Acute Kidney Injury Flashcards
(246 cards)
1
Q
What is acute kidney injury (AKI)?
A
Impairment of kidney filtration and excretory function over days to weeks, leading to retention of waste products
AKI is not a single disease but a heterogeneous group of conditions characterized by increased serum creatinine and reduced urine volume.
2
Q
What percentage of acute-care hospital admissions is complicated by AKI?
A
5-7%
In ICU admissions, this percentage can rise up to 30%.
3
Q
What has been the trend in the incidence of AKI in the United States since 1988?
A
The incidence has grown by more than fourfold
The yearly incidence is estimated at 500 per 100,000 population, which is higher than the yearly incidence of stroke.
4
Q
What is the relationship between serum creatinine (SCr) increases and hospital mortality?
A
Increases as low as 0.3 mg/dL are associated with approximately a fourfold increase in hospital mortality
Higher changes in creatinine and longer duration of elevation correlate with greater morbidity and mortality risk.
5
Q
What are common causes of community-acquired AKI?
A
- Volume depletion
- Heart failure
- Adverse effects of medications
- Urinary tract obstruction
- Malignancy
6
Q
What are the three broad categories of AKI causes?
A
- Prerenal azotemia
- Intrinsic renal parenchymal disease
- Postrenal obstruction
7
Q
What is prerenal azotemia?
A
A rise in SCr or BUN concentration due to inadequate renal plasma flow and intraglomerular hydrostatic pressure
It is the most common form of AKI and is rapidly reversible once blood flow is restored.
8
Q
What clinical conditions are associated with prerenal azotemia?
A
- Hypovolemia
- Decreased cardiac output
- Medications interfering with renal autoregulation
(NSAIDS, ACE-I, ARB)
9
Q
What happens to glomerular filtration rate (GFR) during prerenal azotemia?
A
GFR can be maintained despite reduced renal blood flow through compensatory mechanisms
These mechanisms include angiotensin II-mediated vasoconstriction and myogenic reflexes.
10
Q
What role do NSAIDs play in prerenal azotemia?
A
NSAIDs inhibit renal prostaglandin production, limiting renal afferent vasodilation
This increases the risk of developing prerenal azotemia.
11
Q
What is intrinsic AKI commonly caused by?
A
- Sepsis
- Ischemia
- Nephrotoxins (endogenous and exogenous)
12
Q
How does sepsis lead to AKI?
A
Sepsis can cause decreases in GFR even without overt hypotension, often requiring vasopressor support
Inflammation and mitochondrial dysfunction may also contribute to sepsis-induced AKI.
13
Q
What is the significance of ischemia in AKI?
A
Ischemia can lead to renal tubular injury, particularly in the outer medulla, which is vulnerable to damage
The kidneys receive 20% of cardiac output despite their small mass.
14
Q
What are common risk factors for postoperative AKI?
A
- Underlying chronic kidney disease (CKD)
- Older age
- Diabetes mellitus
- Congestive heart failure
- Emergency procedures
15
Q
What is the pathophysiology of AKI following cardiac surgery?
A
It is multifactorial, including factors like ischemic injury from hypoperfusion and activation of inflammatory processes
Cardiopulmonary bypass can also contribute to AKI.
16
Q
What is the prognosis of type 1 hepatorenal syndrome?
A
It has a particularly poor prognosis, persisting despite volume administration
Type 2 hepatorenal syndrome is less severe and characterized mainly by refractory ascites.
17
Q
What physiological mechanisms help maintain GFR in prerenal azotemia?
A
- Afferent arteriole dilation via myogenic reflex
- Renal biosynthesis of vasodilator prostaglandins
- Tubuloglomerular feedback
18
Q
True or False: AKI can occur without structural damage to the kidneys.
A
True
AKI is a clinical diagnosis and may occur with or without injury to kidney parenchyma.
19
Q
What factors can impair the autoregulatory response of the kidneys?
A
- Atherosclerosis
- Long-standing hypertension
- Older age
20
Q
Fill in the blank: AKI is often attributed to _____, but biopsy confirmation is often lacking.
A
acute tubular necrosis
21
Q
What are the potential complications of AKI in the developing world?
A
- Envenomations
- Malaria
- Leptospirosis
- Crush injuries
22
Q
What is the impact of AKI on long-term kidney health?
A
Increases the risk for chronic kidney disease (CKD) and dialysis-requiring end-stage kidney disease (ESKD)
23
Q
What is the impact of longer duration of cardiopulmonary bypass on AKI?
A
It is a risk factor for AKI.
