Podcast
Questions and Answers
Which statement best illustrates the contemporary understanding of Acute Kidney Injury (AKI) compared to Acute Renal Failure (ARF)?
Which statement best illustrates the contemporary understanding of Acute Kidney Injury (AKI) compared to Acute Renal Failure (ARF)?
- ARF is preferred as it emphasizes the reversible nature of kidney dysfunction better than AKI.
- ARF is now understood to include only cases requiring dialysis, while AKI encompasses all levels of kidney dysfunction.
- AKI focuses exclusively on kidney function declines that result in overt organ failure and mortality.
- AKI recognizes that even small reductions in kidney function, not resulting in organ failure, can be clinically relevant. (correct)
According to the Kidney Disease Improving Global Outcomes (KDIGO) definition, which criterion, if observed in isolation, would NOT be sufficient to diagnose AKI?
According to the Kidney Disease Improving Global Outcomes (KDIGO) definition, which criterion, if observed in isolation, would NOT be sufficient to diagnose AKI?
- Requirement for renal replacement therapy due to rapidly declining kidney function. (correct)
- An increase in serum creatinine to 1.6 times the patient's established baseline value within the past week.
- A documented urine volume of 0.4 mL/kg/hour for a continuous period of six hours.
- A serum creatinine increase of 0.4 mg/dL within a 36-hour period.
Based on the provided data regarding mortality rates in hospitalized patients with AKI, what inference can be made about the relationship between AKI stage and mortality?
Based on the provided data regarding mortality rates in hospitalized patients with AKI, what inference can be made about the relationship between AKI stage and mortality?
- Mortality increases linearly and proportionally with each advancing stage of AKI.
- Non-elective mortality is approximately five times higher than AKI stage 1 mortality.
- Mortality rates are statistically similar between AKI stage 2 and AKI stage 3. (correct)
- Mortality is primarily driven by factors other than AKI stage; the data reflects a weak correlation overall.
Considering the natural history of AKI, as depicted in the provided diagram, which statement is most accurate regarding the long-term implications for a patient who experiences AKI?
Considering the natural history of AKI, as depicted in the provided diagram, which statement is most accurate regarding the long-term implications for a patient who experiences AKI?
Which of the following scenarios is most likely to lead to pre-renal AKI due to 'Low effective arterial blood volume (EABV)' with the LEAST association to hypovolemia?
Which of the following scenarios is most likely to lead to pre-renal AKI due to 'Low effective arterial blood volume (EABV)' with the LEAST association to hypovolemia?
A patient is diagnosed with Acute Tubular Necrosis (ATN) following prolonged hypotension. Which pathological event is MOST directly responsible for the subsequent loss of renal function?
A patient is diagnosed with Acute Tubular Necrosis (ATN) following prolonged hypotension. Which pathological event is MOST directly responsible for the subsequent loss of renal function?
What is the underlying mechanism by which long-term NSAID use can lead to post-renal AKI?
What is the underlying mechanism by which long-term NSAID use can lead to post-renal AKI?
Which medication is LEAST likely to cause crystal nephropathy?
Which medication is LEAST likely to cause crystal nephropathy?
A patient presents with AKI, and the physical exam reveals ecchymosis, asterixis and confusion. Which of the following is the most likely underlying cause?
A patient presents with AKI, and the physical exam reveals ecchymosis, asterixis and confusion. Which of the following is the most likely underlying cause?
Which area of the patient's history would be MOST informative in guiding the differential diagnosis of AKI?
Which area of the patient's history would be MOST informative in guiding the differential diagnosis of AKI?
What condition would be LEAST likely to be considered in the differential diagnosis for volume overload in a patient presenting with AKI?
What condition would be LEAST likely to be considered in the differential diagnosis for volume overload in a patient presenting with AKI?
A patient with AKI develops acute liver failure and hepatic encephalopathy. What component of the differential diagnosis is most relevant given these additional findings?
A patient with AKI develops acute liver failure and hepatic encephalopathy. What component of the differential diagnosis is most relevant given these additional findings?
Why is eGFR not an accurate measure of kidney function in AKI?
Why is eGFR not an accurate measure of kidney function in AKI?
According to the staging criteria for AKI, which of the following meets the criteria for stage 3 AKI?
According to the staging criteria for AKI, which of the following meets the criteria for stage 3 AKI?
A patient with AKI has laboratory results showing increased creatinine and potassium levels. Which diagnostic category would be LEAST helpful in this situation?
A patient with AKI has laboratory results showing increased creatinine and potassium levels. Which diagnostic category would be LEAST helpful in this situation?
In the context of laboratory studies differentiating pre-renal AKI from ATN, which combination of findings would strongly suggest ATN?
In the context of laboratory studies differentiating pre-renal AKI from ATN, which combination of findings would strongly suggest ATN?
A patient with suspected post-renal AKI requires imaging. Which imaging modality should be performed initially to assess for hydronephrosis?
A patient with suspected post-renal AKI requires imaging. Which imaging modality should be performed initially to assess for hydronephrosis?
Under what specific clinical circumstance is a renal biopsy MOST strongly indicated in the evaluation of AKI?
Under what specific clinical circumstance is a renal biopsy MOST strongly indicated in the evaluation of AKI?
