Part 13 - Nephrology Flashcards
1
Q
True or false: AKI is a clinical diagnosis
A
True
p. 1799
2
Q
What is the most common form of AKI?
A
Prerenal
p. 1799
3
Q
What type of AKI is due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal GFR?
A
Prerenal
p. 1799)
4
Q
What are the most common conditions/causes associated with prerenal azotemia?
A
Hypovolemia
Decreased cardiac output
Medications (NSAIDS, inhibitors of angiotensin II)
(p. 1800)
5
Q
True or false: prerenal azotemia involves no parenchymal damage to the kidney
A
True
p. 1800
6
Q
True or false: Prerenal azotemia is rapidly reversible once hemodynamics are restored
A
True
p. 1800
7
Q
Renal blood flow accounts for how many percent of the cardiac output?
A
20%
p. 1800
8
Q
Homeostatic responses occur in response to prerenal azotemia. Mediators of this response include?
A
Angiotensin II
Norepinephrine
Vasopressin
(p. 1800)
9
Q
What is the myogenic reflex?
A
Dilation of the afferent arteriole in the setting of low perfusion pressure to maintain glomerular perfusion
(p. 1800)
10
Q
What are the compensatory mechanisms involved in prerenal azotemia?
A
1) Homeostatic responses
2) Myogenic reflex
3) Tubuloglomerular feedback
(p. 1800)
11
Q
Vasodilators that increase in response to low renal perfusion pressure (in prerenal azotemia)
A
Prostaglandins (prostacyclin, prostaglandin E2)
Kallikrein and kinins
Nitric oxide
(p. 1800)
12
Q
What is the tubuloglomerular feedback?
A
Decreases in solute delivery to the macula dense elicit dilation of the afferent arteriole to maintain glomerular perfusion
(p. 1800)
13
Q
Renal autoregulation usually fails once the systolic blood pressure falls below ____.
A
80 mmHg
p. 1800
14
Q
What is macula densa?
A
Specialized cells within the distal tubule
p. 1800
15
Q
What do you call the dilation of afferent arteriole in response to decreased solute delivery to the macula densa?
A
Tubuloglomerular feedback
p. 1800
16
Q
Effect of NSAIDs to the kidney
A
Limits renal prostaglandin production –> limit renal afferent vasodilation
(p. 1800)
17
Q
Effect of ACE-I and ARBs to the kidney
A
Limit renal efferent vasocontriction
p. 1800
18
Q
Which type of hepatorenal syndrome has the poorer prognosis?
A
Hepatorenal syndrome Type 1
p. 1800
19
Q
Type of hepatorenal syndrome wherein AKI is seen without an alternate cause persisting despite volume administrate and withholding of diuretics
A
Hepatorenal syndrome Type 1
p. 1800
20
Q
Type of hepatorenal syndrome which is characterized mainly by refractory ascites
A
Hepatorenal syndrome Type 2
p. 1800
21
Q
True or false: Decreases in GFR with sepsis can occur even in the absence of overt hypotension
A
True
p. 1801
22
Q
Segment of the proximal tubule that is metabolically very active
A
S3 segment
p. 1802
23
Q
What procedures are most commonly associated with AKI?
A
Cardiac surgery with cardiopulmonary bypass
Vascular procedures with aortic cross clamping
Intraperitoneal procedures
(p. 1802)
24
Q
What are common risk factors for postoperative AKI?
A
Underlying CKD Older age Diabetes Mellitus Congestive heart failure Emergency procedures Longer duration of cardiopulmonary bypass (p. 1802)
25
How does cardiopulmonary bypass cause AKI (mechanisms)?
1) Extracorporeal circuit activation of leukocytes and inflammatory processes
2) Hemolysis with resultant pigment nephropathy
3) Aortic injury with resultant atheroemboli
(p. 1803)
26
What is the abdominal compartment syndrome?
Markedly elevated intraabdominal pressures (usually > 20 mmHg) leading to renal vein compression and reduced GFR
(p. 1803)
27
What do you call markedly elevated intraabdominal pressures (usually above 20 mmHg) that lead to renal vein compression and reduced GFR?
Abdominal compartment syndrome
| p. 1803
28
Microvascular causes of AKI
Thrombotic microangiopathies (APAS, radiation nephritis, malignant nephrosclerosis, TTP-HUS)
Scleroderma
Atheroembolic disease
(p. 1803)
29
Large vessel diseases associated with AKI
```
Renal artery dissection
Thromboembolism
Thrombosis
Renal vein compression or thrombosis
(p. 1803)
```
30
Risk factors for nephrotoxicity
```
Older age
CKD
Prerenal azotemia
Hypoalbuminemia
(p. 1803)
```
31
In contrast-induced nephropathy, when does creatinine begin to rise?
24-48 hours after exposure
| p. 1803
32
In contrast-induced nephropathy, creatinine peaks within ____ day/s.