24
Q
What mechanisms can cause AKI during cardiopulmonary bypass?
A
- Extracorporeal circuit activation of leukocytes and inflammatory processes
- Hemolysis with resultant pigment nephropathy
- Aortic injury with resultant atheroemboli
25
What is atheroembolic disease related to AKI?
It is due to cholesterol crystal embolization leading to occlusion of small arteries within the kidney.
26
What are the consequences of a foreign body reaction in atheroembolic disease?
Intimal proliferation, giant cell formation, and further narrowing of the vascular lumen.
27
What is the mortality rate among cardiovascular patients requiring renal replacement therapy?
40-70%.
28
What percentage of individuals with severe burns experience AKI?
25%.
29
What complications accompany severe burns and acute pancreatitis that may lead to AKI?
* Severe hypovolemia
* Increased neurohormonal activation
* Dysregulated inflammation
* Increased risk of sepsis and acute lung injury
30
What is abdominal compartment syndrome?
A condition where elevated intraabdominal pressures lead to renal vein compression and reduced GFR.
31
What are the microvascular causes of AKI?
* Thrombotic microangiopathies
* Scleroderma
* Atheroembolic disease
32
What is the gold standard for diagnosing renal artery stenosis?
Renal angiography.
33
What makes the kidney particularly susceptible to nephrotoxic agents?
High blood perfusion and concentration of filtered substances along the nephron.
34
What are common nephrotoxic agents associated with AKI?
* Iodinated contrast agents
* Antibiotics
* Chemotherapeutic agents
* Endogenous toxins
35
What is contrast nephropathy?
AKI caused by iodinated contrast agents, particularly in patients with CKD.
36
What characterizes the clinical course of contrast nephropathy?
Rise in SCr beginning 24-48 h post-exposure, peaking within 3-5 days, resolving within 1 week.
37
Which antibiotic is associated with tubular injury leading to AKI?
Vancomycin.
38
What is the effect of aminoglycosides on renal function?
They can cause tubular necrosis and nonoliguric AKI.
39
What is the mechanism of nephrotoxicity for amphotericin B?
It causes renal vasoconstriction and direct tubular toxicity.
40
What environmental toxins can cause AKI?
* Ethylene glycol
* Diethylene glycol
* Aristolochic acid
41
What endogenous compounds can lead to AKI?
* Myoglobin
* Hemoglobin
* Uric acid
* Myeloma light chains
42
What is the pathophysiology of AKI due to myoglobin release?
Intrarenal vasoconstriction and direct proximal tubular toxicity.
43
What are common causes of acute tubulointerstitial disease leading to AKI?
* Proton pump inhibitors
* NSAIDs
* Severe infections
* Infiltrative diseases
44
What is anticoagulant-related nephropathy?
AKI caused by excessive anticoagulation leading to glomerular hemorrhage.
45
What is the significance of early recognition of glomerulonephritis?
Timely treatment may reverse AKI and decrease long-term injury.
46
What defines postrenal AKI?
Acute blockage of urinary flow leading to increased retrograde hydrostatic pressure.
47
What can cause obstruction leading to postrenal AKI?
* Prostate disease
* Blood clots
* Calculi
* Urethral strictures
48
How is AKI defined by current standards?
Rise in SCr of at least 0.3 mg/dL within 48 h or reduction in urine output to <0.5 mL/kg/h for longer than 6 h.
49
What is the definition of AKI?
At least 50% higher than baseline within 1 week, or a reduction in urine output to <0.5 mL/kg per h for longer than 6 h.
50
What distinguishes AKI from CKD?
Recent baseline SCr concentration availability; clues from radiologic studies or laboratory tests.
51
What laboratory findings suggest CKD?
* Small, shrunken kidneys with cortical thinning on renal ultrasound
* Normocytic anemia in the absence of blood loss
* Secondary hyperparathyroidism with hyperphosphatemia and hypocalcemia
52
Why is it challenging to rule out AKI superimposed on CKD?
AKI is a frequent complication in patients with CKD.
53
What indicates a diagnosis of AKI?
Serial blood tests showing a continued substantial rise of SCr.
54
What clinical context should raise suspicion for prerenal azotemia?
Vomiting, diarrhea, glycosuria causing polyuria, use of diuretics, NSAIDs, ACE inhibitors, ARBs.
55
What physical signs are often present in prerenal azotemia?
* Orthostatic hypotension
* Tachycardia
* Reduced jugular venous pressure
* Decreased skin turgor
* Dry mucous membranes
56
What history suggests postrenal AKI?
Prostatic disease, nephrolithiasis, pelvic or paraaortic malignancy.
