Acute Kidney Injury (Acute Renal Failure)


Article Author:
Abhinav Goyal
Parnaz Daneshpajouhnejad


Article Editor:
Khalid Bashir


Editors In Chief:
Dustin Constant
Donald Kushner


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Kyle Blair
Trevor Nezwek
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Daniyal Ameen
Altif Muneeb
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes
Komal Shaheen
Sandeep Sekhon


Updated:
9/9/2019 10:10:14 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] AKI can lead to accumulation of water, sodium, and other metabolic products as well as cause of electrolyte disturbances. It is a very common condition especially among hospitalized patients. It can be seen in up to 7% of hospital admissions and 30% ICU admissions. 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 maybe due to selective hypoperfusion to the kidneys such as those resulting from renal artery stenosis, aortic dissection. Few examples with the mechanism of AKI are listed below:

1. Hypovolemia: Gastrointestinal fluid losses such as diarrhea, vomiting, high ostomy output, etc, Hemorrhage, Severe burns

2. Hypotension from the decreased cardiac output: cardiogenic shock, massive pulmonary embolism, acute coronary syndrome

3. Hypotension from systemic vasodilation: Septic shock, Anaphylaxis, Anesthesia administration, Hepatorenal syndrome

4. Renal vasoconstriction: NSAIDs, Iodinated contrast, Amphotericin B, Calcineurin inhibitors, Hepatorenal syndrome

5. Glomerular efferent arteriolar vasodilation: ACE inhibitors, Angiotensin receptor blockers

Intrinsic renal includes acute tubular necrosis, acute interstitial nephritis among others 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 a renal injury if the exposure to offending factor is prolonged enough to cause cellular damage. Few examples with the mechanisms are listed below:

1. Acute tubular necrosis: Ischemia from prolonged pre-renal injury, drugs such as aminoglycosides, vancomycin, amphotericin B, pentamidine; rhabdomyolysis, intravascular hemolysis

2. Acute interstitial nephritis: Drugs such as beta-lactam antibiotics, penicillins, NSAIDs, PPI, 5-ASA; Infections, Autoimmune conditions (SLE, IgG related disease)

3. Glomerulonephritis: Anti-glomerular basement membrane disease, Immune complex-mediated diseases such as SLE, Post-infectious glomerulonephritis, cryoglobulinemia, IgA nephropathy, Henoch-Schonlein purpura.

4. Intratubular obstruction: Monoclonal gammopathy seen in multiple myeloma, tumor lysis syndrome, toxins such as ethylene glycol. 

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, blood clots 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. Intratubular obstruction by pigments such as myoglobin or crystals such as uric acid in tumor lysis syndrome or immunoglobulin light chains as seen in monoclonal gammopathy may also lead to the same end result. On the other hand, the mechanism of injury in glomerulonephritis may be due to direct immune-mediated injury of the vessels or immune complex deposition leading to an immune response and damage to the glomeruli. 

Histopathology

Histopathology can reliably differentiate intrinsic renal patterrn of AKI from others however the histopathology may not be reliable at narrowing down a specific cause in every situation. Clinical  Renal biopsy is an invasive procedure and usually only pursued in cases where a significant impact on management in expected such as suspected glomerulonephritis. Immunoflourescene patterns and electron microscopy can help differentiate various causes in those cases.

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. Moreover, a careful review of past medical history to reveal any co-morbid conditions can also help narrow down the etiology of AKI e.g. cirrhosis, history of blood clots requiring anticoagulation. 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.

Most common causes of AKI in hospitalized patients are in this order:

  1. ATN – 45%
  2. Prerenal disease – 21%
  3. Acute superimposed on CKD – 13%
  4. Urinary tract obstruction – 10% (most often due to Benign prostatic hypertrophy in older men)
  5. Glomerulonephritis or vasculitis – 4%
  6. AIN – 2%
  7. Atheroemboli – 1%

Evaluation

Evaluation of AKI should include a thorough search for all possible etiologies of AKI including prerenal, intrinsic renal, and post renal disease. The timing onset of AKI can be especially helpful to hospitalized patients. For example, patients labs are being checked every day and creatinine suddenly starts to rise on day 4 then an inciting factor can usually be found in 24-48 hours preceding the onset. It is especially important to look for any radiologic studies that might have been done and utilized iodinated contrast agents which are not an uncommon cause of AKI. It is also extremely important to review the list of medications that the patient is receiving as they can be co-contributors or nephrotoxic and may need their dose modified in view of decreased renal function. ACE inhibitors and ARBs are often the co-contributors to AKI. A good physical exam can also be helpful sometimes e.g. presence of a drug rash may point to Acute interstitial nephritis being the etiology, cyanotic toes could suggest cholesterol emboli in a patient post cardiac catheterization.