According to the provided information, what is the FIRST and MOST critical step in the management of AKI?
According to the provided information, what is the FIRST and MOST critical step in the management of AKI?
According to the information provided, what is the correct action to take when encountering a patient with possible AKI?
According to the information provided, what is the correct action to take when encountering a patient with possible AKI?
Which recommendation regarding diuretic use in AKI reflects current best practice?
Which recommendation regarding diuretic use in AKI reflects current best practice?
Which action is MOST appropriate in the targeted management of AKI secondary to AIN or RPGN?
Which action is MOST appropriate in the targeted management of AKI secondary to AIN or RPGN?
Which of the following is the LEAST effective measure to prevent contrast-induced nephropathy?
Which of the following is the LEAST effective measure to prevent contrast-induced nephropathy?
According to the provided information, what long-term outcome should be a primary concern following an episode of AKI, requiring proactive management and monitoring?
According to the provided information, what long-term outcome should be a primary concern following an episode of AKI, requiring proactive management and monitoring?
What is the underlying criteria for initiating renal replacement therapy (RRT) as indicated by the mnemonic AEIOU?
What is the underlying criteria for initiating renal replacement therapy (RRT) as indicated by the mnemonic AEIOU?
What action is associated with 'maintain circulation' in the context of AKI prevention?
What action is associated with 'maintain circulation' in the context of AKI prevention?
An 80-year-old female with osteoarthritis is admitted with nausea, vomiting, and dehydration. She has been taking ibuprofen for knee pain. Labs reveal: Creatinine 330 µmol/L (Normal 50-120), BUN 14.28 mmol/L (Normal 2.5-8.5), K+ 3.3 mmol/L (Normal 3.5-5.0), Na+ 140 mmol/L (Normal 135-145), urine WBC+, nitrates negative. Which pathogenic mechanism is most likely?
An 80-year-old female with osteoarthritis is admitted with nausea, vomiting, and dehydration. She has been taking ibuprofen for knee pain. Labs reveal: Creatinine 330 µmol/L (Normal 50-120), BUN 14.28 mmol/L (Normal 2.5-8.5), K+ 3.3 mmol/L (Normal 3.5-5.0), Na+ 140 mmol/L (Normal 135-145), urine WBC+, nitrates negative. Which pathogenic mechanism is most likely?
Compared to AKI Stage 1, what changes are expected in management of AKI Stage 3?
Compared to AKI Stage 1, what changes are expected in management of AKI Stage 3?
During a septic episode, a patient prescribed Gentamicin develops AKI, to the level of requiring hospitalization. In addition to managing the sepsis and following the 'STOP AKI' mnemonic, which action is MOST crucial?
During a septic episode, a patient prescribed Gentamicin develops AKI, to the level of requiring hospitalization. In addition to managing the sepsis and following the 'STOP AKI' mnemonic, which action is MOST crucial?
A patient with AKI, metabolic acidosis and hyperkalemia is administered a low volume of IV fluids and provided sodium bicarbonate. What criteria should prompt you to pursue renal replacement therapy?
A patient with AKI, metabolic acidosis and hyperkalemia is administered a low volume of IV fluids and provided sodium bicarbonate. What criteria should prompt you to pursue renal replacement therapy?
You are deciding on imaging for a patient in which you suspect AKI to be occurring. To what should your decision be balanced against?
You are deciding on imaging for a patient in which you suspect AKI to be occurring. To what should your decision be balanced against?
Why is a patient's prior morbidity an important factor in assessing AKI risk?
Why is a patient's prior morbidity an important factor in assessing AKI risk?
During an admission for AKI. When should you conduct an urine analysis and C3/C4 electrophoresis?
During an admission for AKI. When should you conduct an urine analysis and C3/C4 electrophoresis?
Given a scenario where a patient with pulmonary edema secondary to AKI is not responding to diuretics, what action is most likely to be needed?
Given a scenario where a patient with pulmonary edema secondary to AKI is not responding to diuretics, what action is most likely to be needed?
Why is it important to observe a patient and obtain regular blood tests even if they are improving?
Why is it important to observe a patient and obtain regular blood tests even if they are improving?
Why is managing the acute illness that lead to AKI significant?
Why is managing the acute illness that lead to AKI significant?
In a patient with AKI, which scenario BEST illustrates the complex interplay between pre-renal factors and intrinsic renal damage, leading to a sustained reduction in kidney function?
In a patient with AKI, which scenario BEST illustrates the complex interplay between pre-renal factors and intrinsic renal damage, leading to a sustained reduction in kidney function?
Considering the various causes of AKI, which pathophysiological mechanism represents the MOST direct link between systemic inflammation and acute kidney damage?
Considering the various causes of AKI, which pathophysiological mechanism represents the MOST direct link between systemic inflammation and acute kidney damage?
A patient with a history of lupus develops AKI. What combination of findings would MOST strongly suggest a diagnosis of lupus nephritis as the underlying cause, rather than ATN from hypotension?
A patient with a history of lupus develops AKI. What combination of findings would MOST strongly suggest a diagnosis of lupus nephritis as the underlying cause, rather than ATN from hypotension?
In managing AKI, what scenario would warrant the MOST urgent and immediate initiation of renal replacement therapy (RRT) based solely on the AEIOU criteria?