57
What symptoms may indicate acute ureteric obstruction?
Colicky flank pain radiating to the groin.
58
What is the significance of reviewing all medications in AKI evaluation?
Medications can be nephrotoxic and doses may need adjustment for reduced kidney function.
59
What are idiosyncratic reactions to medications in AKI?
Allergic interstitial nephritis, which may present with fever, arthralgias, and a pruritic erythematous rash.
60
What findings may indicate systemic vasculitis with glomerulonephritis in AKI?
Palpable purpura, pulmonary hemorrhage, or sinusitis.
61
What is the typical urine output in oliguria?
<400 mL/24 h.
62
What does preserved urine output indicate in AKI?
Less severe AKI; may be seen in nephrogenic diabetes insipidus or other conditions.
63
What urine color may suggest rhabdomyolysis or hemolysis?
Red or brown urine.
64
What does heavy proteinuria (>3.5 g/d) in AKI suggest?
Possible glomerulonephritis, vasculitis, or nephrotoxic effects on the glomerulus.
65
What urine sediment findings are characteristic of ATN due to ischemic injury?
* Pigmented 'muddy brown' granular casts
* Tubular epithelial cell casts
66
What does a low BUN to creatinine ratio suggest?
Prerenal azotemia, especially if >20:1.
67
What does a FeNa <1% indicate?
Avid tubular sodium reabsorption, suggesting prerenal azotemia.
68
What urine osmolality may indicate prerenal azotemia?
>500 mOsm/kg.
69
What imaging should be performed to evaluate postrenal AKI?
Renal ultrasound or CT scan.
70
What findings on imaging suggest obstruction?
* Dilation of the collecting system
* Hydroureteronephrosis
71
What does the presence of oxalate crystals in urine indicate?
Possible ethylene glycol toxicity.
72
What laboratory findings are associated with thrombotic microangiopathy?
* Thrombocytopenia
* Schistocytes on peripheral blood smear
* Elevated lactate dehydrogenase
* Low haptoglobin
73
What does hyperphosphatemia with hypocalcemia suggest?
Possible rhabdomyolysis or tumor lysis syndrome.
74
What is the significance of elevated serum creatine kinase in AKI?
Indicates rhabdomyolysis.
75
What does an increased anion gap in AKI indicate?
Retention of anions such as phosphate, hippurate, sulfate, and urate.
76
What does a low anion gap suggest?
Possible multiple myeloma due to unmeasured cationic proteins.
77
What role does renal ultrasound play in AKI evaluation?
Helps to investigate obstruction and assess kidney size and echogenicity.
78
What does an enlarged kidney in AKI suggest?
Possible acute interstitial nephritis or infiltrative diseases.
79
What condition is indicated by smaller kidneys in CKD?
CKD usually presents with smaller kidneys unless there are specific conditions such as diabetic nephropathy.
80
What does enlarged kidneys in a patient with AKI suggest?
Possibility of acute interstitial nephritis or infiltrative diseases.
81
What imaging technique should be avoided in severe AKI due to risks?
MRI with gadolinium-based contrast agents (GBCAs) should be avoided.
82
What is the main purpose of a kidney biopsy in AKI?
To provide definitive diagnostic and prognostic information about acute kidney disease.
83
What are BUN and creatinine considered in the context of kidney function?
Functional biomarkers of glomerular filtration.
84
What urine output after furosemide administration may indicate a higher risk of severe AKI?
Urine output <200 mL over 2 h after intravenous furosemide.
85
What does the presence of renal tubular epithelial cells in urine sediment indicate?
Associated with severity and worsening of AKI.
86
What is KIM-1?
A type 1 transmembrane protein expressed in proximal tubular cells injured by nephrotoxins.
87
What does NGAL stand for and where is it expressed?
Neutrophil gelatinase associated lipocalin, expressed in human neutrophils.
88
What does suPAR predict in AKI patients?
The subsequent development of AKI.
89
What combination of biomarkers did the FDA approve for predicting AKI risk?
Insulin-like growth factor binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinase-2 (TIMP-2).
90
What is a hallmark of AKI related to nitrogenous waste products?
Buildup of nitrogenous waste products as indicated by elevated BUN concentration.
91
What complication can arise from expansion of extracellular fluid volume in AKI?
Weight gain, dependent edema, increased jugular venous pressure, and pulmonary edema.
92
What can excessive administration of hypotonic solutions lead to in AKI patients?
Hypoosmolality and hyponatremia.
93
What is a common complication of AKI related to potassium levels?
Hyperkalemia.
94
What type of acidosis is common in AKI?
