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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.
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.

Contents

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

The myriad causes of acute kidney injury are commonly categorised into prerenal, intrinsic, and postrenal.

 
 
 
 
 
Acute kidney
injury
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Prerenal
 
 
Intrinsic
 
 
Postrenal
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Prerenal

Prerenal causes of AKI are those that decrease effective blood flow to the kidney. These include low blood volume, low blood pressure, and heart failure. Changes to the blood vessels supplying the kidney can also lead to prerenal AKI. These 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.

Intrinsic

Those causes that lead to 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, or an obstructed urinary catheter.

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]

  1. Rapid time course (less than 48 hours)
  2. 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

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]

  1. Unexplained AKI
  2. AKI in the presence of the nephritic syndrome
  3. 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. Fluid administration 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] In practice, diuretics may simply mask things, making it more difficult to judge the adequacy of resuscitation.

Renal replacement therapy

Renal replacement therapy, such as 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 and hyperkalemia, the two most serious biochemical manifestations of acute renal failure, may require medical treatment with sodium bicarbonate administration and antihyperkalemic measures, unless dialysis is required.

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 Battle of Britain developed patchy necrosis of renal tubules, leading to a sudden decrease in renal function.[12] During the Korean and Vietnam wars, the incidence of AKI decreased due to better acute management and administration of intravenous fluids.[13]

See also

References

  1. ^ 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.  
  2. ^ Brenner and Rector's The Kidney. Philadelphia: Saunders. 2007. ISBN 1-4160-3110-3.  
  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.  
  4. ^ 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.  
  5. ^ 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.  
  6. ^ Papadakis, Maxine A.; McPhee, Stephen J. (2008). Current Medical Diagnosis and Treatment. McGraw-Hill Professional. ISBN 0-07-159124-9.  
  7. ^ 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.  
  8. ^ 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.  
  9. ^ 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.  
  10. ^ 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.  
  11. ^ 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.  
  12. ^ 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.  
  13. ^ 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.  

Template:Infobox disease Acute renal failure (ARF), also known as acute kidney failure or acute kidney injury, is a rapid loss of renal function due to damage to the kidneys, resulting in retention of nitrogenous (urea and creatinine) and non-nitrogenous waste products that are normally excreted by the kidney. Depending on the severity and duration of the renal dysfunction, this accumulation is accompanied by metabolic disturbances, such as metabolic acidosis (acidification of the blood) and hyperkalaemia (elevated potassium levels), changes in body fluid balance, and effects on many other organ systems. It can be characterised by oliguria or anuria (decrease or cessation of urine production), although nonoliguric ARF may occur. It is a life-threatening medical emergency.

Contents

History

Before the advancement of modern medicine, acute renal failure 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 renal failure due to acute tubular necrosis (ATN) was recognised in the 1940s in the United Kingdom, where crush victims during the Battle of Britain developed patchy necrosis of renal tubules, leading to a sudden decrease in renal function.[1] During the Korean and Vietnam wars, the incidence of ARF decreased due to better acute management and intravenous infusion of fluids.[2]

Causes

Acute renal failure is usually categorised (as in the flowchart below) according to pre-renal, intrinsic and post-renal causes.

 
 
 
 
 
 
 
 
Acute Renal
Failure
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Pre-renal
 
 
Intrinsic
 
 
Post-renal

Pathogenesis

The kidney can regulate its own blood flow and GFR over a wide range of perfusion pressure. When the perfusion pressure falls-as in hypovolemia,shock, heart failure, or narrowing of renal arteries- the resistance vessls in the kidney dilate to facilitate flow. Vasodilator prostaglandins are important, and this mechanism is markedly impaired by NSAIDs. If autoregulation of blood flow fails, the GFR can be maintained by selective consriction of post-glomerular (efferent)arteriole. This is mediated through the release of renin and the generation of angiotensin II, interfere preferentially constricts this vessel. ACE inhibitors interfere with this response. More severe or prolonged under perfusion of the kidneys may lead to failure of these compensatory mechanisms and hence and acute decline in GFR. The renal tubules are intact and become hyperfunctional: that is, tubular reabsorption of sodium and water is increased, partly through physical factors associated with changes in blood and urine flowand partly through influence of angiotensins, aldosterone and vassopressin. this leads to the formation of a low volume of urine which is concentrated (osmolality >600 mOsm/kg) but low in sodium (< 20 mmol/l). These urinary changes may be absent in patients with impaired tubular function, e.g. pre-existing renal impairment, or those who have received loop diuretics.