In managing AKI, what scenario would warrant the MOST urgent and immediate initiation of renal replacement therapy (RRT) based solely on the AEIOU criteria?
Following recovery from an episode of AKI, a patient's creatinine levels have returned to baseline. Which long-term management strategy is MOST critical in preventing future adverse outcomes?
Following recovery from an episode of AKI, a patient's creatinine levels have returned to baseline. Which long-term management strategy is MOST critical in preventing future adverse outcomes?
A patient with known heart failure is admitted with increasing dyspnea and lower extremity edema. Lab results show a rise in creatinine. What is the MOST likely mechanism of AKI in this patient?
A patient with known heart failure is admitted with increasing dyspnea and lower extremity edema. Lab results show a rise in creatinine. What is the MOST likely mechanism of AKI in this patient?
A patient develops AKI following several days of NSAID use for back pain. What is the MOST likely mechanism by which NSAIDs contribute to AKI?
A patient develops AKI following several days of NSAID use for back pain. What is the MOST likely mechanism by which NSAIDs contribute to AKI?
Which of the following scenarios BEST exemplifies how sepsis can lead to intrinsic AKI?
Which of the following scenarios BEST exemplifies how sepsis can lead to intrinsic AKI?
Which of the following intrinsic renal diseases is MOST likely to present with granular, red cell, and other cellular casts in the urine sediment, accompanied by a variable degree of proteinuria?
Which of the following intrinsic renal diseases is MOST likely to present with granular, red cell, and other cellular casts in the urine sediment, accompanied by a variable degree of proteinuria?
A patient with a history of multiple myeloma presents with AKI. What is the MOST likely cause of the AKI in this setting?
A patient with a history of multiple myeloma presents with AKI. What is the MOST likely cause of the AKI in this setting?
A patient is diagnosed with post-renal AKI due to bilateral ureteral obstruction from nephrolithiasis. What is the MOST appropriate next step in management?
A patient is diagnosed with post-renal AKI due to bilateral ureteral obstruction from nephrolithiasis. What is the MOST appropriate next step in management?
A patient undergoing treatment for tuberculosis develops AKI. Which medication is MOST likely to be the cause?
A patient undergoing treatment for tuberculosis develops AKI. Which medication is MOST likely to be the cause?
A patient with AKI is suspected of having acute interstitial nephritis (AIN). Which medication is LEAST likely to be associated with this condition?
A patient with AKI is suspected of having acute interstitial nephritis (AIN). Which medication is LEAST likely to be associated with this condition?
A patient presents with AKI, and the physical exam reveals dry mucous membranes, reduced skin turgor and hypotension. What is the MOST likely underlying cause?
A patient presents with AKI, and the physical exam reveals dry mucous membranes, reduced skin turgor and hypotension. What is the MOST likely underlying cause?
A patient develops pulmonary edema secondary to AKI. Which physical exam finding would be MOST consistent with this condition?
A patient develops pulmonary edema secondary to AKI. Which physical exam finding would be MOST consistent with this condition?
A patient with AKI also exhibits confusion and asterixis. Which diagnostic category is MOST relevant to these findings?
A patient with AKI also exhibits confusion and asterixis. Which diagnostic category is MOST relevant to these findings?
A patient with AKI is being evaluated for possible post-renal obstruction. Which symptom is MOST suggestive of this condition?
A patient with AKI is being evaluated for possible post-renal obstruction. Which symptom is MOST suggestive of this condition?
A patient presents with AKI. Why is relying solely on eGFR problematic in this acute setting?
A patient presents with AKI. Why is relying solely on eGFR problematic in this acute setting?
According to the AKI staging criteria, which laboratory value, in isolation, indicates stage 1 AKI?
According to the AKI staging criteria, which laboratory value, in isolation, indicates stage 1 AKI?
What combination of laboratory findings would STRONGLY suggest prerenal AKI over acute tubular necrosis (ATN)?
What combination of laboratory findings would STRONGLY suggest prerenal AKI over acute tubular necrosis (ATN)?
Which imaging modality is MOST appropriate as a FIRST-LINE investigation for suspected post-renal AKI?
Which imaging modality is MOST appropriate as a FIRST-LINE investigation for suspected post-renal AKI?
When is a renal biopsy MOST indicated in the evaluation of AKI?
When is a renal biopsy MOST indicated in the evaluation of AKI?
A patient is diagnosed with AKI. What is the FIRST and MOST critical step in management?
A patient is diagnosed with AKI. What is the FIRST and MOST critical step in management?
What is the appropriate action regarding nephrotoxic medications in a patient with AKI?
What is the appropriate action regarding nephrotoxic medications in a patient with AKI?
A patient with AKI and volume overload is not responding to diuretics. What action is MOST likely needed?
A patient with AKI and volume overload is not responding to diuretics. What action is MOST likely needed?
A patient with AIN or RPGN being managed for AKI is not responding to first line treatments. When could immunosuppression with glucocorticoids be considered?
A patient with AIN or RPGN being managed for AKI is not responding to first line treatments. When could immunosuppression with glucocorticoids be considered?
What is the BEST strategy to reduce the risk of contrast-induced nephropathy in a patient requiring a CT scan with contrast?
What is the BEST strategy to reduce the risk of contrast-induced nephropathy in a patient requiring a CT scan with contrast?