Metabolic acidosis, usually with an elevated anion gap.
95
What can AKI lead to in terms of phosphate and calcium levels?
Hyperphosphatemia and hypocalcemia.
96
What hematologic complications can arise from AKI?
Anemia and bleeding.
97
What are common cardiac complications associated with AKI?
Arrhythmias, pericarditis, and pericardial effusion.
98
What is a major complication of AKI related to nutrition?
Malnutrition.
99
What is critical in the management of AKI?
Optimization of hemodynamics, correction of fluid and electrolyte imbalances.
100
What is the definitive treatment for hepatorenal syndrome?
Orthotopic liver transplantation.
101
What is required for the treatment of AKI due to rhabdomyolysis?
Early and aggressive volume repletion.
102
What should be done to relieve postrenal AKI?
Prompt recognition and relief of urinary tract obstruction.
103
What is a common complication of AKI in terms of fluid management?
Hypervolemia in oliguric AKI.
104
What is the initial treatment approach for urethral strictures or functional bladder impairment?
Transurethral or suprapubic bladder catheterization
## Footnote
This may be sufficient initially before considering further interventions.
105
How is ureteric obstruction typically treated?
Percutaneous nephrostomy tube placement or ureteral stent placement
## Footnote
This is followed by appropriate diuresis for several days.
106
What is a potential complication of severe polyuria in AKI?
Tubular dysfunction requiring intravenous fluids and electrolytes
## Footnote
This may persist even after relief of obstruction.
107
What is a life-threatening condition associated with hypervolemia in oliguric or anuric AKI?
Acute pulmonary edema
## Footnote
This is particularly concerning in patients with coexisting pulmonary disease.
108
What management strategies are recommended for fluid and sodium in AKI?
Fluid and sodium restriction, and diuretics to increase urinary flow rate
## Footnote
Diuretics may help avoid the need for dialysis.
109
What is the role of furosemide in severe volume overload?
Administered as a bolus (200 mg) followed by an intravenous drip (10-40 mg/h)
## Footnote
May be given with or without a thiazide diuretic.
110
What should be monitored when treating metabolic acidosis in AKI?
pH and serum bicarbonate levels
## Footnote
Treatment is generally reserved for severe cases.
111
What dietary recommendations are given for patients with AKI?
Total energy intake of 20-30 kcal/kg per day and protein intake varies based on AKI severity
## Footnote
Recommendations include specific protein intake ranges based on dialysis needs.
112
What is the typical protein intake recommendation for patients on dialysis?
1.0-1.5 g/kg per day
## Footnote
Up to 1.7 g/kg per day if hypercatabolic and receiving continuous renal replacement therapy.
113
What factors contribute to anemia in AKI?
Multifactorial causes including bone marrow resistance and uremic bleeding
## Footnote
Erythropoiesis-stimulating agents may not be effective.
114
When is dialysis indicated in AKI?
When medical management fails to control volume overload, hyperkalemia, or acidosis
## Footnote
Also indicated in severe complications of uremia.
115
What is a risk associated with late initiation of dialysis?
Avoidable volume, electrolyte, and metabolic complications of AKI
## Footnote
Early initiation may expose patients to unnecessary risks.
116
What are the modes of renal replacement therapy available for AKI?
Hemodialysis, continuous renal replacement therapy (CRRT), and peritoneal dialysis
## Footnote
Each has specific indications and methods of solute clearance.
117
What is the typical schedule for hemodialysis treatment?
3-4 hours per day, three to four times per week
## Footnote
It is the most common form of renal replacement therapy for AKI.
118
What is a significant complication of hemodialysis?
Hypotension
## Footnote
This can cause ischemic injury to recovering organs.
119
What is the advantage of continuous renal replacement therapy (CRRT)?
Treats hemodynamically unstable patients without rapid shifts in volume or electrolytes
## Footnote
CRRT can be performed via convective or diffusive clearance.
120
What is the primary difference between intermittent hemodialysis and CRRT?
Intermittent hemodialysis induces rapid shifts, while CRRT maintains stability
## Footnote
This is crucial for critically ill patients.
121
What is the prognosis for patients who develop AKI?
Increased risk of in-hospital and long-term mortality, longer length of stay, and increased costs
## Footnote
Survivors may develop chronic kidney disease (CKD).
122
How is the relationship between AKI and CKD characterized?
AKI is a risk factor for future development of CKD, and vice versa
## Footnote
Measurement of albuminuria post-AKI can predict kidney disease progression.
123
What is the KDIGO recommendation for AKI management?