Diagnosis

In general, renal failure is diagnosed when either creatinine or blood urea nitrogen tests are markedly elevated in an ill patient, especially when oliguria is present. Previous measurements of renal function may offer comparison, which is especially important if a patient is known to have chronic renal failure as well. If the cause is not apparent, a large amount of blood tests and examination of a urine specimen is typically performed to elucidate the cause of acute renal failure, medical ultrasonography of the renal tract is essential to rule out obstruction of the urinary tract.

Consensus criteria (RIFLE)[3][4] for the diagnosis of ARF are:

  • Risk: serum creatinine increased 1.5 times OR urine production of <0.5 ml/kg/h body weight for 6 hours
  • Injury: creatinine 2.0 times OR urine production <0.5 ml/kg/h for 12 h
  • Failure: creatinine 3.0 times OR creatinine >355 μmol/l (with a rise of >44) OR urine output below 0.3 ml/kg/h for 24 h
  • Loss: persistent ARF or complete loss of kidney function for more than four weeks
  • End-stage Renal Disease: complete loss of kidney function for more than three months

Kidney biopsy may be performed in the setting of acute renal failure, to provide a definitive diagnosis and sometimes an idea of the prognosis, unless the cause is clear and appropriate screening investigations are reassuringly negative.

Treatment

Acute renal failure may be reversible if treated promptly and appropriately. Resuscitation to normotension and a normal cardiac output is key. The main interventions are monitoring fluid intake and output as closely as possible; insertion of a urinary catheter is useful for monitoring urine output as well as relieving possible bladder outlet obstruction, such as with an enlarged prostate. In the absence of fluid overload, administering intravenous fluids is typically the first step to improve renal function. Fluid administration may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid. If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary. Metabolic acidosis and hyperkalemia, the two most serious biochemical manifestations of acute renal failure, may require medical treatment with sodium bicarbonate administration and antihyperkalemic measures, unless dialysis is required.

Should hypotension prove a persistent problem in the fluid replete patient, inotropes such as norepinephrine and/or 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,[5] and at least a suggestion of possible harm. A Swan-Ganz catheter may be used, to measure pulmonary artery occlusion pressure to provide a guide to left atrial pressure (and thus left heart function) as a target for inotropic support.

The use of diuretics such as furosemide, while widespread and sometimes convenient in ameliorating fluid overload, does not reduce the risk of complications and death.[6] In practice, diuretics may simply mask things, making it more difficult to judge the adequacy of resuscitation.

The use of an ACE Inhibitor (such as benazepril) can help protect renal function in patients with advanced renal insufficiency. [7] However, an increase of up to 30% in SCr (serum creatinine) is expected. This is because the ACEI reduces Angiotensin II levels. Angiotensin II causes renal efferent arteriole vasoconstriction, and reduction of angiotensin II leads to vasodialation which in turn reduces GFR. This reduction in GFR causes the predicted increase in SCr.

However, one must not use a NSAID as NSAIDs reduce prostaglandin production. Prostaglandins cause vasodialation of the renal afferent arteriole, and a reduction in prostaglandin leads to vasoconstriction thus reducing GFR. However, this can lead to nephrotoxicity and thus NSAIDs must be avoided. [8]

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.

See also

References

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  1. 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. 
  2. 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. 
  3. 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. 
  4. 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. 
  5. 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. 
  6. 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. 
  7. Fan Fan Hou, M.D., Ph.D., Xun Zhang, M.D., Guo Hua Zhang, M.D., Ph.D., et al. (2006). "Efficacy and Safety of Benazepril for Advanced Chronic Renal Insufficiency". N Engl J Med 354 (2): 131–40. doi:10.1056/NEJMoa053107. PMID 16407508. 
  8. Whelton A. (1999). "Nephrotoxicity of Nonsteroidal Anti-Inflamatory Drugs: Physiologic Foundations and Clinical Implications". Am J Med 106: 13S–24S. doi:10.1016/S0002-9343(99)00113-8. 

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