Acute Kidney Injury (Acute Renal Failure)


Article Author:
Abhinav Goyal
Abdul Siddiqui
Parnaz Daneshpajouhnejad


Article Editor:
Khalid Bashir


Editors In Chief:
Susan Johnson
Alexandra Caley


Managing Editors:
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Benjamin Eovaldi
Radia Jamil
Sobhan Daneshfar
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Hajira Basit
Phillip Hynes


Updated:
6/18/2019 7:38:03 PM

Introduction

Acute kidney injury (AKI), formerly known as acute renal failure (ARF) denotes a sudden and often reversible reduction in the kidney function, as measured by glomerular filtration rate (GFR).  [1][2][3] There is no clear definition of AKI. Several different criteria have been used in research studies such as RIFLE, AKIN (Acute Kidney Injury Network) or KDIGO (Kidney Disease: Improving Global Outcomes) criteria. However, KDIGO is the most recent and most commonly used. According to KDIGO, AKI is the presence of any of the following:

  1. Increase in serum creatinine by 0.3 mg/dL or more (26.5 micromoles/L or more) within 48 hours
  2. Increase in serum creatinine to 1.5 times or more baseline, within the prior 7 days
  3. Urine volume less than  0.5 mL/kg/h for at least 6 hours

Etiology

The etiology of AKI has always been traditionally divided into three categories: pre-renal, renal and post-renal. Each of these categories has several different causes associated with them. [4][5]

Pre-renal includes any reduced blood flow to the kidney. This may be part of a systemic hypoperfusion resulting from hypovolemia or hypotension; or may be due to selective hypoperfusion to the kidneys such as those resulting from renal artery stenosis, aortic dissection.

Renal includes acute tubular necrosis which can result from several different causes. Prolonged renal ischemia, sepsis, and nephrotoxins being the most common ones. It is worthwhile mentioning that pre-renal injury can convert into renal injury if the exposure to offending factor is prolonged enough to cause cellular damage.

Post-renal mainly includes obstructive causes which lead to congestion of the filtration system and thus eventually lead to shutting down of the kidneys. The most common ones being renal/ureteral calculi, tumors or any urethral obstruction. Another noteworthy fact is that a unilateral obstruction may not always present as AKI especially if the obstruction is gradual such as a tumor because a normal working contralateral kidney may be able to compensate for the function of the affected kidney. Therefore, the most common etiology of post-renal AKI is bladder outlet obstruction.

Epidemiology

AKI is a very commonly seen in patients admitted to the hospital. It is often an important factor that contributes to decision to hospitalize for other conditions, if not being the sole reason for hospitalization. AKI is one of the most clinically impactful diseases since it affects patient management to a great extent regarding the treatment options for their primary disease. Most drugs or procedures that use contrast media may need to delay due to co-existent AKI. Most of the drugs are renally excreted, and dosages might need to be adjusted to account for the reduced renal function. Sometimes, it may even necessitate frequent monitoring of drug levels, for example, Vancomycin. AKI is thus an important contributor to longer hospital stays and patient morbidity. [6][7][8]

Pathophysiology

Pathogenesis of AKI is etiology driven. The common endpoint in all acute tubular necrosis is a cellular insult either secondary to ischemia or direct toxins which result in effacement of the brush border and eventually cell death thus shutting down the function of tubular cells.

History and Physical

The history and physical exam should focus on determining the etiology of AKI and the timeline of progression. If the history points towards hypovolemia or hypotension, then the treatment is guided towards volume repletion. The physician needs to look for inciting events such as diarrhea, nausea, vomiting which may have caused volume loss or any over the counter drugs such as NSAIDs or other nephrotoxins. One of the important signs to look for on physical exam is orthostatic vital signs since they are an important clue for hypovolemia and in an appropriate clinical context would guide treatment. History and physical are very important in AKI because more often than not, labs are unable to provide a clear answer as to the etiology of AKI.

Evaluation

All patients presenting with AKI warrant a basic lab panel including a basic metabolic panel. Sometimes, urine electrolytes can be helpful in suggesting an etiology of the AKI. Renal ultrasound can be helpful if obstructive causes are suspected. However, routine renal ultrasound for every patient with AKI is not warranted. Urine sediment examination can also provide important clues as to the etiology such as muddy brown casts seen in acute tubular necrosis. [9][10]

There are markers of tubular function that can be calculated to help distinguish an etiology like the fractional excretion of sodium and urea, urine osmolality but the sensitivity of all these markers is very poor, and they are affected by many drugs very commonly used in clinical practice such as diuretics. Therefore, no single marker can be reliably used in isolation to distinguish pre-renal from renal causes of AKI, which is a common misconception in clinical practice.