Patients should be under nephrologist supervision for aggressive secondary prevention of kidney disease
## Footnote
This includes monitoring and managing risk factors.
124
What is acute kidney injury (AKI)?
Impairment of kidney filtration and excretory function over days to weeks, leading to retention of waste products
## Footnote
AKI is not a single disease but a heterogeneous group of conditions characterized by increased serum creatinine and reduced urine volume.
125
What percentage of acute-care hospital admissions is complicated by AKI?
5-7%
## Footnote
In ICU admissions, this percentage can rise up to 30%.
126
What has been the trend in the incidence of AKI in the United States since 1988?
The incidence has grown by more than fourfold
## Footnote
The yearly incidence is estimated at 500 per 100,000 population, which is higher than the yearly incidence of stroke.
127
What is the relationship between serum creatinine (SCr) increases and hospital mortality?
Increases as low as 0.3 mg/dL are associated with approximately a fourfold increase in hospital mortality
## Footnote
Higher changes in creatinine and longer duration of elevation correlate with greater morbidity and mortality risk.
128
What are common causes of community-acquired AKI?
* Volume depletion
* Heart failure
* Adverse effects of medications
* Urinary tract obstruction
* Malignancy
129
What are the three broad categories of AKI causes?
* Prerenal azotemia
* Intrinsic renal parenchymal disease
* Postrenal obstruction
130
What is prerenal azotemia?
A rise in SCr or BUN concentration due to inadequate renal plasma flow and intraglomerular hydrostatic pressure
## Footnote
It is the most common form of AKI and is rapidly reversible once blood flow is restored.
131
What clinical conditions are associated with prerenal azotemia?
* Hypovolemia
* Decreased cardiac output
* Medications interfering with renal autoregulation
132
What happens to glomerular filtration rate (GFR) during prerenal azotemia?
GFR can be maintained despite reduced renal blood flow through compensatory mechanisms
## Footnote
These mechanisms include angiotensin II-mediated vasoconstriction and myogenic reflexes.
133
What role do NSAIDs play in prerenal azotemia?
NSAIDs inhibit renal prostaglandin production, limiting renal afferent vasodilation
## Footnote
This increases the risk of developing prerenal azotemia.
134
What is intrinsic AKI commonly caused by?
* Sepsis
* Ischemia
* Nephrotoxins (endogenous and exogenous)
135
How does sepsis lead to AKI?
Sepsis can cause decreases in GFR even without overt hypotension, often requiring vasopressor support
## Footnote
Inflammation and mitochondrial dysfunction may also contribute to sepsis-induced AKI.
136
What is the significance of ischemia in AKI?
Ischemia can lead to renal tubular injury, particularly in the outer medulla, which is vulnerable to damage
## Footnote
The kidneys receive 20% of cardiac output despite their small mass.
137
What are common risk factors for postoperative AKI?
* Underlying chronic kidney disease (CKD)
* Older age
* Diabetes mellitus
* Congestive heart failure
* Emergency procedures
138
What is the pathophysiology of AKI following cardiac surgery?
It is multifactorial, including factors like ischemic injury from hypoperfusion and activation of inflammatory processes
## Footnote
Cardiopulmonary bypass can also contribute to AKI.
139
What is the prognosis of type 1 hepatorenal syndrome?
It has a particularly poor prognosis, persisting despite volume administration
## Footnote
Type 2 hepatorenal syndrome is less severe and characterized mainly by refractory ascites.
140
What physiological mechanisms help maintain GFR in prerenal azotemia?
* Afferent arteriole dilation via myogenic reflex
* Renal biosynthesis of vasodilator prostaglandins
* Tubuloglomerular feedback
141
True or False: AKI can occur without structural damage to the kidneys.
True
## Footnote
AKI is a clinical diagnosis and may occur with or without injury to kidney parenchyma.
142
What factors can impair the autoregulatory response of the kidneys?
* Atherosclerosis
* Long-standing hypertension
* Older age
143
Fill in the blank: AKI is often attributed to _____, but biopsy confirmation is often lacking.
acute tubular necrosis
144
What are the potential complications of AKI in the developing world?
* Envenomations
* Malaria
* Leptospirosis
* Crush injuries
145
What is the impact of AKI on long-term kidney health?
Increases the risk for chronic kidney disease (CKD) and dialysis-requiring end-stage kidney disease (ESKD)
146
What is the impact of longer duration of cardiopulmonary bypass on AKI?
It is a risk factor for AKI.
147
What mechanisms can cause AKI during cardiopulmonary bypass?