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. Urine protein, urine osmolality, and urine albumin to creatinine ratios can also be helpful clues in determining the etiology of AKI. Older patients without any obvious etiology should also be subjected to Serum and Urine protein electrophoresis (SPEP and UPEP) to rule out monoclonal gammopathy from multiple myeloma. Renal ultrasound can be helpful if obstructive causes are suspected. However, routine renal ultrasound for every patient with AKI is not warranted. CT non-contrast is another important radiographic modality and can be used to look for nephrolithiasis or urolithiasis. Urine sediment examination can also provide important clues as to the etiology such as muddy brown casts seen in acute tubular necrosis. Sterile pyuria is the most sensitive sign of acute interstitial nephritis. [9][10]

A kidney biopsy is an excellent but infrequently utilized tool. It is usually indicated in patients with rapidly declining renal function without apparent cause or to find out the exact etiology of AKI in the setting where multiple etiologies could be responsible. It is a test not without risks due to the possibility of complications such as bleeding (especially in patients with platelet dysfunction from uremia). 

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.

Lastly, attention also needs to be paid to the overall clinical picture. It is important to assess the volume status of the patient to exclude possible cardiorenal or hepatorenal syndrome. The cardiorenal syndrome is usually due to poor glomerular filtration due to venous congestion along with a lack of forward flow in some cases due to poor cardiac output. Hepatorenal syndrome is due to the differential distribution of circulation volume with systemic vasodilation and splanchnic vasoconstriction leading to the diversion of blood into the periphery and limitation of blood supply to kidneys. 

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. Diuretics may be required during the oliguric phase of ATN if significant volume overload develops. 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. Another key issue may be a limitation of dietary ingestion of potassium and phosphorus. Sometimes, AKI may need short-term renal replacement therapy till the kidney function recovers. Dialysis is usually required to manage the complications of AKI such as severe hyperkalemia, uremic pericarditis, pulmonary edema, etc. 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] When required dialysis in this setting is usually performed through a double lumen central venous catheter. Continuous renal replacement therapy can also be utilized in patients who cannot tolerate hemodialysis due to hypotension. It is a much slower continuous type of dialysis. Correction of some of the metabolic abnormalities along with dialysis may be required. Metabolic acidosis is one such instance where systemic administration of citrate or bicarbonate is often required to maintain a suitable blood pH. The requirement for renal replacement therapy should be reevaluated in these patients on a daily basis while they are hospitalized and at least weekly thereafter until the kidney function is stable. Renal replacement therapy is usually required for short term ranging from a few days to a few weeks in most cases however Acute tubular necrosis can take up to months to recover and may, therefore, require intermittent hemodialysis support during that time.

There are certain specific treatments that are required for acute kidney injury in specific circumstances such as administration of vasoactive medications and colloids for treatment of hepatorenal syndrome, cautious diuresis in cardiorenal syndrome. Acute kidney injury from various glomerunephritides may require immunosuppressive medications for treatment. Acute interstitial nephritis which does not recover with supportive care may benefit from a trial of steroids. Post renal obstruction may need to be relieved operatively in certain situations. For example, benign prostatic hypertrophy may require surgical relief of bladder outlet obstruction. Urethral calculi may require ureteral stenting and lithotripsy. 

It is also important to note that in certain situation the risk of acute kidney injury may be decreased by taking some measures. For example, in high-risk patients such as those with compromised renal function at baseline it may be beneficial to administer peri-procedure intravenous fluids to prevent contrast-induced nephropathy when performing cardiac catheterization, etc. 

Differential Diagnosis

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

Prognosis

 Most cases of acute kidney injury recover completely with supportive management however the prognosis mostly depends on the etiology of AKI. Most cases of pre-renal AKI recover completely with correction of the underlying insult if caught early however the persistence of underlying insult may lead to acute tubular necrosis in which case the damage may not be completely reversible. The other consideration to keep in mind is that although recovery from individual episode may be complete or partial, repeated AKIs can lead to a cumulative worsening of renal function. Therefore, it is important to follow these patients either to the normalization of renal function or until its stable to decide whether that is gonna be their new baseline. 

Complications

Most common complications include metabolic derangements such as:

  1. Hyperkalemia- If severe it can lead to arrythmias because of which renal replacement therapy is required in cases of severe hyperkalemia.
  2. Metabolic acidosis- Inability of kidney to excrete acids leads to metabolic acidosis and may necessitate systemic administration of bicarbonate or citrate buffers.
  3. Hyperphosphatemia- Can usually be prevented by decreasing dietary ingestion or using phosphorus binders.
  4. Other effects include pulmonary edema from volume overload, peripheral edema from an inability to excrete body water. This is especially common in the oliguric phase of acute tubular necrosis. It may necessitate use of diuretics or renal replacement therapy.

