AKI Flashcards
(242 cards)
1
Q
A 65-year-old male patient with a baseline serum creatinine of 1.0 mg/dL is admitted with acute kidney injury. His current serum creatinine is 2.9 mg/dL, and his urine output has been 0.4 mL/kg/h for the past 14 hours. According to the staging system in Table 310-1, what is the severity of his AKI?
A. Stage 1
B. Stage 2
C. Stage 3
D. Not classifiable
A
Answer: B (Stage 2)
Explanation: The patient meets Stage 2 criteria: serum creatinine is 2.0–2.9 times baseline (2.9 mg/dL vs. 1.0 mg/dL) and urine output is <0.5 mL/kg/h for ≥12 hours.
2
Q
A 12-year-old patient with acute kidney injury has an eGFR of 30 mL/min per 1.73 m². According to Table 310-1, which of the following statements is correct?
A. The patient meets Stage 3 criteria due to eGFR <35 mL/min per 1.73 m².
B. The patient meets Stage 2 criteria because serum creatinine is not provided.
C. The patient does not meet AKI criteria because eGFR is not used for staging in adults.
D. The patient must have anuria for ≥12 hours to qualify for Stage 3.
A
Answer: A (The patient meets Stage 3 criteria due to eGFR <35 mL/min per 1.73 m².)
Explanation: For patients <18 years, a decrease in eGFR to <35 mL/min per 1.73 m² qualifies as Stage 3 AKI, per the table.
3
Q
Which of the following scenarios would classify a patient as having Stage 1 AKI based on Table 310-1?
A. Serum creatinine increases from 1.2 mg/dL to 1.6 mg/dL, and urine output is 0.4 mL/kg/h for 8 hours.
B. Serum creatinine increases from 1.8 mg/dL to 3.6 mg/dL, and urine output is 0.2 mL/kg/h for 24 hours.
C. Serum creatinine is 4.5 mg/dL (newly elevated), and the patient is anuric for 6 hours.
D. Serum creatinine is 2.5 times baseline, and urine output is 0.3 mL/kg/h for 18 hours.
A
Answer: A (Serum creatinine increases from 1.2 mg/dL to 1.6 mg/dL, and urine output is 0.4 mL/kg/h for 8 hours.)
Explanation: This meets Stage 1 criteria: creatinine increase ≥0.3 mg/dL (0.4 mg/dL) OR 1.5–1.9 times baseline, and urine output <0.5 mL/kg/h for 6–12 hours.
4
Q
What is the myogenic reflex in relation to the afferent arteriole?
A
It leads to dilation in the setting of low perfusion pressure, maintaining glomerular perfusion.
This reflex is a response to changes in blood pressure within the renal arterioles.
5
Q
Which vasodilator substances are synthesized intrarenally in response to low renal perfusion pressure?
A
Prostaglandins (prostacyclin, prostaglandin E2), kallikrein, kinins, and possibly nitric oxide (NO).
These substances help in regulating blood flow within the kidneys.
6
Q
What is tubuloglomerular feedback?
A
A mechanism where decreases in solute delivery to the macula densa elicit dilation of the afferent arteriole to maintain glomerular perfusion.
The macula densa are specialized cells located in the distal tubule.
7
Q
What role does nitric oxide (NO) play in tubuloglomerular feedback?
A
It mediates the dilation of the afferent arteriole in response to decreased solute delivery.
NO is a key signaling molecule in various physiological processes.
8
Q
What is the limit of renal autoregulation during systemic hypotension?
A
Renal autoregulation usually fails once systolic blood pressure falls below 80 mmHg.
This indicates a critical threshold for maintaining glomerular filtration rate (GFR).
9
Q
True or False: Autoregulation mechanisms can always maintain GFR regardless of systemic blood pressure.
A
False.
There are limits to these counterregulatory mechanisms.
10
Q
A 72-year-old patient with heart failure is admitted with worsening renal function. His blood pressure is 90/60 mmHg, and his serum creatinine has risen from 1.2 mg/dL to 1.8 mg/dL over 48 hours. Urinalysis shows no casts or cellular debris. Which of the following is the most likely mechanism contributing to his acute kidney injury?
A. Direct tubular toxicity from nephrotoxic medications
B. Glomerular inflammation due to immune complex deposition
C. Reduced intraglomerular hydrostatic pressure from decreased renal perfusion
D. Obstructive uropathy from bladder outlet obstruction
A
Answer: C (Reduced intraglomerular hydrostatic pressure from decreased renal perfusion)
Explanation: The patient’s presentation (hypotension, elevated creatinine without active sediment) is classic for prerenal azotemia, where reduced renal perfusion leads to decreased glomerular filtration. This is reversible with restoration of blood flow.
10
Q
A 55-year-old woman with osteoarthritis develops acute kidney injury after starting high-dose ibuprofen for chronic back pain. Her serum creatinine increases from 0.9 mg/dL to 1.4 mg/dL. Which of the following best explains the pathophysiology of her AKI?
A. NSAIDs inhibit angiotensin II, reducing efferent arteriolar constriction.
B. NSAIDs block prostaglandin-mediated afferent arteriolar vasodilation.
C. NSAIDs cause direct tubular necrosis due to oxidative stress.
D. NSAIDs induce glomerular capillary inflammation.
A
Answer: B (NSAIDs block prostaglandin-mediated afferent arteriolar vasodilation.)
Explanation: NSAIDs impair renal autoregulation by inhibiting prostaglandins, which normally dilate the afferent arteriole to maintain glomerular perfusion. This reduces intraglomerular pressure and GFR, leading to prerenal azotemia.
11
Q
Which of the following clinical scenarios is most likely to progress from prerenal azotemia to acute tubular necrosis (ATN)?
A. A patient with mild dehydration who receives IV fluids within 6 hours.
B. A patient with septic shock and prolonged hypotension (>12 hours).
C. A patient with nephrotic syndrome and heavy proteinuria.
D. A patient with unilateral renal artery stenosis.
A
Answer: B (A patient with septic shock and prolonged hypotension (>12 hours).)
Explanation: Prolonged renal hypoperfusion (e.g., from severe hypotension) can lead to ischemic tubular necrosis, transitioning from reversible prerenal azotemia to intrinsic AKI (ATN).
12
Q
What factors determine the robustness of the autoregulatory response and the risk of prerenal azotemia?
A
Atherosclerosis, long-standing hypertension, and older age
These factors lead to hyalinosis and myointimal hyperplasia, resulting in structural narrowing of intrarenal arterioles.
13
Q
What is the effect of CKD on renal afferent vasodilation?
A
It may operate at maximal capacity to maximize GFR in response to reduced functional renal mass
This is a compensatory mechanism due to the loss of renal function.
14
Q
How do NSAIDs affect renal function?
A
They inhibit renal prostaglandin production, limiting renal afferent vasodilation
This can reduce the kidney’s ability to increase blood flow in response to low perfusion.
15
Q
What is the role of ACE inhibitors and ARBs in renal function?
A
They limit renal efferent vasoconstriction
This effect is important in maintaining GFR, especially in cases of renal artery stenosis.