* Extracorporeal circuit activation of leukocytes and inflammatory processes
* Hemolysis with resultant pigment nephropathy
* Aortic injury with resultant atheroemboli
148
What is atheroembolic disease related to AKI?
It is due to cholesterol crystal embolization leading to occlusion of small arteries within the kidney.
149
What are the consequences of a foreign body reaction in atheroembolic disease?
Intimal proliferation, giant cell formation, and further narrowing of the vascular lumen.
150
What is the mortality rate among cardiovascular patients requiring renal replacement therapy?
40-70%.
151
What percentage of individuals with severe burns experience AKI?
25%.
152
What complications accompany severe burns and acute pancreatitis that may lead to AKI?
* Severe hypovolemia
* Increased neurohormonal activation
* Dysregulated inflammation
* Increased risk of sepsis and acute lung injury
153
What is abdominal compartment syndrome?
A condition where elevated intraabdominal pressures lead to renal vein compression and reduced GFR.
154
What are the microvascular causes of AKI?
* Thrombotic microangiopathies
* Scleroderma
* Atheroembolic disease
155
What is the gold standard for diagnosing renal artery stenosis?
Renal angiography.
156
What makes the kidney particularly susceptible to nephrotoxic agents?
High blood perfusion and concentration of filtered substances along the nephron.
157
What are common nephrotoxic agents associated with AKI?
* Iodinated contrast agents
* Antibiotics
* Chemotherapeutic agents
* Endogenous toxins
158
What is contrast nephropathy?
AKI caused by iodinated contrast agents, particularly in patients with CKD.
159
What characterizes the clinical course of contrast nephropathy?
Rise in SCr beginning 24-48 h post-exposure, peaking within 3-5 days, resolving within 1 week.
160
Which antibiotic is associated with tubular injury leading to AKI?
Vancomycin.
161
What is the effect of aminoglycosides on renal function?
They can cause tubular necrosis and nonoliguric AKI.
162
What is the mechanism of nephrotoxicity for amphotericin B?
It causes renal vasoconstriction and direct tubular toxicity.
163
What environmental toxins can cause AKI?
* Ethylene glycol
* Diethylene glycol
* Aristolochic acid
164
What endogenous compounds can lead to AKI?
* Myoglobin
* Hemoglobin
* Uric acid
* Myeloma light chains
165
What is the pathophysiology of AKI due to myoglobin release?
Intrarenal vasoconstriction and direct proximal tubular toxicity.
166
What are common causes of acute tubulointerstitial disease leading to AKI?
* Proton pump inhibitors
* NSAIDs
* Severe infections
* Infiltrative diseases
167
What is anticoagulant-related nephropathy?
AKI caused by excessive anticoagulation leading to glomerular hemorrhage.
168
What is the significance of early recognition of glomerulonephritis?
Timely treatment may reverse AKI and decrease long-term injury.
169
What defines postrenal AKI?
Acute blockage of urinary flow leading to increased retrograde hydrostatic pressure.
170
What can cause obstruction leading to postrenal AKI?
* Prostate disease
* Blood clots
* Calculi
* Urethral strictures
171
How is AKI defined by current standards?
Rise in SCr of at least 0.3 mg/dL within 48 h or reduction in urine output to <0.5 mL/kg/h for longer than 6 h.
172
What is the definition of AKI?
At least 50% higher than baseline within 1 week, or a reduction in urine output to <0.5 mL/kg per h for longer than 6 h.
173
What distinguishes AKI from CKD?
Recent baseline SCr concentration availability; clues from radiologic studies or laboratory tests.
174
What laboratory findings suggest CKD?
* Small, shrunken kidneys with cortical thinning on renal ultrasound
* Normocytic anemia in the absence of blood loss
* Secondary hyperparathyroidism with hyperphosphatemia and hypocalcemia
175
Why is it challenging to rule out AKI superimposed on CKD?
AKI is a frequent complication in patients with CKD.
176
What indicates a diagnosis of AKI?
Serial blood tests showing a continued substantial rise of SCr.
177
What clinical context should raise suspicion for prerenal azotemia?
Vomiting, diarrhea, glycosuria causing polyuria, use of diuretics, NSAIDs, ACE inhibitors, ARBs.
178
What physical signs are often present in prerenal azotemia?
* Orthostatic hypotension
* Tachycardia
* Reduced jugular venous pressure
* Decreased skin turgor
* Dry mucous membranes
179
What history suggests postrenal AKI?
Prostatic disease, nephrolithiasis, pelvic or paraaortic malignancy.
180
What symptoms may indicate acute ureteric obstruction?
Colicky flank pain radiating to the groin.