Treatment / Management

With the exception of post-renal AKI, most cases are an overlap between pre-renal and acute tubular necrosis type of AKI.   [11][12] The best way to determine if the AKI is pre-renal or not is a fluid challenge. If the clinical scenario doesn't contradict it, all patients with acute renal dysfunction should receive a fluid challenge. They require close monitoring of the urine output and renal function. If the renal function improves with fluid, that is the best indicator of a pre-Renal AKI. Acute tubular necrosis is very slow to recover and can take weeks to months for complete recovery of renal function. It may not normalize at all sometimes. Another important thing to consider for these patients is to avoid any further insult to the kidneys such as nephrotoxic drugs. Any and all medications need to be renally dosed once a patient develops AKI. Sometimes, AKI may need short-term renal replacement therapy till the kidney function recovers. This is seen especially in the oliguric phase of acute tubular necrosis, where the patient is prone to develop multiple electrolyte and acid-base abnormalities as well as fluid overload.[13]

Differential Diagnosis

  • Renal calculi
  • Sickle cell anemia
  • Chronic renal failure
  • Dehydration
  • Gastrointestinal bleeding
  • Heart failure
  • Urinary tract infection

Pearls and Other Issues

Mild AKI can often be managed, outpatient. AKI more often than not is a co-existent problem for hospitalized patients and usually is appropriate for these patients to be on the general medical floor unless they also have an electrolyte imbalance or significant volume overload, in which case, they may require a higher level of care. The most important issues to realize for clinicians dealing with AKI is to appropriately adjust the dose of any medications these patients are taking and avoiding nephrotoxic medications as much as possible. The other important thing to consider is an appropriate fluid challenge whenever possible.

Enhancing Healthcare Team Outcomes

AKI does have significant morbidity and mortality. The aim today is to try and prevent the condition in the first place by employing a multidisciplinary team approach. All healthcare workers must be aware of the condition and its causes. The pharmacist should ensure that at the first signs of creatinine elevation that the patient is on no nephrotoxic medications. The nurse should ensure that the patient is well hydrated prior to any contrast study and is making adequate urine. For those who do develop AKI, the nurse should educate the patient on agents to avoid to prevent worsening of the renal injury. Plus, close follow up with a nephrologist is highly recommended. Finally, the patient should have a dietary consult because the restriction of salt and fluid are vital when managing AKI. Similarly, the patient should avoid a high potassium diet when there is renal dysfunction. Because AKI induces a catabolic state, the patient should be encouraged to eat at least 1800 calories per day. [14][15][16](Level V)

Outcomes

The outcomes for patients with AKI depends on the cause of the renal dysfunction, the presence of any underlying kidney disease and duration of the renal dysfunction. In the past, it was widely believed that AKI was fully reversible in all patients. Studies now show that in patients with a low eGFR, not only is there a higher risk of progressing to end-stage renal disease but it also increases the mortality rate. In addition, AKI can also worsen the quality of life compared to the general population. Individuals who have a sudden increase in creatinine, usually tend to have the worst prognosis. Today, in-hospital mortality for patients with AKI varies between 30-50%, especially when dialysis is required. Negative prognostic factors include:

  • Advanced age
  • Oliguria
  • Use of vasopressors
  • Multiorgan dysfunction
  • Need for blood transfusions
  • Hypotension

Over the long term, at least 12-15% of patients with AKI may require permanent dialysis. Mortality is increased in patients with high APACHE lll score, advanced age and persistent elevation of creatinine.[17][18] (Level V)


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Acute Kidney Injury (Acute Renal Failure) - Questions

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What is the most common cause of acute renal failure in children?



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Which of the following does not cause renal failure in trauma patients?



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A post-pneumonectomy patient develops renal failure. Which of the following is not consistent with prerenal failure?



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A patient received gentamicin sulfate 3 mg/kg every 8 hours to treat a life-threatening infection. Following the administration of this drug, the patient complained of nausea and vomiting. Fluid balance indicates a blood urea nitrogen of 46 mg/dl, creatinine of 2.6 mg/l, sodium of 148 mEq/l, and potassium of 4.8 mEq/l. These laboratory results suggest which of the following?