16
Q
In which patients is the effect of ACE inhibitors and ARBs particularly pronounced?
A
Patients with bilateral renal artery stenosis or unilateral renal artery stenosis
This is critical when there is a solitary functioning kidney.
17
Q
What is the risk associated with the combined use of NSAIDs and ACE inhibitors or ARBs?
A
It poses a particularly high risk for developing prerenal azotemia
This combination can severely impair the autoregulatory mechanisms of the kidneys.
18
Q
Fill in the blank: Atherosclerosis, long-standing hypertension, and older age can lead to ______.
A
hyalinosis and myointimal hyperplasia
19
Q
A 68-year-old man with a history of hypertension and coronary artery disease presents with oliguria and a serum creatinine increase from 1.1 mg/dL to 2.3 mg/dL over 48 hours. He was recently started on lisinopril and ibuprofen for back pain. Which of the following is the most likely contributing mechanism to his AKI?
A. Acute tubular necrosis from rhabdomyolysis
B. Postrenal obstruction due to benign prostatic hyperplasia
C. Prerenal azotemia from impaired renal autoregulation
D. Glomerulonephritis secondary to immune complex deposition
A
Answer: C (Prerenal azotemia from impaired renal autoregulation)
Explanation: The combination of ACE-I (lisinopril) and NSAIDs (ibuprofen) disrupts renal autoregulation by reducing efferent arteriolar constriction (ACE-I) and blocking compensatory afferent vasodilation (NSAIDs), leading to decreased GFR. This is a classic prerenal azotemia scenario.
20
Q
A 45-year-old woman with systemic lupus erythematosus (SLE) develops AKI with hematuria, proteinuria, and red blood cell casts on urinalysis. Her blood pressure is 160/100 mmHg. Which of the following is the most likely cause of her AKI?
A. Prerenal azotemia from hypovolemia
B. Intrinsic AKI due to acute glomerulonephritis
C. Postrenal obstruction from nephrolithiasis
D. Tubular injury from aminoglycoside toxicity
A
Answer: B (Intrinsic AKI due to acute glomerulonephritis)
Explanation: The findings of hematuria, proteinuria, and RBC casts point to glomerular inflammation, likely lupus nephritis, a form of intrinsic AKI. Hypertension further supports glomerular pathology
21
Q
A 60-year-old man with metastatic prostate cancer presents with anuria and a serum creatinine of 5.8 mg/dL (baseline 1.0 mg/dL). Renal ultrasound reveals bilateral hydronephrosis. Which of the following is the most urgent intervention?
A. Intravenous fluids to restore renal perfusion
B. High-dose glucocorticoids for vasculitis
C. Relief of bladder outlet obstruction with a Foley catheter
D. Discontinuation of NSAIDs
A
Answer: C (Relief of bladder outlet obstruction with a Foley catheter)
Explanation: Anuria + bilateral hydronephrosis indicates postrenal AKI from obstruction (e.g., prostate cancer compressing the urethra). Immediate catheterization is required to restore urine flow.
22
Q
What hemodynamic profile do individuals with advanced liver disease exhibit?
A
A profile resembling prerenal azotemia in the setting of total-body volume overload
This is characterized by reduced systemic vascular resistance due to primary arterial vasodilation in the splanchnic circulation.
23
Q
What activates vasoconstrictor responses in advanced liver disease?
A
Primary arterial vasodilation in the splanchnic circulation
This results in a hemodynamic profile similar to hypovolemia.
24
What is a common complication in individuals with advanced liver disease?
Acute Kidney Injury (AKI)
## Footnote
AKI can be triggered by volume depletion and spontaneous bacterial peritonitis.
25
What characterizes type 1 hepatorenal syndrome?
AKI persists despite volume administration and withholding of diuretics
## Footnote
This syndrome is associated with a particularly poor prognosis.
26
How does type 2 hepatorenal syndrome differ from type 1?
It is characterized mainly by refractory ascites
## Footnote
Type 2 is considered a less severe form.
27
What is the definition of hepatorenal syndrome?
Difficult to distinguish from prerenal azotemia
## Footnote
It is characterized by specific renal dysfunction in the context of liver disease.
28
What are the most common causes of intrinsic AKI?
* Sepsis
* Ischemia
* Nephrotoxins (both endogenous and exogenous)
## Footnote
These causes underscore the multifactorial nature of intrinsic AKI.
29
What can occur when prerenal azotemia advances?
Tubular injury
## Footnote
This progression often leads to acute tubular necrosis.
30
What is often lacking in cases of sepsis and ischemia regarding AKI?
Human biopsy confirmation of tubular necrosis
## Footnote
Inflammation, apoptosis, and altered regional perfusion may contribute to the condition without frank necrosis.
31
What are other potential causes of AKI in settings such as sepsis?
* Drug-induced interstitial nephritis
* Glomerulonephritis
## Footnote
These conditions can complicate the diagnosis and management of AKI.
32
How can causes of intrinsic AKI be catalogued?
Anatomically according to the major site of renal parenchymal damage
## Footnote
This includes glomeruli, tubulointerstitium, and vessels.
33
What are the hemodynamic effects of sepsis?
Generalized arterial vasodilation mediated by cytokines leading to a reduction in GFR
## Footnote
Cytokines upregulate the expression of inducible NO synthase in the vasculature.
34
What can cause reduction in GFR during sepsis?
Excessive efferent arteriole vasodilation or renal vasoconstriction
## Footnote
Renal vasoconstriction can be due to activation of the sympathetic nervous system, renin-angiotensin-aldosterone system, or increased levels of vasopressin or endothelin.
35
What are the effects of endothelial damage in sepsis?
* Increased microvascular leukocyte adhesion
* Migration
* Thrombosis
* Permeability
* Increased interstitial pressure
* Reduction in local flow to tubules
* Activation of reactive oxygen species
## Footnote
These effects may injure renal tubular cells.
36
What viral infections can lead to AKI?
* Hantavirus
* Dengue virus
* SARS-CoV-2
## Footnote
AKI can be an important complication of these viral infections.
37
What is known about the pathophysiology of AKI due to viral infections?
It remains incompletely understood
## Footnote
Some reports indicate infection of the kidney with SARS-CoV-2, while others find less direct involvement.
38
What is a significant immune response associated with SARS-CoV-2?
A large release of cytokines into the circulation, known as 'cytokine storm'
## Footnote
This cytokine storm may cause diffuse intrarenal vasoconstriction.
39
What state is associated with SARS-CoV-2 that can impair intrarenal blood flow?
A generalized hypercoagulable state
## Footnote
This state may contribute to the impairment of intrarenal blood flow.
40
Fill in the blank: The hemodynamic effects of sepsis can lead to a reduction in _______.
GFR
41
True or False: Sepsis leads to renal vasodilation.
False
42
List the mechanisms that can cause renal vasoconstriction during sepsis.
* Activation of the sympathetic nervous system
* Renin-angiotensin-aldosterone system
* Increased levels of vasopressin
* Increased levels of endothelin
43
What percentage of cardiac output do healthy kidneys receive?
20%
44
What percentage of resting oxygen consumption do kidneys account for?