181
What is the significance of reviewing all medications in AKI evaluation?
Medications can be nephrotoxic and doses may need adjustment for reduced kidney function.
182
What are idiosyncratic reactions to medications in AKI?
Allergic interstitial nephritis, which may present with fever, arthralgias, and a pruritic erythematous rash.
183
What findings may indicate systemic vasculitis with glomerulonephritis in AKI?
Palpable purpura, pulmonary hemorrhage, or sinusitis.
184
What is the typical urine output in oliguria?
<400 mL/24 h.
185
What does preserved urine output indicate in AKI?
Less severe AKI; may be seen in nephrogenic diabetes insipidus or other conditions.
186
What urine color may suggest rhabdomyolysis or hemolysis?
Red or brown urine.
187
What does heavy proteinuria (>3.5 g/d) in AKI suggest?
Possible glomerulonephritis, vasculitis, or nephrotoxic effects on the glomerulus.
188
What urine sediment findings are characteristic of ATN due to ischemic injury?
* Pigmented 'muddy brown' granular casts
* Tubular epithelial cell casts
189
What does a low BUN to creatinine ratio suggest?
Prerenal azotemia, especially if >20:1.
190
What does a FeNa <1% indicate?
Avid tubular sodium reabsorption, suggesting prerenal azotemia.
191
What urine osmolality may indicate prerenal azotemia?
>500 mOsm/kg.
192
What imaging should be performed to evaluate postrenal AKI?
Renal ultrasound or CT scan.
193
What findings on imaging suggest obstruction?
* Dilation of the collecting system
* Hydroureteronephrosis
194
What does the presence of oxalate crystals in urine indicate?
Possible ethylene glycol toxicity.
195
What laboratory findings are associated with thrombotic microangiopathy?
* Thrombocytopenia
* Schistocytes on peripheral blood smear
* Elevated lactate dehydrogenase
* Low haptoglobin
196
What does hyperphosphatemia with hypocalcemia suggest?
Possible rhabdomyolysis or tumor lysis syndrome.
197
What is the significance of elevated serum creatine kinase in AKI?
Indicates rhabdomyolysis.
198
What does an increased anion gap in AKI indicate?
Retention of anions such as phosphate, hippurate, sulfate, and urate.
199
What does a low anion gap suggest?
Possible multiple myeloma due to unmeasured cationic proteins.
200
What role does renal ultrasound play in AKI evaluation?
Helps to investigate obstruction and assess kidney size and echogenicity.
201
What does an enlarged kidney in AKI suggest?
Possible acute interstitial nephritis or infiltrative diseases.
202
What condition is indicated by smaller kidneys in CKD?
CKD usually presents with smaller kidneys unless there are specific conditions such as diabetic nephropathy.
203
What does enlarged kidneys in a patient with AKI suggest?
Possibility of acute interstitial nephritis or infiltrative diseases.
204
What imaging technique should be avoided in severe AKI due to risks?
MRI with gadolinium-based contrast agents (GBCAs) should be avoided.
205
What is the main purpose of a kidney biopsy in AKI?
To provide definitive diagnostic and prognostic information about acute kidney disease.
206
What are BUN and creatinine considered in the context of kidney function?
Functional biomarkers of glomerular filtration.
207
What urine output after furosemide administration may indicate a higher risk of severe AKI?
Urine output <200 mL over 2 h after intravenous furosemide.
208
What does the presence of renal tubular epithelial cells in urine sediment indicate?
Associated with severity and worsening of AKI.
209
What is KIM-1?
A type 1 transmembrane protein expressed in proximal tubular cells injured by nephrotoxins.
210
What does NGAL stand for and where is it expressed?
Neutrophil gelatinase associated lipocalin, expressed in human neutrophils.
211
What does suPAR predict in AKI patients?
The subsequent development of AKI.
212
What combination of biomarkers did the FDA approve for predicting AKI risk?
Insulin-like growth factor binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinase-2 (TIMP-2).
213
What is a hallmark of AKI related to nitrogenous waste products?
Buildup of nitrogenous waste products as indicated by elevated BUN concentration.
214
What complication can arise from expansion of extracellular fluid volume in AKI?
Weight gain, dependent edema, increased jugular venous pressure, and pulmonary edema.
215
What can excessive administration of hypotonic solutions lead to in AKI patients?
Hypoosmolality and hyponatremia.
216
What is a common complication of AKI related to potassium levels?
Hyperkalemia.
217
What type of acidosis is common in AKI?
Metabolic acidosis, usually with an elevated anion gap.
218
What can AKI lead to in terms of phosphate and calcium levels?