A patient recovers from an episode of AKI. What long-term outcome should be of PRIMARY concern, requiring proactive management and monitoring?
A patient recovers from an episode of AKI. What long-term outcome should be of PRIMARY concern, requiring proactive management and monitoring?
A patient with AKI develops severe, refractory hyperkalemia despite medical management. According to the AEIOU criteria, what intervention should definitely be considered?
A patient with AKI develops severe, refractory hyperkalemia despite medical management. According to the AEIOU criteria, what intervention should definitely be considered?
A patient at risk of AKI is being managed in the intensive care unit. What action is MOST directly associated with 'maintaining circulation' to prevent AKI in this context?
A patient at risk of AKI is being managed in the intensive care unit. What action is MOST directly associated with 'maintaining circulation' to prevent AKI in this context?
Following initial treatment, a patient’s AKI is improving. Why is continued observation and regular blood tests still important?
Following initial treatment, a patient’s AKI is improving. Why is continued observation and regular blood tests still important?
Following a patient’s AKI, an evaluation shows that the acute issue leading to the AKI has resolved. Why is managing this acute illness still significant?
Following a patient’s AKI, an evaluation shows that the acute issue leading to the AKI has resolved. Why is managing this acute illness still significant?
A patient with AKI shows signs of metabolic acidosis requiring sodium bicarbonate. Under what circumstances should you pursue renal replacement therapy (RRT)?
A patient with AKI shows signs of metabolic acidosis requiring sodium bicarbonate. Under what circumstances should you pursue renal replacement therapy (RRT)?
In a patient presenting with symptoms of AKI, what factor should most influence the decision concerning the use of imaging?
In a patient presenting with symptoms of AKI, what factor should most influence the decision concerning the use of imaging?
Why is assessing a patient's prior morbidity an important factor in assessing AKI risk?
Why is assessing a patient's prior morbidity an important factor in assessing AKI risk?
A patient develops AKI following aortic dissection. What is the MOST probable pathogenic mechanism?
A patient develops AKI following aortic dissection. What is the MOST probable pathogenic mechanism?
Outside of addressing the AEIOU criteria for Renal Replacement Therapy, what is the next step for treating a patient?
Outside of addressing the AEIOU criteria for Renal Replacement Therapy, what is the next step for treating a patient?
Which of the following laboratory findings would suggest ATN instead of pre-renal AKI?
Which of the following laboratory findings would suggest ATN instead of pre-renal AKI?
Which of the following is an indication for immediate Renal Replacement Therapy?
Which of the following is an indication for immediate Renal Replacement Therapy?
Which of the following is least likely to cause crystal nephropathy?
Which of the following is least likely to cause crystal nephropathy?
Which measure is least effective in preventing Contrast-Induced Nephropathy?
Which measure is least effective in preventing Contrast-Induced Nephropathy?
A patient with known cirrhosis presents with AKI. Which pathophysiological process is MOST likely contributing to the development of pre-renal AKI in this patient?
A patient with known cirrhosis presents with AKI. Which pathophysiological process is MOST likely contributing to the development of pre-renal AKI in this patient?
A patient with AKI has a urine microscopy report showing muddy brown casts. Which of the following etiologies does muddy brown casts strongly suggest?
A patient with AKI has a urine microscopy report showing muddy brown casts. Which of the following etiologies does muddy brown casts strongly suggest?
Following treatment with a loop diuretic for fluid overload, a patient with heart failure develops AKI. What is the MOST likely pathogenic mechanism?
Following treatment with a loop diuretic for fluid overload, a patient with heart failure develops AKI. What is the MOST likely pathogenic mechanism?
A patient with AKI is suspected of having a urinary tract obstruction. After initial assessment, further intervention is deemed necessary. In addition to nephrostomy tubes and bladder catheters, what technique is MOST appropriate for bypassing an obstruction in the ureter?
A patient with AKI is suspected of having a urinary tract obstruction. After initial assessment, further intervention is deemed necessary. In addition to nephrostomy tubes and bladder catheters, what technique is MOST appropriate for bypassing an obstruction in the ureter?
A patient is started on gentamicin for a severe infection and subsequently develops AKI. What is the MOST important step in preventing further kidney damage from the medication?
A patient is started on gentamicin for a severe infection and subsequently develops AKI. What is the MOST important step in preventing further kidney damage from the medication?
Flashcards
Acute Kidney Injury (AKI)
Acute Kidney Injury (AKI)
Kidney injury marked by decreased renal function, measured by serum creatinine or urine output, occurring over hours-days.
KDIGO Definition of AKI
KDIGO Definition of AKI
Increase in serum creatinine by ≥0.3 mg/dL within 48 hours, or ≥1.5 times baseline within prior seven days, or urine volume <0.5 mL/kg/hour for six hours.
Prerenal AKI
Prerenal AKI
Reduced perfusion to the kidney, which can occur in hypovolemic, euvolemic, or hypervolemic states.