10%
45
What percentage of the human body mass do kidneys constitute?
0.5%
46
Which region of the kidneys is one of the most hypoxic areas in the body?
Renal medulla
47
Why is the outer medulla particularly vulnerable to ischemic damage?
Architecture of the blood vessels that supply oxygen and nutrients to the tubules
48
What leads to inflammation and reduced local blood flow in the outer medulla?
Enhanced leukocyte-endothelial interactions in small vessels
49
Which segment of the proximal tubule depends on oxidative metabolism for survival?
S3 segment
50
What role does mitochondrial dysfunction play in renal tubular injury?
It is due to ischemia and mitochondrial release of reactive oxygen species
51
Is transient ischemia alone sufficient to cause severe AKI in a normal kidney?
No
52
What clinical conditions increase the risk of AKI during ischemia?
Limited renal reserve (e.g., CKD or older age) or coexisting insults such as sepsis, vasoactive or nephrotoxic drugs, rhabdomyolysis, or systemic inflammatory states
53
Prerenal azotemia and ischemia-associated AKI represent a continuum of what?
Manifestations of renal hypoperfusion
54
What may be a common underlying cause of the reduction in GFR seen in AKI?
Persistent preglomerular vasoconstriction
55
What factors are implicated in vasoconstriction during AKI?
* Activation of tubuloglomerular feedback from enhanced delivery of solute to the macula densa following proximal tubule injury
* Increased basal vascular tone and reactivity to vasoconstrictive agents
* Decreased vasodilator responsiveness
56
What are other contributors to low GFR in AKI?
* Backleak of filtrate across damaged and denuded tubular epithelium
* Mechanical obstruction of tubules from necrotic debris
57
What is ischemia-associated AKI?
A serious complication in the postoperative period, especially after major operations involving significant blood loss and intraoperative hypotension.
58
Which surgical procedures are most commonly associated with AKI?
* Cardiac surgery with cardiopulmonary bypass
* Vascular procedures with aortic cross clamping
* Intraperitoneal procedures
59
What percentage of cardiac and vascular surgery procedures experience severe AKI requiring dialysis?
~1%
60
What are common risk factors for postoperative AKI?
* Underlying CKD
* Older age
* Diabetes mellitus
* Congestive heart failure
* Emergency procedures
61
What is the pathophysiology of AKI following cardiac surgery?
Multifactorial.
62
How does the age and comorbidities of surgical patients relate to AKI risk?
More surgical procedures are performed on older patients with comorbidities that predispose them to AKI and hasten progression of ESKD.
63
What is a risk factor for AKI related to cardiopulmonary bypass duration?
Longer duration of cardiopulmonary bypass.
64
What mechanisms may cause AKI during cardiopulmonary bypass?
* Extracorporeal circuit activation of leukocytes and inflammatory processes
* Hemolysis with resultant pigment nephropathy
* Aortic injury with resultant atheroemboli
65
What causes AKI from atheroembolic disease?
Cholesterol crystal embolization resulting in partial or total occlusion of multiple small arteries within the kidney.
66
What can happen over time due to a foreign body reaction from atheroembolic disease?
Intimal proliferation, giant cell formation, and further narrowing of the vascular lumen.
67
What is the typical time frame for the decline in renal function due to AKI from atheroembolic disease?
Generally subacute, over a period of weeks rather than days.
68
What increases the risk of AKI in postoperative patients?
* High doses of exogenous vasopressors
* Blood-product perfusion
69
What is the mortality rate among cardiovascular patients requiring renal replacement therapy?
As high as 40–70%.
70
True or False: Even milder forms of postoperative AKI do not increase the risk of progression to chronic kidney disease.
False.
71
A 32-year-old man presents with acute kidney injury (creatinine 4.2 mg/dL from baseline 0.9 mg/dL), hemolytic anemia, thrombocytopenia, and neurologic symptoms. Peripheral smear shows schistocytes. Which of the following is the most likely underlying pathology?
A. Acute tubular necrosis from sepsis
B. Thrombotic microangiopathy (TTP/HUS)
C. Tubulointerstitial nephritis from PPIs
D. Cholesterol emboli syndrome
Answer: B (Thrombotic microangiopathy [TTP/HUS])
Explanation: The triad of AKI, microangiopathic hemolytic anemia (schistocytes), and thrombocytopenia is classic for TTP/HUS, a vascular cause of intrinsic AKI. Neurologic symptoms further support TTP.
72
A 55-year-old woman develops oliguric AKI (creatinine 3.8 mg/dL) 5 days after starting high-dose IV penicillin for endocarditis. Urinalysis shows white blood cells and eosinophils. Which of the following is the most likely diagnosis?
A. Acute tubular necrosis from ischemia
B. Allergic tubulointerstitial nephritis
C. Glomerulonephritis from immune complexes
D. Obstructive uropathy from crystalluria
Answer: B (Allergic tubulointerstitial nephritis)
Explanation: Drug-induced tubulointerstitial nephritis (e.g., from penicillin) presents with AKI, WBCs/eosinophils in urine, and often fever/rash. The timing after drug exposure is key.
73
A 70-year-old man with diabetes and hypertension is found to have AKI (creatinine 5.0 mg/dL) after coronary angiography. Urine microscopy reveals muddy brown casts and renal tubular epithelial cells. Which of the following is the most likely cause?
A. Contrast-induced acute tubular necrosis
B. Cholesterol crystal embolization
C. Prerenal azotemia from dehydration
D. Postrenal obstruction from BPH
Answer: A (Contrast-induced acute tubular necrosis)
Explanation: Muddy brown casts and tubular epithelial cells are pathognomonic for acute tubular necrosis (ATN). The temporal association with iodinated contrast exposure points to contrast-induced ATN.
74
What frequently accompanies severe burns and acute pancreatitis?
Extensive fluid losses into the extravascular compartments of the body
## Footnote
This fluid loss can lead to severe complications.
75
What percentage of individuals with >10% total body surface area involvement experience AKI?
25%
## Footnote
AKI stands for acute kidney injury.
76
What are the primary factors leading to AKI in burns and acute pancreatitis?
Severe hypovolemia, decreased cardiac output, increased neurohormonal activation, dysregulated inflammation, increased risk of sepsis, acute lung injury
## Footnote
These factors can facilitate the development and progression of AKI.
77
What condition can develop from massive fluid resuscitation for trauma, burns, and acute pancreatitis?
Abdominal compartment syndrome
## Footnote
This condition is characterized by markedly elevated intraabdominal pressures.
78
What intraabdominal pressure is typically associated with abdominal compartment syndrome?
>20 mmHg
## Footnote
Elevated pressures can lead to renal vein compression and reduced GFR.
79
What can compromise oxygen and metabolic substrate delivery to the tubules and glomeruli?
Diseases of the vasculature leading to ischemia
## Footnote
These diseases can significantly affect kidney function.
80
What are microvascular causes of AKI?
* Thrombotic microangiopathies
* Scleroderma
* Some chemotherapeutic agents
* Atheroembolic disease
## Footnote
Examples of thrombotic microangiopathies include cocaine use and certain chemotherapeutic agents.
