Acute kidney injury
| Acute kidney injury | |
|---|---|
| Classification and external resources | |
 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. |
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| ICD-10 | N17. |
| ICD-9 | 584 |
| DiseasesDB | 11263 |
| MedlinePlus | 000501 |
| eMedicine | med/1595 |
| MeSH | D007675 |
Acute kidney injury (AKI), previously called acute renal failure (ARF),[1] is a rapid loss of kidney function. Its causes are numerous and include low blood volume, exposure to toxins, and prostate enlargement. AKI is diagnosed on the basis of clinical history, such as decreased urine production, and characteristic laboratory findings, such as elevated blood urea nitrogen and creatinine. Depending on its severity, AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, changes in body fluid balance, and effects to other organ systems. Management includes supportive care, such as renal replacement therapy, as well as treatment of the underlying disorder.
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Epidemiology
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.[2]
Causes
| Type | UOsm | UNa | FeNa | BUN/Cr |
|---|---|---|---|---|
| Prerenal | >500 | <10 | <1% | >20 |
| Intrinsic | <350 | >20 | >2% | <15 |
| Postrenal | <350 | >40 | >4% | >15 |
The myriad causes of acute kidney injury are commonly categorised into prerenal, intrinsic, and postrenal.
Prerenal
Prerenal causes of AKI are those that decrease effective blood flow to the kidney. These include systemic causes, such as low blood volume, low blood pressure, and heart failure, as well as local changes to the blood vessels supplying the kidney. The latter include renal artery stenosis, which is a narrowing of the renal artery that supplies the kidney, and renal vein thrombosis, which is the formation of a blood clot in the renal vein that drains blood from the kidney. Renal ischaemia ultimately results in functional disorder, depression of GFR, or both. These causes the inadequate cardiac output and hypovoumia or vascular diseases causing reduces perfusion of kidneys.
Intrinsic
Sources of damage to the kidney itself are dubbed intrinsic. Intrinsic AKI can be due to damage to the glomeruli, renal tubules, or interstitium. Common causes of each are glomerulonephritis, acute tubular necrosis (ATN), and acute interstitial nephritis (AIN), respectively.
Postrenal
Postrenal AKI is a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasia, kidney stones, obstructed urinary catheter, bladder stone, bladder, ureteral or renal malignancy. It is useful to perform a bladder scan or a post void residual to rule out urinary retention. A renal ultrasound will demonstrate hydronephrosis if present. A CT scan of the abdomen will also demonstrate bladder distension or hydronephrosis, however, in case of acute renal failure, the use of IV contrast is contraindicated. On the basic metabolic panel, the ratio of BUN to creatinine may indicate post renal failure.
Diagnosis
Acute kidney injury is diagnosed on the basis of clinical history and laboratory data. A diagnosis is made when there is rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria.
Definition
Introduced by the Acute Kidney Injury Network (AKIN), specific criteria exist for the diagnosis of AKI:[3]
- Rapid time course (less than 48 hours)
- Reduction of kidney function
- Rise in serum creatinine
- Absolute increase in serum creatinine of ≥0.3 mg/dl (≥26.4 μmol/l)
- Percentage increase in serum creatinine of ≥50%
- Reduction in urine output, defined as <0.5 ml/kg/hr for more than 6 hours
- Rise in serum creatinine
Staging
The RIFLE criteria, proposed by the Acute Dialysis Quality Initiative (ADQI) group, aid in the staging of patients with AKI:[4][5]
- Risk: serum creatinine increased 1.5 times or urine production of <0.5 ml/kg for 6 hours
- Injury: doubling of creatinine or urine production <0.5 ml/kg for 12 hours
- Failure: tripling of creatinine or creatinine >355 μmol/l (with a rise of >44) (>4 mg/dl) OR urine output below 0.3 ml/kg for 24 hours
- Loss: persistent AKI or complete loss of kidney function for more than 4 weeks
- End-stage renal disease: complete loss of kidney function for more than 3 months
Further testing
Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. These may include renal ultrasound and kidney biopsy. Indications for renal biopsy in the setting of AKI include:[6]
- Unexplained AKI
- AKI in the presence of the nephritic syndrome
- Systemic disease associated with AKI
Treatment
The management of AKI hinges on identification and treatment of the underlying cause. 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, iodinated contrasts such as those used for CT scans, and others.
Monitoring of renal 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.
Specific therapies
In prerenal AKI without fluid overload, administration of intravenous fluids is typically the first step to improve renal function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid.
Should low blood pressure prove a persistent problem in the fluid-replete patient, inotropes such as norepinephrine and dobutamine may be given to improve cardiac output and hence renal perfusion. While a useful pressor, there is no evidence to suggest that dopamine is of any specific benefit,[7] and may be harmful.