Absolute hypovolemia
Absolute hypovolemia
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Acute tubular necrosis (ATN)
Acute tubular necrosis (ATN)
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Glomerular disease
Glomerular disease
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Intra-tubular obstruction
Intra-tubular obstruction
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Post-renal AKI
Post-renal AKI
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NSAIDs cause pre-renal AKI
NSAIDs cause pre-renal AKI
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NSAIDs cause intra-renal AKI
NSAIDs cause intra-renal AKI
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Signs/Symptoms of AKI
Signs/Symptoms of AKI
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Suspect AKI in unwell patients
Suspect AKI in unwell patients
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Important areas of AKI history
Important areas of AKI history
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Urea and electrolytes for investigation
Urea and electrolytes for investigation
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eGFR in AKI
eGFR in AKI
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Post-void residual volume (PVR)
Post-void residual volume (PVR)
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Ultrasound of the kidneys, ureters, bladder (KUB)
Ultrasound of the kidneys, ureters, bladder (KUB)
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CT non-contrast
CT non-contrast
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AKI Management
AKI Management
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General management of AKI
General management of AKI
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Adjustment of drug doses which are renally cleared to prevent drug toxicity
Adjustment of drug doses which are renally cleared to prevent drug toxicity
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Targeted AKI management
Targeted AKI management
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Complications of AKI
Complications of AKI
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Include complications of AKI
Include complications of AKI
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Renal replacement therapy (AEIOU)
Renal replacement therapy (AEIOU)
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Prevention Steps of AKI
Prevention Steps of AKI
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AKI vs ARF
AKI vs ARF
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Causes of Absolute Hypovolemia
Causes of Absolute Hypovolemia
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Low Effective Arterial Blood Volume (EABV)
Low Effective Arterial Blood Volume (EABV)
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Drug-induced prerenal AKI
Drug-induced prerenal AKI
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Radiocontrast media's effect
Radiocontrast media's effect
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Small blood vessel injury AKI
Small blood vessel injury AKI
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Larger renal vessel injury AKI
Larger renal vessel injury AKI
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Ureteral Obstruction
Ureteral Obstruction
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Bladder obstruction
Bladder obstruction
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Prostate Obstruction
Prostate Obstruction
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Urethral Obstruction
Urethral Obstruction
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AKIs from External Obstruction
AKIs from External Obstruction
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ACEi/ARB AKI Mechanism
ACEi/ARB AKI Mechanism
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Aminoglycosides/Amphotericin B/Cisplatin
Aminoglycosides/Amphotericin B/Cisplatin
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Acyclovir/Ampicillin AKI
Acyclovir/Ampicillin AKI
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Signs of hypovolemia
Signs of hypovolemia
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Signs of volume overload
Signs of volume overload
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Signs of uremia
Signs of uremia
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Oliguria or anuria
Oliguria or anuria
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General Inspection Signs
General Inspection Signs
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Signs detectable at Head & Neck
Signs detectable at Head & Neck
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Face and Neck Signs
Face and Neck Signs
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Abdomen Signs
Abdomen Signs
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Other signs of general AKI
Other signs of general AKI
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Differential diagnosis of volume overload
Differential diagnosis of volume overload
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Differential diagnosis of uraemic encephalopathy
Differential diagnosis of uraemic encephalopathy
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Anuria and GFR
Anuria and GFR
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Urine sample results of AKI
Urine sample results of AKI
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Creatinine levels relationship to GFR
Creatinine levels relationship to GFR
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AKI Staging Criteria
AKI Staging Criteria
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AKI Lab examination examinations
AKI Lab examination examinations