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

Acute kidney injury (AKI) does have significant morbidity and mortality if it is left untreated. The aim today is to try and prevent the condition in the first place by employing an interprofessional team approach. All healthcare workers must be aware of the condition, its causes, and potential complications.

The pharmacist should ensure that at the first signs of creatinine elevation that the patient is on no nephrotoxic medications. The patient should be educated that the regular consumption of NSAIDs is harmful to the kidney. the patient should be instructed to remain compliant with his blood pressure medications, since uncontrolled hypertension can worsen kidney injury.

The nurse practitioner should ensure that the patient is well hydrated prior to any contrast study and is making adequate urine. For those who do develop Acute kidney injury, the nurse should educate the patient on agents (eg NSAIDs) 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 Acute kidney injury. Similarly, the patient should avoid a high potassium diet when there is renal dysfunction. Because acute kidney injury induces a catabolic state, the patient should be encouraged to eat at least 1800 calories per day. [14][15][16](Level V)

Finally, the primary care provider should closely monitor renal function and it is worsening, a prompt nephrologist consult is recommended. Only through an interprofessional approach can the morbidity of acute kidney injury be lowered. If the kidney injury is allowed to progress, end-stage renal disease is the outcome. 

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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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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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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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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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 rarely a feature of acute renal failure?



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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 of the following is associated with renal failure?



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A 40-year-old male patient is brought to the emergency department with a complaint of the worst headache in his life. On examination, he does not have any neurological deficit. A computed tomogram (CT) is done, which shows subarachnoid hemorrhage in the right Sylvian fissure. He is being planned for CT cerebral angiogram. It is noted that he has diabetes. Which of the following interventions can help prevent the development of acute renal failure due to contrast-induced nephropathy in this patient?



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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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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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A 65-year-old female with diabetes mellitus presents with complaints of decreased urination, nausea, fatigue, and swelling in her legs. One week ago, she was started on medication for the treatment of her urinary tract infection. Today, her blood tests show elevated BUN and serum creatinine levels. Which of the following medications most likely precipitated her current symptoms?



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A 32-year-old man is brought by his neighbor to the emergency department after being found on the floor in the parking lot. The neighbor mentions that the patient has a history of recreational drug use. There is a pool of urine around him. He is confused, not oriented to time or place, and does not recall anything related to the event. His blood pressure is 110/70 mmHg, and his heart rate is 120/min. He talks and moves all his extremities. His electrolytes and liver function tests are normal. He has a CPK of 30,000 units/L. His urine toxicology screen is positive for cocaine and cannabinoids. The patient is at the greatest risk of which of the following complications?



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A 78-year-old woman who lives in a nursing home is brought to the emergency department due to a day of lethargy and confusion. She is febrile and disoriented. Past medical history includes diabetes mellitus and hypertension. During the hospitalization, she received gentamicin sulfate 3 mg/kg every 8 hours to treat a life-threatening infection. Following the administration of this drug, the patient became more irritable and vomited several times. Fluid balance indicates a blood urea nitrogen of 46 mg/dL, creatinine of 2.6 mg/dL, sodium of 148 mEq/L, and potassium of 4.8 mEq/L. Which of the following is the most appropriate next step in the management of this patient?



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A 66-year-old male presents to the emergency department complaining of severe lower abdominal pain and an inability to urinate. He reports that he last urinated approximately eight hours ago. When asked to urinate, only a few drops dribble. Further assessment reveals that the patient has experienced progressively worsening difficulty with urinating over the past two years, and he usually wakes up three times a night for urination. He has lived alone for the past five years since his wife passed away. He has not seen a doctor since then. His temperature is 98.8 F (37.1 C), blood pressure is 140/95 mmHg, pulse rate is 105/min, and respiratory rate is 21/min. He appears to be in severe pain. Physical examination reveals a distended bladder and significant tenderness to palpation over the inferior aspect of his abdomen. Which of the following sets of laboratory values is most likely to be found in the urinalysis of this patient?



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A 65-year-old male is admitted to the emergency department after falling from the second floor of a building when he was working as a construction manager in a rural area. He was not rescued until 5 hours after the accident. Upon entrance to the emergency department, he is found to have multiple lacerations as well as a pelvic fracture. His past medical history includes diabetes and benign prostatic hyperplasia, for which he takes metformin and tamsulosin, respectively. Besides, he has a family history of autoimmune diseases. Serum studies show sodium 135 mEq/L, creatinine 1.6 mg/dL, and blood urea nitrogen 38 mg/dL. Urinalysis shows sodium 12 mEq/L, creatinine 18 mg/dL, and osmolality 590 mOsm/kg. Which of the following is the most likely cause of this patient's increased creatinine level?