81
What are large-vessel diseases associated with AKI?
* Renal artery dissection
* Thromboembolism
* Thrombosis
* Renal vein compression
## Footnote
These conditions can severely impact renal blood flow.
82
What is the gold standard for direct visualization of the renal vasculature?
Renal angiography
## Footnote
This diagnostic tool is crucial for identifying renal artery stenosis and other vascular issues.
83
What conditions can renal angiography help diagnose?
* Renal artery stenosis
* Large vessel vasculitis
* Fibromuscular disease
* Renal vein obstruction
## Footnote
Accurate diagnosis is essential for effective treatment.
84
A 65-year-old patient develops acute kidney injury following hemorrhagic shock. Laboratory studies show elevated endothelin-1 and thromboxane A2 levels. Which of the following pathophysiologic mechanisms is most directly responsible for the sustained reduction in renal blood flow in this patient?
A. Tubular obstruction from desquamated cells
B. Vasoconstriction mediated by endothelin and thromboxane A2
C. Backleak of filtrate due to loss of tubular integrity
D. Mitochondrial injury in proximal tubular cells
Answer: B (Vasoconstriction mediated by endothelin and thromboxane A2)
Explanation: The figure highlights that endothelin, thromboxane A2, and other mediators cause microvascular vasoconstriction, which sustains ischemia. This is the primary driver of reduced renal perfusion post-injury.
85
In experimental models of ischemic AKI, administration of a nitric oxide (NO) donor prior to renal ischemia is found to attenuate injury. Which of the following best explains this protective effect?
A. NO inhibits leukocyte-endothelial adhesion
B. NO promotes vasodilation to counteract vasoconstrictors
C. NO prevents cytoskeletal breakdown in tubular cells
D. NO reduces mitochondrial oxidative stress
Answer: B (NO promotes vasodilation to counteract vasoconstrictors)
Explanation: The figure lists NO as a vasodilator that opposes vasoconstrictors (e.g., endothelin, angiotensin II). Preserving renal blood flow via vasodilation mitigates ischemic damage.
86
A kidney biopsy from a patient with prolonged ischemic AKI shows tubular lumina filled with cellular debris and patchy necrosis of tubular epithelial cells. Which of the following processes best accounts for these findings?
A. Leukocyte activation causing vascular obstruction
B. Tubular obstruction from desquamated cells and backleak of filtrate
C. Apoptosis due to mitochondrial injury
D. Loss of endothelial nitric oxide synthase (eNOS) activity
Answer: B (Tubular obstruction from desquamated cells and backleak of filtrate)
Explanation: The "Tubular" section of the figure describes desquamation of cells leading to obstruction and backleak, which correlate with the biopsy findings of luminal debris and necrosis.
87
What is the susceptibility of the kidney to nephrotoxic agents?
The kidney has very high susceptibility to nephrotoxic agents due to extremely high blood perfusion and concentration of filtered substances along the nephron.
88
What results from high-concentration exposure of toxins to kidney cells?
High-concentration exposure of toxins to tubular, interstitial, and endothelial cells leads to nephrotoxic injury.
89
What types of substances can cause nephrotoxic injury?
Nephrotoxic injury occurs in response to pharmacologic compounds, endogenous substances, and environmental exposures.
90
Which structures of the kidney are vulnerable to toxic injury?
All structures of the kidney are vulnerable, including the tubules, interstitium, vasculature, and collecting system.
91
What are common risk factors for nephrotoxicity?
Risk factors for nephrotoxicity include older age, chronic kidney disease (CKD), and prerenal azotemia.
92
How does hypoalbuminemia affect nephrotoxin-associated AKI?
Hypoalbuminemia may increase the risk of some forms of nephrotoxin-associated AKI due to increased free circulating drug concentrations.
93
Fill in the blank: The kidney has very high susceptibility to _______ due to extremely high blood perfusion.
[nephrotoxic agents]
94
True or False: Only the tubules of the kidney are vulnerable to nephrotoxic injury.
False
95
What condition may lead to increased free circulating drug concentrations and potentially nephrotoxic injury?
Hypoalbuminemia
96
What are iodinated contrast agents used for?
They are used for cardiovascular and computed tomography (CT) imaging.
97
What is the risk of AKI in individuals with normal renal function after exposure to iodinated contrast agents?
Negligible.
98
In which condition does the risk of contrast nephropathy increase significantly?
Chronic kidney disease (CKD), particularly diabetic nephropathy.
99
What is the typical clinical course of contrast nephropathy?
Rise in serum creatinine (SCr) beginning 24–48 hours after exposure, peaking within 3–5 days, and resolving within 1 week.
100
Is severe, dialysis-requiring AKI common in contrast nephropathy?
Uncommon, except in significant preexisting CKD.
101
Which patients are particularly susceptible to contrast nephropathy?
Patients with multiple myeloma and/or renal disease.
102
What are common findings in contrast nephropathy?
* Low fractional excretion of sodium (FeNa)
* Relatively benign urinary sediment without features of tubular necrosis.
103
What are the proposed mechanisms for contrast nephropathy?
1. Hypoxia in the renal outer medulla due to renal microcirculation perturbations
2. Cytotoxic damage to the tubules or via oxygen-free radicals
3. Transient tubule obstruction with precipitated contrast material.
104
What other diagnostic agents can cause AKI?
* High-dose gadolinium for MRI
* Oral sodium phosphate solutions used as bowel purgatives.
105
What condition has gadolinium been associated with in patients with advanced kidney disease?
Nephrogenic systemic fibrosis (NSF).
106
Which group of gadolinium-based contrast media has been associated with NSF?
Group I gadolinium-based contrast media.
107
What is the risk of AKI associated with standard doses of group II gadolinium-based contrast media?
Very low.
108
109
What is vancomycin associated with in terms of kidney injury?
Vancomycin may be associated with AKI from tubular injury, particularly when trough levels are high and when used in combination with other nephrotoxic antibiotics.
## Footnote
Vancomycin can also crystallize in tubules and cause intratubular obstruction.
110
What types of kidney injury do aminoglycosides and amphotericin B cause?
Both cause tubular necrosis.
## Footnote
Nonoliguric AKI accompanies 10–30% of courses of aminoglycoside antibiotics.
111
What is the urine volume characteristic of nonoliguric AKI?
Urine volume >400 mL/day.
## Footnote
This occurs even when plasma levels of aminoglycosides are in the therapeutic range.
112
After how many days of therapy do symptoms of AKI typically manifest with aminoglycosides?
5–7 days of therapy.
## Footnote
AKI can present even after the drug has been discontinued.
113
What is a common finding associated with aminoglycoside-induced AKI?
Hypomagnesemia.
## Footnote
This is frequently observed in patients with AKI due to aminoglycosides.
114
What mechanism does amphotericin B use to cause renal vasoconstriction?
Increase in tubuloglomerular feedback.
## Footnote
Amphotericin B also has direct tubular toxicity mediated by reactive oxygen species.
115
What is the relationship between amphotericin B nephrotoxicity and dosage?
Nephrotoxicity is dose and duration dependent.