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Checklists for AKI
Checklists for AKI
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The Use of Diuretics in AKI
The Use of Diuretics in AKI
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Contrast induced nephropathy recommendation
Contrast induced nephropathy recommendation
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Study Notes
- Acute Kidney Injury (AKI) is a syndrome marked by decreased renal function
- It is measured by serum creatinine or urine output
- It occurs over hours to days
- It has different etiologies and may be multifactorial
- AKI is common, occurring in up to 18% of hospital patients and ~50% of ICU patients
- The term AKI has largely replaced acute renal failure (ARF)
- This reflects the recognition that smaller decrements in kidney function that do not result in overt organ failure are of substantial clinical relevance and are associated with increased morbidity and mortality
- KDIGO defines AKI as any of the following:
- Increase in serum creatinine by ≥0.3 mg/dL (≥26.5 micromol/L) within 48 hours
- Increase in serum creatinine to ≥1.5 times baseline, presumed to have occurred within the prior seven days
- Urine volume <0.5 mL/kg/hour for six hours
Mortality
- AKI leads to high mortality rates in hospitalized patients
- Non-elective mortality is at 3.20%
- AKI stage 1 is at 16.30%
- AKI stage 2 is at 33.00%
- AKI stage 3 is at 36.10%
Natural History
- Natural history of AKI shown on graphs displays:
- Prerenal Initiation Extension Maintenance Repair
- AKI; No CKD Progression
- AKI; CKD Progression
- AKI on CKD; CKD Progression
- RRT is indicated
Causes of AKI (exposures and susceptibilities for non-specific AKI)
- Sepsis
- Critical illness
- Circulatory shock
- Burns
- Trauma
- Cardiac surgery (especially with CPB)
- Major noncardiac surgery
- Nephrotoxic drugs
- Radiocontrast agents
- Poisonous plants and animals
- Susceptibilities include:
- Dehydration or volume depletion
- Advanced age
- Female gender
- Black race
- CKD
- Chronic diseases (heart, lung, liver)
- Diabetes mellitus
- Cancer
- Anemia
Causes of AKI divided into pre-renal, renal, and post-renal categories
- Pre-renal causes involve factors that reduce blood flow to the kidneys:
- Hypovolaemia
- Sepsis
- CCF
- Renal Artery Stenosis
- ACE Inhibitors
- Renal causes include intrinsic kidney diseases:
- Ischaemia
- Nephrotoxins
- Glomerulonephritis
- Interstitial nephritis
- Hepatorenal Syndrome
- HUS / TTP
- Post-Renal causes are due to obstruction of urine flow:
- Stone
- Tumour
- Prostate
- Blocked Catheter
Pre-Renal AKI
- Pre-renal AKI occurs when there is reduced perfusion to the kidney
- Can occur in hypovolemic, euvolemic or hypervolemic states
- Causes include:
- Absolute hypovolemia (hemorrhage, over-diuresis, vomiting and diarrhea)
- Low effective arterial blood volume (EABV): heart failure, cirrhosis, sepsis, third spacing of fluid
- Anatomical: renal artery stenosis
- Drug-induced: NSAIDs, ACE inhibitors, diuretics
- Iodinated radiocontrast media: alters renal vascular autoregulation (afferent arteriole vasoconstriction)
Intra-Renal AKI
- Occurs when there is a structural or functional change at the level of the nephron
- Can occur independently or as a transformation of a pre-renal AKI
- Causes include:
- Acute tubular necrosis (ATN): the most common cause of AKI due to ischemic or toxic injury to the cells of the proximal convoluted tubules, which results in effacement of the brush border and eventually cell death, thus shutting down the function of tubular cells
- Acute interstitial nephritis (AIN): most often eosinophilic nephritis that can be drug-induced (NSAIDs, penicillin), infection-induced (tuberculosis, legionella) or immune-mediated (sarcoidosis, SLE or IgG-related disease (IgG4-RD)
- Intrinsic Renal vascular disease: affects both small-and large-sized blood vessels within the kidneys.
- Small blood vessels include small vessel vasculitides and diseases that cause microangiopathy and hemolytic anemia (MAHA), including thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP/HUS), scleroderma, Athero-embolic disease, and malignant hypertension
- Larger vessels include renal infarction from aortic dissection, systemic thromboembolism, or renal artery abnormality (such as aneurysm) and acute renal vein thrombosis.
- Severe AKI from renal vascular catastrophe suggests bilateral involvement or involvement of a solitary functioning kidney
- Glomerular disease: 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
- Classified as either primary or secondary
- Two general patterns are observed with considerable overlap in some diseases:
- Nephritic pattern: produces an active urine sediment with dysmorphic red cells and white cells; granular, red cell, and other cellular casts; and a variable degree of proteinuria. Rapidly progressive glomerulonephritis (RPGN), which causes AKI or subacute kidney injury, always presents with a nephritic pattern
- Nephrotic pattern: is a rare cause of AKI in the hospitalized patient but may occur in patients with very large amounts of proteinuria Intra-tubular obstruction: Intratubular obstruction by pigments such as myoglobin (rhabdomyolysis) or crystals such as uric acid in tumour lysis syndrome or immunoglobulin light chains, as seen in monoclonal gammopathy may also lead to the same result
Post-Renal AKI
- Post-renal AKI is associated with an obstructive pathology leading to congestion of the kidneys
- Causes of post-Renal Aki can be Divided Anatomically:
- Ureters: nephrolithiasis, retroperitoneal fibrosis
- Bladder: bladder cancer
- Prostate: benign prostatic hyperplasia (BPH), prostate cancer
- Urethra: urethral stricture