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Acute Kidney Injury (Acute Renal Failure) - References

References

Muroya Y,He X,Fan L,Wang S,Xu R,Fan F,Roman RJ, Enhanced Renal Ischemia-Reperfusion Injury in Aging and Diabetes. American journal of physiology. Renal physiology. 2018 Sep 12     [PubMed]
Palevsky PM, Endpoints for Clinical Trials of Acute Kidney Injury. Nephron. 2018 Sep 11     [PubMed]
Zuber K,Davis J, The ABCs of chronic kidney disease. JAAPA : official journal of the American Academy of Physician Assistants. 2018 Sep 10     [PubMed]
Moresco RN,Bochi GV,Stein CS,De Carvalho JAM,Cembranel BM,Bollick YS, Urinary kidney injury molecule-1 in renal disease. Clinica chimica acta; international journal of clinical chemistry. 2018 Sep 7     [PubMed]
Crabbs TA, Acute Kidney Injury (AKI)-The Toxicologic Pathologist's Constant Companion. Toxicologic pathology. 2018 Sep 6     [PubMed]
Winther-Jensen M,Kjaergaard J,Lassen JF,Køber L,Torp-Pedersen C,Hansen SM,Lippert F,Kragholm K,Christensen EF,Hassager C, Use of renal replacement therapy after out-of-hospital cardiac arrest in Denmark 2005-2013. Scandinavian cardiovascular journal : SCJ. 2018 Sep 5     [PubMed]
Park S,Lee S,Lee A,Paek JH,Chin HJ,Na KY,Chae DW,Kim S, Awareness, incidence and clinical significance of acute kidney injury after non-general anesthesia: A retrospective cohort study. Medicine. 2018 Aug     [PubMed]
Kirkley MJ,Boohaker L,Griffin R,Soranno DE,Gien J,Askenazi D,Gist KM, Acute kidney injury in neonatal encephalopathy: an evaluation of the AWAKEN database. Pediatric nephrology (Berlin, Germany). 2018 Aug 28     [PubMed]
Sanguankeo A,Upala S, Limitations of Fractional Excretion of Urea in Clinical Practice. Hepatology (Baltimore, Md.). 2018 Sep 4     [PubMed]
Brkovic V,Milinkovic M,Kravljaca M,Lausevic M,Basta-Jovanovic G,Marković-Lipkovski J,Naumovic R, Does the pathohistological pattern of renal biopsy change during time? Pathology, research and practice. 2018 Aug 10     [PubMed]
Cahn A,Melzer-Cohen C,Pollack R,Chodick G,Shalev V, Acute renal outcomes with SGLT-2 inhibitors - real world data analysis. Diabetes, obesity     [PubMed]
Abdelsalam M,Elnagar SSE,Mohamed AH,Tawfik M,Sayed Ahmed N, Community Acquired Acute Kidney Injury in Mansoura Nephrology Dialysis Unit: One Year Prospective Observational Study. Nephron. 2018 Sep 11     [PubMed]
Azzalini L,Vilca LM,Lombardo F,Poletti E,Laricchia A,Beneduce A,Maccagni D,Demir OM,Slavich M,Giannini F,Carlino M,Margonato A,Cappelletti A,Colombo A, Incidence of contrast-induced acute kidney injury in a large cohort of all-comers undergoing percutaneous coronary intervention: Comparison of five contrast media. International journal of cardiology. 2018 Sep 1     [PubMed]
Hobson C,Lysak N,Huber M,Scali S,Bihorac A, Epidemiology, outcomes, and management of acute kidney injury in the vascular surgery patient. Journal of vascular surgery. 2018 Sep     [PubMed]
Doi K,Nishida O,Shigematsu T,Sadahiro T,Itami N,Iseki K,Yuzawa Y,Okada H,Koya D,Kiyomoto H,Shibagaki Y,Matsuda K,Kato A,Hayashi T,Ogawa T,Tsukamoto T,Noiri E,Negi S,Kamei K,Kitayama H,Kashihara N,Moriyama T,Terada Y, The Japanese Clinical Practice Guideline for acute kidney injury 2016. Journal of intensive care. 2018     [PubMed]
Sarin SK,Choudhury A, Management of acute-on-chronic liver failure: an algorithmic approach. Hepatology international. 2018 Aug 16     [PubMed]
Huang ST,Ke TY,Chuang YW,Lin CL,Kao CH, Renal complications and subsequent mortality in acute critically ill patients without pre-existing renal disease. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. 2018 Sep 10     [PubMed]
Helgason D,Long TE,Helgadottir S,Palsson R,Sigurdsson GH,Gudbjartsson T,Indridason OS,Gudmundsdottir IJ,Sigurdsson MI, Acute kidney injury following coronary angiography: a nationwide study of incidence, risk factors and long-term outcomes. Journal of nephrology. 2018 Sep 5     [PubMed]

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