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The doctor recommends that a patient collect early morning urine before ingestion of any fluids. What is the reason for this recommendation?



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Which of the following is not a cause of postrenal kidney failure?



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A 69-year-old man with diverticular disease has an elective sigmoid resection. Intravenous D5 0.45 normal saline is given at 100 ml per hour. His urine output initially is approximately 40 ml per hour, but drops to 20 ml per hour on post-op day 4. Arterial blood gas is remarkable for a pH of 7.27 and PCO2 of 28 mmHg. Potassium is 5.6 mEq/L, BUN is 90 mg/dL, and creatinine is 5.0 mg/dL. Urine sodium is 80 mEq/L. What is the most likely diagnosis?



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Which of the following is FALSE about renal impairment?



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In a patient with renal failure, edema is most likely to appear in the morning around which of the following?



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Which of the following is an indication for initiation of hemodialysis in a patient with acute renal failure?



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What type of renal failure is caused by obstruction secondary to prostate enlargement?



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In a patient with acute renal failure, what type of diet is not recommended?



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What is the most common cause of death associated with acute renal failure?



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What is the most common cause of renal failure after an acute myocardial infarction?



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Why are levels of blood urea nitrogen elevated in cases of acute renal failure?



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Which of the following is TRUE regarding the prognosis of a patient who has shown some improvement following an episode of acute renal failure two weeks ago?



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Which of the following is NOT associated with postoperative renal failure?



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Which of the following is rarely a feature of acute renal failure?



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What is the most common cause of acute renal failure in hospitalized patients?



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When should hemodialysis be initiated in cases of acute renal failure?



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A 67-year-old female who is status post abdominal aortic aneurysm repair has a foley catheter in place. She has a blood pressure of 116/72 and pulse of 113. Her urine output drops to 44 cc/hour and creatinine rises to 2.9 mg/dL. Which diagnostic test should be ordered first?



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A patient with acute renal failure has a potassium of 6.9 mEq/L. What other diagnostic study should be done emergently?



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A 69-year-old male is hospitalized with a myocardial infarction and is treated with percutaneous angioplasty and stent. He developed urosepsis on his third day of hospitalization and was started on ampicillin and gentamicin. On day 4 he was in congestive heart failure and was treated with intravenous furosemide. On day 5 he was given ibuprofen for a fever. On day 6 he was in renal failure. Urinalysis showed 15 WBC/HPF, 2 RBC/HPF, and eosinophils. Creatinine is 4.5 mg/dL and complement levels are very low. What was the most likely cause of the renal failure?



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What type of acute renal failure is associated with medication nephrotoxicity?



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A 50-year-old woman is brought to the emergency department by her husband due to flank and pelvic pain, nausea, and vomiting. Blood tests reveal levels of sodium at 130 meq/L, potassium at 6.2 meq/l, bicarbonate at 20 meq/L, blood urea nitrogen at 30 mg/dL, and creatinine at 3.0 mg/dL. Which of the following is the most likely pathogenesis of her signs and symptoms?



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What type of acute renal failure is associated with hypovolemia?



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Which laboratory feature is not associated with acute renal failure?



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Which of the following is associated with renal failure?



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Which interventions can help prevent the development of acute renal failure due to contrast-induced nephropathy?



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A 62-year-old female is seen for possible acute renal failure. Select the finding that would be of most concern?



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Which of the following is not true of the Kidney Disease: Improving Global Outcomes (KDIGO) definition of acute kidney injury (AKI)?



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The patient who is functionally anephric, and who withdraws from dialytic therapy, dies primarily because of:



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After being administered gentamicin for a serious bone infection, the patient experiences nausea and vomiting. Lab work reveals the following: sodium 145 mEq/L, potassium 5.0 mEq/L, BUN 42 mg/dL, and creatinine 2.7 mg/L. What do these lab results indicate?



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A 14-year-old girl is rescued from the rubble of a collapsed hotel 3 days after an earthquake. She is conscious, hemodynamically stable, and has crush injuries to both legs. You are at a field hospital and can do basic labs. An ECG shows sinus bradycardia at 40 bpm with a wide QRS. Her potassium is 7 mmol/L and creatinine is 6.0 mg/dL. What is the definitive treatment for her condition?



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A client was not feeling well and presented to the emergency department. A workup reveals that the client has developed acute renal failure. Which of the following is true regarding acute renal failure? Select all that apply.



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Acute Kidney Injury (Acute Renal Failure) - References

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