- External: retroperitoneal mass, ovarian tumors
- Obstruction at or distal to the level of the bladder can cause a post-renal AKI in both kidneys
- Unless there is a solitary kidney, a unilateral obstruction may not cause post-renal AKI as the unaffected kidney may be able to compensate for the reduced function of the affected kidney
Medications associated with AKI
- ACE inhibitors and Angiotensin receptor blockers (ARBs): GFR alteration affecting vascular tone of afferent and efferent arterioles, altering interglomerular blood flow
- Aminoglycosides, Amphotericin B, and Cisplatin: tubular cell toxicity causing direct toxicity to the epithelial cells of the proximal convoluted tubules
- Rifampin and Proton pump inhibitors: cause Interstitial nephritis, which is an inflammatory reaction within the interstitium of the kidney
- Acyclovir and Ampicillin: Crystal nephropathy causing precipitates of insoluble crystals
Non-steroidal anti-inflammatory drugs (NSAIDs)
- NSAIDs can be implicated in multiple causes of renal impairment so their use should be restricted in patients at risk of AKI
- Pre-renal: NSAIDs block prostaglandin mediated vasodilation of the afferent arteriole, which limits the kidney's ability to regulate local blood flow
- Intra-renal: NSAIDs can cause acute interstitial nephritis (AIN)
- Post-renal: long term NSAID use can cause renal papillary necrosis where the medullary papilla sloughs off, causing obstruction to urine flow
Clinical Signs of AKI
- Typical clinical findings of AKI may include:
- Oliguria or anuria
- Signs of hypovolemia: dry mucous membranes, reduced skin turgor, tachycardia, hypotension
- Signs of volume overload: hypertension, pulmonary oedema, peripheral oedema, elevated jugular venous pulse
- Signs of uremia: ecchymosis due to platelet dysfunction, uremic encephalopathy (asterixis, confusion, seizures)
- Signs of post-renal obstruction: palpable or tender distended bladder
Symptoms of AKI
- Symptoms include
- The presenting history will provide clues to the likely cause of the AKI
- AKI can be challenging to recognize as it is often asymptomatic
- The condition that is causing the AKI (sepsis) can present with non-specific symptoms of fatigue, nausea, and confusion. These symptoms can often be mistaken as symptoms of the underlying cause It is important to suspect AKI in any acutely unwell patient
Important areas of the history
- Reason for admission to hospital (sepsis, burns)
- Lower urinary tract symptoms (frequency, urgency, incomplete emptying)
- Known to have a solitary kidney
- Underlying medical conditions (heart failure, cirrhosis, SLE)
- Use of medications known to be nephrotoxic (NSAIDs, diuretics, penicillin, cisplatin)
- Recent imaging investigations using iodinated contrast, particularly if delivered arterially (CT with contrast, angiogram)
Differential Diagnosis
- Volume Overload:
- Congestive cardiac failure
- Liver disease
- Pleural Effusion
- Exacerbation of Pre-existing Chronic lung disease
- Protein-losing enteropathy
- Lymphoedema
- Uraemic Encephalopathy:
- Acute liver failure and Hepatic encephalopathy
- Sepsis (Lactic acidosis)
- Hypertensive encephalopathy
- Metabolic encephalopathy i.e Diabetic keto acidosis/Hyperosmolar coma
- Hypoglycaemia
- Fluid and electrolyte disturbances, such as hyponatremia and hypermagnesemia
- Drug toxicity
- Wernicke-Korsakoff encephalopathy
Laboratory Investigations
- Urea and electrolytes: creatinine, blood urea nitrogen (BUN), calcium, phosphate, potassium, sodium
- eGFR does not apply in AKI, only in steady state
- Anuria is a GFR of 0mls/min, irrespective of the serum creatinine or eGFR
- Early recognition of AKI is currently impeded by the widespread use of serum creatinine as the biomarker
- Serum creatinine is a late, insensitive, highly confounded, nonspecific biomarker of kidney function
- It may take as long as 72 hours postinjury to detect a rise in serum creatinine for a number of reasons
- It takes 2–3 days for serum creatinine to reach a new equilibrium postinjury.
Staging of AKI
- AKI is staged for severity according to the following criteria:
- Stage 1: 1.5-1.9 times baseline OR ≥0.3 mg/dl (≥26.5 µmol/l) increase; Urine output <0.5 ml/kg/h for 6-12 hours
- Stage 2: 2.0-2.9 times baseline; Urine output <0.5 ml/kg/h for ≥12 hours
- Stage 3: 3.0 times baseline OR Increase in serum creatinine to ≥4.0mg/dl (≥353.6 µmol/l) OR Initiation of renal replacement therapy OR, In patients < 18 years, decrease in eGFR to <35 ml/min per 1.73 m²; Urine output <0.3 ml/kg/h for ≥24 hours OR Anuria for ≥12 hours
Other diagnostic tests
- Full blood count: anaemia, leukocytopenia, thrombocytopenia
- Liver function tests: serum albumin
- Venous blood gas (VBG) or ABG: Assess for acidaemia, Lactate( sepsis)
- Tests for Aetiology: ASOT, Vasculitic screening, C3,C4. Electrophoresis
- CK: Rhabdomyolysis
- Category Sub-category Test Explanation
- Diagnostic & Supportive Investigations and Investigations for Aetiology Bloods ABG ↑ lactate (sepsis, ischaemia) ↓ pH (acidosis)
- FBC ↓ platelets (HUS, DIC, TTP) ↑ WCC (infection, sepsis)
- U&E ↑ creatinine (renal dysfunction) ↑ potassium (renal dysfunction)
- Osmolality See ATN vs pre-renal AKI
- CK ↑ CK (rhabdomyolysis)
- GN screen C3/C4, electrophoresis, antibodies, ASOT
Urine Studies
- Urine analysis: proteinuria, albuminuria, haemoglobinuria, haematuria, WBC, glucose
- Urine volume measurement: oliguria, anuria
- Urinary microscopy and sediment: casts, crystals. Pigmented, muddy brown, granular casts are visible in the urine sediment of a patient with acute tubular necrosis
- Urine osmolarity and specific gravity: dehydration, less commonly used in clinical practice
- Urinary eosinophil count: useful in the evaluation of AIN (rare), less commonly used in clinical practice