## Footnote
This drug binds to tubular membrane cholesterol and introduces pores.
116
What are some clinical features of amphotericin B nephrotoxicity?
Clinical features include:
* Polyuria
* Hypomagnesemia
* Hypocalcemia
* Nongap metabolic acidosis
## Footnote
These features arise from the nephrotoxic effects of the drug.
117
How can acyclovir cause AKI?
Acyclovir can precipitate in tubules and cause AKI by tubular obstruction, particularly when given as an intravenous bolus at high doses or in the setting of hypovolemia.
## Footnote
High doses of 500 mg/m2 are particularly risky.
118
Which drugs are frequently associated with AKI due to tubular toxicity?
Foscarnet, pentamidine, tenofovir, and cidofovir.
## Footnote
These drugs can lead to AKI secondary to tubular toxicity.
119
What can cause AKI secondary to acute interstitial nephritis?
Exposure to many antibiotics, including:
* Penicillins
* Cephalosporins
* Quinolones
* Sulfonamides
* Rifampin
## Footnote
These antibiotics can lead to a type of kidney injury characterized by inflammation.
120
What are the two chemotherapeutic agents that accumulate in proximal tubular cells?
Cisplatin and carboplatin
121
What is the effect of intensive hydration regimens on cisplatin nephrotoxicity?
They have reduced the incidence of cisplatin nephrotoxicity
122
What type of toxicity does cisplatin represent?
Dose-limiting toxicity
123
What condition may ifosfamide cause that is characterized by bleeding in the urinary tract?
Hemorrhagic cystitis
124
What is one manifestation of tubular toxicity from ifosfamide?
Type II renal tubular acidosis (Fanconi syndrome)
125
What are two symptoms associated with ifosfamide's tubular toxicity?
* Polyuria
* Hypokalemia
126
What is a potential consequence of ifosfamide use regarding kidney function?
Modest decline in GFR
127
What do antiangiogenesis agents like bevacizumab cause in relation to kidney health?
Proteinuria and hypertension
128
What type of kidney injury can result from antiangiogenesis agents?
Thrombotic microangiopathy
129
Which other antineoplastic agents can cause thrombotic microangiopathy?
* Mitomycin C
* Gemcitabine
130
What are immune checkpoint inhibitors associated with in terms of kidney health?
Immune-related adverse events
131
What specific immune-related adverse event can occur in the kidney due to immune checkpoint inhibitors?
Acute interstitial nephritis
132
Fill in the blank: Ifosfamide may cause _______ as a side effect.
Hemorrhagic cystitis
133
True or False: Cisplatin and carboplatin are known to cause apoptosis in proximal tubular cells.
True
134
135
What is ethylene glycol metabolized to that may cause AKI?
Oxalic acid, glycolaldehyde, and glyoxylate
## Footnote
These metabolites may cause acute kidney injury through direct tubular injury and tubular obstruction.
136
What industrial agent has caused outbreaks of severe AKI due to adulteration of pharmaceutical preparations?
Diethylene glycol
## Footnote
This agent has been linked to significant health crises worldwide.
137
What metabolite is thought to be responsible for tubular injury in cases of diethylene glycol exposure?
2-hydroxyethoxyacetic acid (HEAA)
## Footnote
HEAA is a toxic metabolite that leads to kidney damage.
138
What contamination of foodstuffs has led to nephrolithiasis and AKI?
Melamine
## Footnote
Melamine can cause kidney stones and acute kidney injury through intratubular obstruction or direct tubular toxicity.
139
What were the causes of 'Chinese herb nephropathy' and 'Balkan nephropathy'?
Aristolochic acid
## Footnote
This compound was found in contaminated medicinal herbs and farming products.
140
What is the expected trend regarding environmental toxins and chronic tubular interstitial disease?
The list of environmental toxins is likely to grow
## Footnote
This growth will contribute to a better understanding of previously catalogued idiopathic chronic tubular interstitial disease.
141
True or False: Ethylene glycol ingestion can lead to direct tubular injury.
True
## Footnote
Ethylene glycol metabolites cause acute kidney injury through various mechanisms.
142
Fill in the blank: Diethylene glycol has caused outbreaks of severe AKI due to _______.
[adulteration of pharmaceutical preparations]
143
True or False: Melamine only causes AKI through direct tubular toxicity.
False
## Footnote
Melamine can also cause AKI through intratubular obstruction.
144
What are some endogenous compounds that may cause AKI?
Myoglobin, hemoglobin, uric acid, myeloma light chains
## Footnote
These compounds can lead to kidney injury through various mechanisms.
145
How can myoglobin be released into the bloodstream?
By injured muscle cells
## Footnote
Myoglobin release can occur due to muscle damage.
146
What condition can lead to the release of hemoglobin?
Massive hemolysis
## Footnote
Hemolysis is the breakdown of red blood cells, leading to pigment nephropathy.
147
What is rhabdomyolysis and what can cause it?
A condition resulting from muscle injury, caused by:
* Traumatic crush injuries
* Muscle ischemia
* Compression during coma or immobilization
* Prolonged seizure activity
* Excessive exercise
* Heat stroke
* Malignant hyperthermia
* Infections
* Metabolic disorders
* Myopathies
## Footnote
Rhabdomyolysis can lead to the release of myoglobin and subsequent kidney injury.
148
What are pathogenic factors for AKI due to endogenous toxins?
Intrarenal vasoconstriction, direct proximal tubular toxicity, mechanical obstruction of the distal nephron lumen
## Footnote
These factors can exacerbate kidney injury when endogenous toxins are present.
149
What is Tamm-Horsfall protein and where is it produced?
The most common protein in urine, produced in the thick ascending limb of the loop of Henle
## Footnote
It plays a role in the precipitation of myoglobin and hemoglobin in acidic urine.
150
What syndrome may follow initiation of cytotoxic therapy in patients with high-grade lymphomas?
Tumor lysis syndrome
## Footnote
This syndrome can also occur spontaneously or with treatment for solid tumors or multiple myeloma.
151
What is a significant biochemical feature of tumor lysis syndrome?
Massive release of uric acid, often exceeding 15 mg/dL
## Footnote
This high level of uric acid can lead to precipitation in renal tubules.
152
What other features accompany tumor lysis syndrome?
Hyperkalemia, hyperphosphatemia
## Footnote
These electrolyte imbalances can complicate the clinical picture.
153
How do myeloma light chains contribute to AKI?
By causing glomerular damage, direct tubular toxicity, and binding to Tamm-Horsfall protein
## Footnote
This binding can lead to obstructing intratubular casts.
154
What condition can cause AKI by intense renal vasoconstriction and volume depletion?
Hypercalcemia
## Footnote
Hypercalcemia can also be seen in conditions like multiple myeloma.
155
What type of disease can lead to AKI and is characterized by an inflammatory infiltrate?
Acute tubulointerstitial disease
## Footnote
This can be associated with allergic responses and sometimes eosinophilia.
156
Name two commonly used drugs associated with acute tubulointerstitial nephritis.
* Proton pump inhibitors
* NSAIDs
## Footnote
These drugs can trigger allergic responses leading to kidney inflammation.