The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to Wegener's granulomatosis may respond to steroid medication. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as aminoglycoside, penicillin, NSAIDs, or acetaminophen.
If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary.
Diuretic agents
The use of diuretics such as furosemide, while widespread and sometimes convenient in ameliorating fluid overload, does not reduce the risk of complications or death.[8]
Renal replacement therapy
Renal replacement therapy, such as with hemodialysis, may be instituted in some cases of AKI. A systematic review of the literature in 2008 demonstrated no difference in outcomes between the use of intermittent hemodialysis and continuous venovenous hemofiltration (CVVH).[9] Among critically ill patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis.[10][11]
Complications
Metabolic acidosis, hyperkalemia, and pulmonary edema[12] 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. Depending on the cause, a proportion of patients will never regain full renal function, thus having end-stage renal failure requiring lifelong dialysis or a kidney transplant.
History
Before the advancement of modern medicine, acute kidney injury might be referred to as uremic poisoning. Uremia was the term used to describe the contamination of the blood with urine. Starting around 1847 this term was used to describe reduced urine output, now known as 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 recognised in the 1940s in the United Kingdom, where crush injury victims during the London Blitz developed patchy necrosis of renal tubules, leading to a sudden decrease in renal function.[13] During the Korean and Vietnam wars, the incidence of AKI decreased due to better acute management and administration of intravenous fluids.[14]
See also
- Chronic kidney disease
- Dialysis
- Renal failure
- BUN-to-creatinine ratio
References
- ↑ Webb S, Dobb G (December 2007). "ARF, ATN or AKI? It's now acute kidney injury". Anaesthesia and Intensive Care 35 (6): 843–4. PMID 18084974.
- ↑ Brenner and Rector's The Kidney. Philadelphia: Saunders. 2007. ISBN 1-4160-3110-3.
- ↑ Mehta RL, Kellum JA, Shah SV, et al. (2007). "Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury". Critical Care (London, England) 11 (2): R31. doi:10.1186/cc5713. PMID 17331245. PMC 2206446. http://ccforum.com/content/11/2/R31.
- ↑ Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P (2004). "Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group". Crit Care 8 (4): R204–12. doi:10.1186/cc2872. PMID 15312219.
- ↑ Lameire N, Van Biesen W, Vanholder R (2005). "Acute renal failure". Lancet 365 (9457): 417–30. doi:10.1016/S0140-6736(05)17831-3. PMID 15680458.
- ↑ Papadakis, Maxine A.; McPhee, Stephen J. (2008). Current Medical Diagnosis and Treatment. McGraw-Hill Professional. ISBN 0-07-159124-9.
- ↑ Holmes CL, Walley KR (2003). "Bad medicine: low-dose dopamine in the ICU". Chest 123 (4): 1266–75. doi:10.1378/chest.123.4.1266. PMID 12684320.
- ↑ Uchino S, Doig GS, Bellomo R, et al (2004). "Diuretics and mortality in acute renal failure". Crit. Care Med. 32 (8): 1669–77. doi:10.1097/01.CCM.0000132892.51063.2F. PMID 15286542.
- ↑ Pannu N, Klarenbach S, Wiebe N, Manns B, Tonelli M (February 2008). "Renal replacement therapy in patients with acute renal failure: a systematic review". JAMA : the Journal of the American Medical Association 299 (7): 793–805. doi:10.1001/jama.299.7.793. PMID 18285591. http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=18285591.
- ↑ Bellomo R, Cass A, Cole L, et al. (October 2009). "Intensity of continuous renal-replacement therapy in critically ill patients". The New England Journal of Medicine 361 (17): 1627–38. doi:10.1056/NEJMoa0902413. PMID 19846848. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=19846848&promo=ONFLNS19.
- ↑ Palevsky PM, Zhang JH, O'Connor TZ, et al. (July 2008). "Intensity of renal support in critically ill patients with acute kidney injury". The New England Journal of Medicine 359 (1): 7–20. doi:10.1056/NEJMoa0802639. PMID 18492867. PMC 2574780. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=18492867&promo=ONFLNS19.
- ↑ http://beavermedic.wordpress.com/2010/01/19/the-kidneys/
- ↑ Bywaters EG, Beall D (1941). "Crush injuries with impairment of renal function.". Br Med J 1 (1): 427–32. doi:10.1136/bmj.1.4185.427. PMID 9527411. http://jasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=9527411.
- ↑ Schrier RW, Wang W, Poole B, Mitra A (2004). "Acute renal failure: definitions, diagnosis, pathogenesis, and therapy". J. Clin. Invest. 114 (1): 5–14. doi:10.1172/JCI22353. PMID 15232604.
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