Laboratory Studies in Prerenal AKI and ATN
- Prerenal AKI vs ATN include:
- Urine Sodium <20 vs >30
- Urine Osmolarity >500mosm/L vs <350mosm/L
- Fractional Excretion of Sodium <1% vs >2%
- BUN:Creatinine Ratio >20 vs <20
- Urine Specific Gravity >1.02 vs <1.01
- Urine Sediment Normal/Hyaline Casts vs Muddy Brown Casts
- Response to Fluid Challenge Good vs Poor
Imaging Investigations
- Post-void residual volume (PVR): can be assessed rapidly using a bedside bladder scanner
- Ultrasound of the kidneys, ureters and bladder (KUB): assess kidney size, hydronephrosis, postrenal obstruction, renal lesions
- CT non-contrast: radiopaque and non-radiopaque calculi, ureteric obstruction
- CT urogram: investigate for urinary tract bleeding
- CT triphasic kidneys: dedicated cross-sectional imaging for renal lesions (often used to clarify masses seen on ultrasound)
Renal Biopsy
- Indications of renal biopsy include
- ARF of unknown etiology
- Suspicion of glomerulonephritis, systemic disease (e.g., vasculitis), or AIN as the cause of ARF
- ATN not recovering after 4 to 6 weeks of dialysis with no more recurrent insults
Management
- Mainstay of AKI management is prompt identification and removal of the causative agent(s) while providing supportive treatment for the AKI itself
- Recognition of AKI in its early stages, and early response geared to prevent progression to more severe stages
General management of AKI includes
- Withdrawal of nephrotoxic medication
- Adjustment of drug doses which are renally cleared to prevent drug toxicity
- Fluid resuscitation can rapidly improve renal function in hypovolemia/hypotension
- Urinary catheterization can be used where there is difficulty in measuring urine output or to relieve urinary obstruction
- Assess for evidence of sepsis and initiate the sepsis six care bundle if required
- Many hospitals are using an ABCDE or STOP AKI checklist to prompt AKI management
Diuretics
- Do not use diuretics to prevent AKI
- Do not use diuretics to treat AKI, except in the management of volume overload
Targeted management options include
- Immunosuppression with glucocorticoids can be considered in AIN or RPGN to slow the progression to irreversible injury
- Patients with obstructive uropathy may need an indwelling bladder catheter, nephrostomy tubes or ureteric stent insertion depending on the site and cause of the obstruction
Contrast-Induced Nephropathy
- It is a cause of toxic ATN and a potential cause of inpatient AKI
- It should be suspected if a hospitalized patient develops intrinsic AKI and had an indication for intravascular administration of radiographic contrast media
- Patient-related risk factors for contrast-induced nephropathy include:
- Advanced age
- Diabetes mellitus
- Underlying chronic kidney disease (CKD) such as diabetic nephropathy, and concomitant use of certain nephrotoxic drugs (e.g., NSAIDs)
- The course of contrast-induced nephropathy is typically mild (unless CKD is already present), with creatinine levels peaking after 3–5 days and returning to baseline within one week
- Measures to prevent contrast-induced nephropathy include:
- Adequate hydration with isotonic fluids before and after administration of contrast medium
- Use low osmolar, non ionic contrast in slimmest voume possible may be useful in high risk patients
- Discontinuing nephrotoxic substances before contrast administration
- No Role for N Acetyl cysteine or sodium bicarbonate
- Fear of CIN should not prevent a necessary radiologic investigation
Complications of AKI
- AKI can be a significant cause of morbidity and mortality, especially in patients admitted to Intensive Care
- Having poorer pre-morbid status prior to developing the AKI is a significant negative predictor for recovery
- Recognition and prompt management of an AKI are essential in preventing permanent damage or progression to chronic kidney disease (CKD)
- Include fluid overload (leg oedema, pulmonary oedema pleural effusions)
- Electrolyte derangement (hyperphosphatemia hyperkalaemia)
- Acid-base disorder (metabolic acidosis)
- End-organ complications of uraemia
- Chronic kidney disease (CKD)
- End-stage renal disease (ESRD)
- Death
Indications of Renal Replacement Therapy
- Indications for RRT can be remembered by the mnemonic AEIOU:
- Acidosis with a Ph < 7.0mmol/
- Electrolyte imbalance: K+ >7.0mmol/L or refractory hyperkalaemia
- Intoxication: poisons such as ethylene glycol and lithium
- Overload: severe pulmonary oedema with oliguria or diuretic resistant
- Uraemia symptoms: encephalopathy or pericarditis
AKI Preventative measures: the 4 'M's
- Monitor patient
- Observations and EWS
- Regular blood tests
- Fluid charts
- Urine volumes
- Maintain circulation
- Hydration
- Resuscitation
- Oxygenation)
- Minimize kidney insults
- Nephrotoxic medications i.e. NSAIDS, Gentamycin
- Surgery or high-risk interventions
- iodinated contrast
- Hospital-acquired infection
- Manage the acute illness
- Sepsis, Heart failure, Liver failure
Clinical Scenario for AKI
- An 80-year-old female with Osteoarthritis is admitted with nausea and vomiting for 2 days
- The patient is taking Ibuprofen 2-3 times per day for the last month
- She is clinically dehydrated with dry mucous membranes, poor skin turgor B/P 90/50
- Laboratory results include:
- Serum Creatinine 330 µmol/L (50 - 120 µmol/L)
- Blood Urea Nitrogen (BUN) 14.28 mmol/L (2.5 – 8.5 mmol/L)
- Serum Potassium (K+) 3.3 mmol/L (3.5-5.0 mmol/L)
- Serum Sodium (Na+) 140 mmol/L (135-145 mmol/L)
- Urine WBC +, Nitrates Neg, Protein Neg Blood Neg
- The likely cause for patient presentation is the use of Non-steroidal anti-inflammatory drugs (NDAIDs) causing AKI
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