157
What severe conditions can also cause AKI apart from drug-related causes?
Severe infections and infiltrative malignant or nonmalignant diseases
## Footnote
An example of a nonmalignant disease is sarcoidosis.
158
What condition results from excessive anticoagulation with warfarin or other anticoagulants?
Anticoagulant-Related Nephropathy
## Footnote
This condition can cause AKI through glomerular hemorrhage.
159
How does anticoagulant-related nephropathy lead to AKI?
Formation of obstructing red blood cell casts within the kidney tubule and tubular injury
## Footnote
This occurs due to glomerular hemorrhage.
160
What diseases can lead to AKI by compromising the filtration barrier and blood flow?
Glomerulonephritis
## Footnote
This involves glomerular podocytes, mesangial, and/or endothelial cells.
161
What is the approximate percentage of AKI cases attributed to glomerulonephritis?
~5%
## Footnote
Early recognition and treatment are crucial for improving outcomes.
162
What treatments may help reverse AKI caused by glomerulonephritis?
* Immunosuppressive agents
* Therapeutic plasma exchange
## Footnote
Timely treatment may decrease subsequent longer-term injury.
163
What is postrenal AKI?
Postrenal AKI occurs when the normally unidirectional flow of urine is acutely blocked either partially or totally.
164
What is the consequence of obstruction to urinary flow in postrenal AKI?
It leads to increased retrograde hydrostatic pressure and interference with glomerular filtration.
165
Where can obstruction to urinary flow occur?
From the renal pelvis to the tip of the urethra.
166
Does normal urinary flow rate rule out partial obstruction?
No, normal urinary flow rate does not rule out the presence of partial obstruction.
167
Why can preservation of urine output be misleading in postrenal AKI?
Because GFR is normally two orders of magnitude higher than the urinary flow rate.
168
What must occur for moderate to severe AKI to be observed in individuals with two healthy functional kidneys?
Obstruction must affect both kidneys.
169
What can cause AKI in the setting of unilateral obstruction?
Significant underlying CKD or reflex vasospasm of the contralateral kidney.
170
What is a common cause of postrenal AKI?
Bladder neck obstruction.
171
What conditions can lead to bladder neck obstruction?
* Prostate disease (benign prostatic hypertrophy or prostate cancer)
* Neurogenic bladder
* Therapy with anticholinergic drugs.
172
What can obstructed Foley catheters cause?
Postrenal AKI if not recognized and obstruction relieved.
173
What are other causes of lower tract obstruction?
* Blood clots
* Calculi
* Urethral strictures.
174
What can cause ureteric obstruction?
* Intraluminal obstruction (e.g., calculi, blood clots, sloughed renal papillae)
* Infiltration of the ureteric wall (e.g., neoplasia)
* External compression (e.g., retroperitoneal fibrosis, neoplasia, abscess, or inadvertent surgical damage).
175
What is the pathophysiology of postrenal AKI?
It involves hemodynamic alterations triggered by an abrupt increase in intratubular pressures.
176
What initially occurs in the pathophysiology of postrenal AKI?
An initial period of hyperemia from afferent arteriolar dilation.
177
What follows the initial hyperemia in postrenal AKI?
Intrarenal vasoconstriction from the generation of angiotensin II, thromboxane A2, and vasopressin.
178
What reduction occurs in the pathophysiology of postrenal AKI?
A reduction in NO production.
179
What are secondary reductions in glomerular function due to?
Underperfusion of glomeruli and possibly changes in the glomerular ultrafiltration coefficient.
180
What is the primary suspicion in cases of prerenal azotemia?
Suspected in the setting of vomiting, diarrhea, glycosuria causing polyuria, and several medications including diuretics, NSAIDs, ACE inhibitors, and ARBs.
## Footnote
Prerenal azotemia results from reduced renal perfusion.
181
Which physical signs are often present in prerenal azotemia?
Orthostatic hypotension, tachycardia, reduced jugular venous pressure, decreased skin turgor, dry mucous membranes.
## Footnote
These signs indicate volume depletion.
182
What conditions can be associated with reductions in renal blood flow?
Congestive heart failure, liver disease, nephrotic syndrome.
## Footnote
These conditions can alter intrarenal hemodynamics leading to reduced GFR.
183
What does extensive vascular disease raise the possibility of?
Renal artery disease, especially if kidneys are asymmetric in size.
## Footnote
Asymmetry may indicate underlying vascular pathology.
184
What signs may be associated with atheroembolic disease?
Livedo reticularis and other signs of emboli to the legs.
## Footnote
Atheroembolic disease can lead to AKI through embolization of renal arteries.
185
What is an important clue to the causation of AKI?
The presence of sepsis.
## Footnote
Sepsis can lead to multifactorial pathophysiology of AKI.
186
What history would suggest the possibility of postrenal AKI?
History of prostatic disease, nephrolithiasis, or pelvic or paraaortic malignancy.
## Footnote
These conditions can lead to urinary obstruction.
187
What symptom suggests acute ureteric obstruction?
Colicky flank pain radiating to the groin.
## Footnote
This symptom is indicative of obstruction in the urinary tract.
188
What can be accompanying symptoms of bladder enlargement?
Abdominal fullness and suprapubic pain.
## Footnote
These symptoms may indicate urinary retention due to obstruction.
189
What is required for definitive diagnosis of obstruction?
Radiologic investigations.
## Footnote
Imaging helps confirm the presence and location of obstruction.
190
Why is a careful review of all medications important in AKI evaluation?
Medications can be nephrotoxic and doses must be adjusted for reductions in kidney function.
## Footnote
Understanding medication effects is crucial for patient safety.
191
What is a common misconception regarding equations that estimate GFR?
Reductions in true GFR are not reflected by these equations because they depend on SCr and the patient being in a steady state.
## Footnote
In AKI, changes in SCr lag behind changes in filtration rate.
192
What can lead to allergic interstitial nephritis?
Idiosyncratic reactions to a wide variety of medications.
## Footnote
Symptoms may include fever, arthralgias, and a pruritic erythematous rash.
193
What should be considered for definitive diagnosis of interstitial nephritis?
A kidney biopsy.
## Footnote
Biopsy can provide conclusive evidence of interstitial nephritis.
194
What symptoms may indicate systemic vasculitis with glomerulonephritis?
Palpable purpura, pulmonary hemorrhage, or sinusitis.
## Footnote
These symptoms suggest an underlying systemic condition affecting the kidneys.
195
What underlying disease should be considered if a patient has a history of autoimmune disease?
Worsening of the autoimmune disease such as systemic lupus erythematosus.
## Footnote
Autoimmune diseases can exacerbate renal function.
196
What condition should be considered in pregnant patients with AKI?
Preeclampsia.
## Footnote
Preeclampsia can significantly affect renal function during pregnancy.
197
What should a tense abdomen prompt consideration of?
Acute abdominal compartment syndrome.
## Footnote
Measurement of bladder pressure can facilitate diagnosis.
198
What may be clues to the diagnosis of rhabdomyolysis?
Signs and/or symptoms of limb ischemia.
## Footnote
Rhabdomyolysis can lead to AKI through muscle breakdown.
