

References

  1. PMID 18084974
    .
  2. ^
    McGraw-Hill Professional
    .
  3. PMID 17331245
    .
  4. ^
    S2CID 208230983
    .
  5. ^
    PMID 31790176
    .
  6. ISBN 978-0-07-139140-5
    .
  7. ^
    S2CID 33811639
    .
  8. ISBN 978-0-07-143692-2
    .
  9. ^
    ISBN 978-0-07-139140-5
    .
  10. ISBN 978-0-19-956313-5
    .
  11. PMID 25540591
    .
  12. S2CID 46171014
    .
  13. PMID 15312219
    .
  14. S2CID 37093076
    .
  15. PMID 29862965
    .
  16. ISBN 978-0-07-159124-9
    .
  17. ^
    PMID 26838799. (CC-BY 4.0) Archived 2017-10-16 at the Wayback Machine
  18. PMID 19188307
    .
  19. ^
    OCLC 899727756.{{cite book}}: CS1 maint: location missing publisher (link
    )
  20. ^
    PMID 25376763
    .
  21. ^
    PMID 35330795
    .
  22. ^
    PMID 18492867
    .
  23. PMID 12684320
    .
  24. S2CID 2642777
    .
  25. PMID 16794108
    .
  26. PMID 18285591
    .
  27. PMID 19846848
    .
  28. ^ Schoenfelder, T; Chen, X; Bless, HH (March 2017). "Effects of continuous and intermittent renal replacement therapies among adult patients with acute kidney injury". GMS Health Technol Assess. 13 (Doc01 (20170301)). Archived from the original on 8 August 2017. Retrieved 8 August 2017.
  29. S2CID 25491242
    .
  30. S2CID 233484979
    .
  31. PMID 23882341
    .
  32. S2CID 85529862
    .
  33. PMID 29136086
    .
  34. S2CID 5496234
    .
  35. S2CID 11909307
    .
  36. PMID 32238366
    .
  37. PMID 28801674
    .
  38. PMID 19398670
    .
  39. S2CID 9298414
    .
  40. PMID 22113526
    .
  41. ^ "Renal Medicine: Acute Kidney Injury (AKI)". Renalmed.co.uk. 2012-05-23. Archived from the original on 2013-08-08. Retrieved 2013-07-17.
  42. S2CID 35174532
    .
  43. ISBN 978-1-4160-3110-9
    .
  44. ^ Torio CM, Andrews RM. National Inpatient Hospital Costs: The Most Expensive Conditions by Payer, 2011. HCUP Statistical Brief #160. Agency for Healthcare Research and Quality, Rockville, MD. August 2013. "Statistical Brief #160". Archived from the original on 2017-03-14. Retrieved 2017-05-01.
  45. ^ Pfuntner A., Wier L.M., Stocks C. Most Frequent Conditions in U.S. Hospitals, 2011. HCUP Statistical Brief #162. September 2013. Agency for Healthcare Research and Quality, Rockville, MD. "Most Frequent Conditions in U.S. Hospitals, 2011 #162". Archived from the original on 2016-03-04. Retrieved 2016-02-09.
  46. PMID 25229340
    .
  47. ^ "oliguria | Origin and meaning of oliguria by Online Etymology Dictionary". www.etymonline.com. Retrieved 2021-01-29.
  48. PMID 20783577
    .
  49. PMID 15232604
    .

External links

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