Hyperphosphatemia and hypocalcemia.
219
What hematologic complications can arise from AKI?
Anemia and bleeding.
220
What are common cardiac complications associated with AKI?
Arrhythmias, pericarditis, and pericardial effusion.
221
What is a major complication of AKI related to nutrition?
Malnutrition.
222
What is critical in the management of AKI?
Optimization of hemodynamics, correction of fluid and electrolyte imbalances.
223
What is the definitive treatment for hepatorenal syndrome?
Orthotopic liver transplantation.
224
What is required for the treatment of AKI due to rhabdomyolysis?
Early and aggressive volume repletion.
225
What should be done to relieve postrenal AKI?
Prompt recognition and relief of urinary tract obstruction.
226
What is a common complication of AKI in terms of fluid management?
Hypervolemia in oliguric AKI.
227
What is the initial treatment approach for urethral strictures or functional bladder impairment?
Transurethral or suprapubic bladder catheterization
## Footnote
This may be sufficient initially before considering further interventions.
228
How is ureteric obstruction typically treated?
Percutaneous nephrostomy tube placement or ureteral stent placement
## Footnote
This is followed by appropriate diuresis for several days.
229
What is a potential complication of severe polyuria in AKI?
Tubular dysfunction requiring intravenous fluids and electrolytes
## Footnote
This may persist even after relief of obstruction.
230
What is a life-threatening condition associated with hypervolemia in oliguric or anuric AKI?
Acute pulmonary edema
## Footnote
This is particularly concerning in patients with coexisting pulmonary disease.
231
What management strategies are recommended for fluid and sodium in AKI?
Fluid and sodium restriction, and diuretics to increase urinary flow rate
## Footnote
Diuretics may help avoid the need for dialysis.
232
What is the role of furosemide in severe volume overload?
Administered as a bolus (200 mg) followed by an intravenous drip (10-40 mg/h)
## Footnote
May be given with or without a thiazide diuretic.
233
What should be monitored when treating metabolic acidosis in AKI?
pH and serum bicarbonate levels
## Footnote
Treatment is generally reserved for severe cases.
234
What dietary recommendations are given for patients with AKI?
Total energy intake of 20-30 kcal/kg per day and protein intake varies based on AKI severity
## Footnote
Recommendations include specific protein intake ranges based on dialysis needs.
235
What is the typical protein intake recommendation for patients on dialysis?
1.0-1.5 g/kg per day
## Footnote
Up to 1.7 g/kg per day if hypercatabolic and receiving continuous renal replacement therapy.
236
What factors contribute to anemia in AKI?
Multifactorial causes including bone marrow resistance and uremic bleeding
## Footnote
Erythropoiesis-stimulating agents may not be effective.
237
When is dialysis indicated in AKI?
When medical management fails to control volume overload, hyperkalemia, or acidosis
## Footnote
Also indicated in severe complications of uremia.
238
What is a risk associated with late initiation of dialysis?
Avoidable volume, electrolyte, and metabolic complications of AKI
## Footnote
Early initiation may expose patients to unnecessary risks.
239
What are the modes of renal replacement therapy available for AKI?
Hemodialysis, continuous renal replacement therapy (CRRT), and peritoneal dialysis
## Footnote
Each has specific indications and methods of solute clearance.
240
What is the typical schedule for hemodialysis treatment?
3-4 hours per day, three to four times per week
## Footnote
It is the most common form of renal replacement therapy for AKI.
241
What is a significant complication of hemodialysis?
Hypotension
## Footnote
This can cause ischemic injury to recovering organs.
242
What is the advantage of continuous renal replacement therapy (CRRT)?
Treats hemodynamically unstable patients without rapid shifts in volume or electrolytes
## Footnote
CRRT can be performed via convective or diffusive clearance.
243
What is the primary difference between intermittent hemodialysis and CRRT?
Intermittent hemodialysis induces rapid shifts, while CRRT maintains stability
## Footnote
This is crucial for critically ill patients.
244
What is the prognosis for patients who develop AKI?
Increased risk of in-hospital and long-term mortality, longer length of stay, and increased costs
## Footnote
Survivors may develop chronic kidney disease (CKD).
245
How is the relationship between AKI and CKD characterized?
AKI is a risk factor for future development of CKD, and vice versa
## Footnote
Measurement of albuminuria post-AKI can predict kidney disease progression.
246
What is the KDIGO recommendation for AKI management?
Patients should be under nephrologist supervision for aggressive secondary prevention of kidney disease
## Footnote
This includes monitoring and managing risk factors.