199
A 70-year-old man with a history of hypertension presents with acute kidney injury. His BUN/creatinine ratio is 25:1, urine specific gravity is 1.025, and urine osmolality is 550 mOsm/kg. Urine sediment shows hyaline casts. He has been taking ibuprofen for chronic back pain. Which of the following is the most likely diagnosis?
A. Sepsis-associated AKI
B. Prerenal azotemia
C. Rhabdomyolysis
D. Multiple myeloma
Answer: B (Prerenal azotemia)
Explanation: The findings of elevated BUN/creatinine ratio (>20:1), high urine specific gravity (>1.020), high urine osmolality (>500 mOsm/kg), and hyaline casts are classic for prerenal azotemia. The use of NSAIDs (ibuprofen) further supports this diagnosis by impairing renal autoregulation.
200
A 45-year-old woman develops acute kidney injury following a severe bacterial infection. Her urine sediment shows granular casts and renal tubular epithelial cell casts. Her FeNa is 2%. Which of the following is the most likely cause of her AKI?
A. Prerenal azotemia
B. Ischemia-associated AKI
C. Nephrotoxin-associated AKI
D. Hemolysis
Answer: B (Ischemia-associated AKI)
Explanation: The presence of granular casts and renal tubular epithelial cell casts with a FeNa >1% suggests intrinsic AKI, specifically ischemia-associated AKI, which is common in the setting of sepsis or hypotension.
201
A 60-year-old man with a history of multiple myeloma presents with acute kidney injury. Laboratory studies reveal a monoclonal spike on serum electrophoresis, anemia, and a low anion gap. Which of the following additional findings would most support the diagnosis of myeloma-associated AKI?
A. Elevated creatine kinase
B. Hyperphosphatemia and hypocalcemia
C. Positive urine heme with few RBCs
D. High haptoglobin
Answer: B (Hyperphosphatemia and hypocalcemia)
Explanation: In multiple myeloma-associated AKI, hyperphosphatemia and hypocalcemia may occur due to bone resorption and renal failure. The monoclonal spike and low anion gap further support this diagnosis. Elevated creatine kinase (A) suggests rhabdomyolysis, while positive urine heme with few RBCs (C) suggests hemolysis.
202
A 32-year-old bodybuilder is found unconscious after a 24-hour gym session. His urine is tea-colored and dipstick shows 3+ blood but only 2-3 RBCs/hpf. Serum CK is 85,000 U/L. Which of the following best explains his acute kidney injury?
A. Acute glomerulonephritis
B. Rhabdomyolysis with myoglobinuria
C. Hemolytic uremic syndrome
D. Contrast-induced nephropathy
Answer: B (Rhabdomyolysis with myoglobinuria)
Explanation: The clinical scenario of prolonged exertion with tea-colored urine, dipstick-positive blood without RBCs on microscopy, and extremely elevated CK is classic for rhabdomyolysis-induced AKI from myoglobinuria.
203
A 65-year-old man develops AKI 48 hours after coronary angiography. His serum creatinine peaks on day 3 at 3.2 mg/dL (baseline 1.0 mg/dL) and improves by day 7. Which nephrotoxic mechanism is most likely?
A. Acute interstitial nephritis
B. Contrast nephropathy
C. Aminoglycoside toxicity
D. Tumor lysis syndrome
Answer: B (Contrast nephropathy)
Explanation: The temporal relationship with contrast exposure, characteristic creatinine curve (rise in 1-2 days, peak at 3-5 days, recovery by 7 days) is diagnostic of contrast-induced nephropathy.
204
A 58-year-old woman with breast cancer develops AKI after her first cycle of chemotherapy. Labs show potassium 5.8 mEq/L, phosphate 8.2 mg/dL, calcium 6.9 mg/dL, and uric acid 12 mg/dL. What is the most likely cause?
A. Cisplatin nephrotoxicity
B. Tumor lysis syndrome
C. Multiple myeloma cast nephropathy
D. Aminoglycoside toxicity
Answer: B (Tumor lysis syndrome)
Explanation: The biochemical triad of hyperphosphatemia, hypocalcemia and hyperuricemia following chemotherapy is pathognomonic for tumor lysis syndrome, which can cause AKI through urate and phosphate crystal deposition.
205
A 45-year-old woman presents with acute kidney injury, hemoptysis, and sinusitis. Laboratory studies reveal positive anti-neutrophil cytoplasmic antibodies (ANCA). Which of the following is the most likely underlying pathology?
A. Poststreptococcal glomerulonephritis
B. ANCA-associated vasculitis
C. Thrombotic thrombocytopenic purpura (TTP)
D. Tubulointerstitial nephritis
Answer: B (ANCA-associated vasculitis)
Explanation: The triad of AKI, hemoptysis (lung hemorrhage), and sinusitis with positive ANCA is classic for ANCA-associated vasculitis (e.g., granulomatosis with polyangiitis). This requires urgent immunosuppressive therapy.
206
A 60-year-old man develops acute kidney injury 1 week after coronary angiography. On examination, he has livedo reticularis and tender purple toe lesions. Laboratory studies show eosinophilia and hypocomplementemia. Which of the following is the most likely diagnosis?
A. Contrast-induced nephropathy
B. Cholesterol crystal embolization
C. Acute interstitial nephritis
D. Hemolytic uremic syndrome
Answer: B (Cholesterol crystal embolization)
Explanation: The findings of livedo reticularis, purple toes (retinal plaques may also be seen), eosinophilia, and AKI after vascular manipulation (angiography) are pathognomonic for cholesterol crystal embolization ("atheroembolic disease"). Hypocomplementemia further supports this diagnosis.
207
A 25-year-old woman presents with acute kidney injury, thrombocytopenia, and confusion. Peripheral blood smear shows schistocytes. Which of the following additional findings would most strongly suggest thrombotic thrombocytopenic purpura (TTP) rather than Shiga toxin-induced HUS?
A. Recent diarrheal illness
B. Severely reduced ADAMTS13 activity (<10%)
C. Elevated lactate dehydrogenase (LDH)
D. Hypocomplementemia
Answer: B (Severely reduced ADAMTS13 activity (<10%))
Explanation: While both TTP and STEC-HUS present with AKI, thrombocytopenia, and schistocytes, ADAMTS13 activity <10% is diagnostic of TTP. A diarrheal prodrome (A) would suggest STEC-HUS, and LDH elevation (C) occurs in both. Hypocomplementemia (D) is seen in other conditions like lupus.
208
What is prerenal azotemia characterized by in terms of serum creatinine (SCr) levels?
Modest rises in SCr that return to baseline with improvement in hemodynamic status
## Footnote
This condition indicates a pre-renal cause of acute kidney injury (AKI) often related to decreased blood flow to the kidneys.
209
How does contrast nephropathy affect serum creatinine levels?
Rise in SCr within 24–48 hours, peak within 3–5 days, and resolution within 5–7 days
## Footnote
This condition is often seen following exposure to contrast agents in imaging studies.
210
What pattern of serum creatinine rise is associated with atheroembolic disease?
Subacute rises in SCr, although severe AKI with rapid increases in SCr can occur
## Footnote
This condition is often related to emboli from atherosclerotic plaques affecting renal blood flow.
211
What is the characteristic timing of SCr rise with epithelial cell toxins like aminoglycoside antibiotics?
Delayed rise in SCr for 3–5 days to 2 weeks after initial exposure
## Footnote
This delay is crucial for recognizing drug-induced nephrotoxicity.
212
What laboratory finding is common in acute kidney injury (AKI)?
Anemia
## Footnote
Anemia in AKI is often multifactorial and not solely related to red blood cell production.
213
What can peripheral eosinophilia indicate in the context of AKI?
Interstitial nephritis, atheroembolic disease, polyarteritis nodosa, or Churg-Strauss vasculitis
## Footnote
This finding can help differentiate causes of AKI.
214
What severe condition may cause anemia in the absence of bleeding?
Hemolysis, multiple myeloma, or thrombotic microangiopathy
## Footnote
Examples of thrombotic microangiopathy include hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP).
215
What laboratory findings are associated with thrombotic microangiopathy?
Thrombocytopenia, schistocytes on peripheral blood smear, elevated lactate dehydrogenase level, low haptoglobin content
## Footnote
These findings are critical for diagnosing conditions like HUS and TTP.
216
What is the significance of measuring ADAMTS13 levels in suspected TTP or HUS cases?
It helps evaluate the presence of von Willebrand factor cleaving protease
## Footnote
Low levels of ADAMTS13 are indicative of TTP.
217
What percentage of atypical HUS patients have mutations in genes related to the alternative complement pathway?
60–70%
## Footnote
Atypical HUS is more prevalent in adults and genetic testing is important for diagnosis.
218
What electrolyte imbalances are commonly seen in AKI?
Hyperkalemia, hyperphosphatemia, and hypocalcemia
## Footnote
These imbalances can lead to various complications in patients with AKI.
219
What does marked hyperphosphatemia with hypocalcemia suggest?
Rhabdomyolysis or tumor lysis syndrome
## Footnote
This combination of electrolyte disturbances is critical for diagnosis.
220
How do serum creatine kinase levels vary in rhabdomyolysis versus tumor lysis syndrome?
Elevated in rhabdomyolysis; normal or marginally elevated in tumor lysis syndrome
## Footnote
Serum uric acid levels are markedly elevated in tumor lysis syndrome.
221
What does an increased anion gap indicate in uremia?
Retention of anions such as phosphate, hippurate, sulfate, and urate
## Footnote
An increased anion gap may suggest various underlying causes of renal failure.
222
What might the co-occurrence of an increased anion gap and an osmolal gap suggest?
Ethylene glycol poisoning
## Footnote
This condition may also lead to oxalate crystalluria and deposition in kidney tissue.
223
What does a low anion gap suggest in the context of AKI?
Diagnosis of multiple myeloma due to presence of unmeasured cationic proteins
## Footnote
This finding can help differentiate multiple myeloma from other causes of AKI.
224
What laboratory tests are helpful for diagnosing glomerulonephritis and vasculitis?
Depressed complement levels and high titers of ANAs, ANCAs, Anti-GBM antibodies, and cryoglobulins
## Footnote
These tests are essential for identifying autoimmune causes of kidney injury.
225
What is prerenal azotemia characterized by in terms of serum creatinine (SCr) levels?
Modest rises in SCr that return to baseline with improvement in hemodynamic status
## Footnote
This condition indicates a pre-renal cause of acute kidney injury (AKI) often related to decreased blood flow to the kidneys.
226
How does contrast nephropathy affect serum creatinine levels?
Rise in SCr within 24–48 hours, peak within 3–5 days, and resolution within 5–7 days
## Footnote
This condition is often seen following exposure to contrast agents in imaging studies.
227
What pattern of serum creatinine rise is associated with atheroembolic disease?
Subacute rises in SCr, although severe AKI with rapid increases in SCr can occur
## Footnote
This condition is often related to emboli from atherosclerotic plaques affecting renal blood flow.
228
What is the characteristic timing of SCr rise with epithelial cell toxins like aminoglycoside antibiotics?
Delayed rise in SCr for 3–5 days to 2 weeks after initial exposure
## Footnote
This delay is crucial for recognizing drug-induced nephrotoxicity.
229
What laboratory finding is common in acute kidney injury (AKI)?
Anemia
## Footnote
Anemia in AKI is often multifactorial and not solely related to red blood cell production.
230
What can peripheral eosinophilia indicate in the context of AKI?
Interstitial nephritis, atheroembolic disease, polyarteritis nodosa, or Churg-Strauss vasculitis
## Footnote
This finding can help differentiate causes of AKI.
231
What severe condition may cause anemia in the absence of bleeding?
Hemolysis, multiple myeloma, or thrombotic microangiopathy
## Footnote
Examples of thrombotic microangiopathy include hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP).
232
What laboratory findings are associated with thrombotic microangiopathy?
Thrombocytopenia, schistocytes on peripheral blood smear, elevated lactate dehydrogenase level, low haptoglobin content
## Footnote
These findings are critical for diagnosing conditions like HUS and TTP.
233
What is the significance of measuring ADAMTS13 levels in suspected TTP or HUS cases?
It helps evaluate the presence of von Willebrand factor cleaving protease
## Footnote
Low levels of ADAMTS13 are indicative of TTP.
234
What percentage of atypical HUS patients have mutations in genes related to the alternative complement pathway?
60–70%
## Footnote
Atypical HUS is more prevalent in adults and genetic testing is important for diagnosis.
235
What electrolyte imbalances are commonly seen in AKI?
Hyperkalemia, hyperphosphatemia, and hypocalcemia
## Footnote
These imbalances can lead to various complications in patients with AKI.
236
What does marked hyperphosphatemia with hypocalcemia suggest?
Rhabdomyolysis or tumor lysis syndrome
## Footnote
This combination of electrolyte disturbances is critical for diagnosis.
237
How do serum creatine kinase levels vary in rhabdomyolysis versus tumor lysis syndrome?
Elevated in rhabdomyolysis; normal or marginally elevated in tumor lysis syndrome
## Footnote
Serum uric acid levels are markedly elevated in tumor lysis syndrome.
238
What does an increased anion gap indicate in uremia?
Retention of anions such as phosphate, hippurate, sulfate, and urate
## Footnote
An increased anion gap may suggest various underlying causes of renal failure.
239
What might the co-occurrence of an increased anion gap and an osmolal gap suggest?
Ethylene glycol poisoning
## Footnote
This condition may also lead to oxalate crystalluria and deposition in kidney tissue.
240
What does a low anion gap suggest in the context of AKI?
Diagnosis of multiple myeloma due to presence of unmeasured cationic proteins
## Footnote
This finding can help differentiate multiple myeloma from other causes of AKI.
241
What laboratory tests are helpful for diagnosing glomerulonephritis and vasculitis?
Depressed complement levels and high titers of ANAs, ANCAs, Anti-GBM antibodies, and cryoglobulins
## Footnote
These tests are essential for identifying autoimmune causes of kidney injury.