3-5 days
| p. 1803
33
Contrast-induced nephropathy resolves within how many days?
1 week
| p. 1803
34
Mechanisms involved in contrast-induced nephropathy
1) Hypoxia in the renal outer medulla due to perturbations in renal microcirculation and occlusion of small vessels
2) cytotoxic damage to the tubules directly or via the generation of oxygen free radicals
3) transient tubule obstruction with precipitated contrast material
(p. 1803)
35
AKI secondary to aminoglycosides typically manifest after how many days of therapy?
5-7 days
| p. 1803
36
True or false: AKI secondary to aminoglycosides can present even after the drug has been discontinued.
True
| p. 1803
37
What electrolyte abnormality is a common finding in AKI secondary to aminoglycoside use?
Hypomagnesemia
| p. 1803
38
True or false: Nephrotoxicity from Amphotericin B is dose and duration dependent.
True
| p. 1803
39
Metabolic/electrolyte abnormalities found in AKI secondary to Amphotericin B use
Hypomagnesemia
Hypocalcemia
Non-gap metabolic acidosis
(p. 1803)
40
AKI secondary to acute interstitial nephritis can occur as a consequence of exposure to what medications?
```
Penicillins
Cephalosporins
Quinolones
Sulfonamides
Rifampin
(p. 1804)
```
41
What are the renal adverse effects of Ifosfamide?
```
Hemorrhagic cystitis
Type II RTA (Fanconi's syndrome)
Hypokalemia
Modest decline in GFR
(p. 1804)
```
42
What is the renal adverse effect of bevacizumab?
Proteinuria
Hypertension via injury to the glomerular microvasculature (thrombotic microangiopathy)
(p. 1804)
43
Cause of "Chinese herb nephropathy" and "Balkan nephropathy"
Aristolochic acid
| p. 1804
44
What is the most common protein in urine which is produced in the thick ascending limb of the loop of Henle?
Uromodulin
| p. 1804
45
What serum level of uric acid leads to precipitation of uric acid in the renal tubules and AKI?
>15 mg/dL
| p. 1804
46
Definition of AKI (according to Harrison's)
1) Rise from the baseline of at least 0.3 mg/dL within 48 hours OR
2) At least 50% higher than baseline within 1 week OR
3) Reduction in urine output to less than 0.5 ml/kg per hour for longer than 6 hours
(p. 1805)
47
Characteristic urine sediment findings in AKI secondary to ATN
1) Pigmented "muddy brown" granular casts
2) Tubular epithelial cell casts
(p. 1805)
48
Finding of oxalate crystals in AKI should prompt an evaluation for _____ toxicity.
Ethylene glycol
| p. 1805
49
True or false: Anemia is common in AKI.
True
| p. 1807
50
What is the fractional excretion of sodium (FeNa) in prerenal azotemia?
<1%
| Pp. 1806-1807
51
What is the fractional excretion of sodium (FeNa) in ischemic AKI?
Frequently above 1%
| p. 1807
52
Why is fractional excretion of sodium (FeNa) in ischemic AKI frequently above 1%?
Because of tubular injury and resultant inability to reabsorb sodium
(p. 1807)
53
Ischemia and nephrotoxin-associated AKI that can present with FeNa < 1%
Sepsis (often early in the course)
Rhabdomyolysis
Contrast nephropathy
(p. 1807)
54
Causes of RBC or RBC casts in urine
```
Glomerulonephritis
Vasculitis
Malignant hypertension
Thrombotic microangiopathy
(p. 1807, Figure 334-6)
```
55
Causes of WBCs or WBC casts in urine
```
Interstitial nephritis
Glomerulonephritis
Pyelonephritis
Allograft rejection
Malignant infiltration of the kidney
(p. 1807, Figure 334-6)
```
56
Causes of renal tubular epithelial cells (RTE), RTE casts, or pigmented casts in the urine
```
Acute tubular necrosis
Tubulointerstitial nephritis
Acute cellular allograft rejection
Myoglobinuria
Hemoglobinuria
(p. 1807, Figure 334-6)
```
57
Causes of granular casts in the urine
```
Acute tubular necrosis
Glomerulonephritis
Vasculitis
Tubulointerstitial nephritis
(p. 1807, Figure 334-6)
```
58
Causes of eosinophiluria
```
Allergic interstitial nephritis
Atheroembolic disease
Pyelonephritis
Cystitis
Glomerulonephritis
(p. 1807, Figure 334-6)
```
59
Causes of crystalluria
Acute uric acid nephropathy
Calcium oxalate (ethylene glycol intoxication)
Drugs or toxins (acyclovir, indinavir, sulfadiazine, amoxicillin)
(p. 1807, Figure 334-6)
60
True or false: Enlarged kidneys in a patient with AKI suggests the possibility of acute interstitial nephritis
True
| p. 1808
61
Biomarker for AKI that is a type 1 transmembrane protein abundantly expressed in proximal tubular cells injured by ischemia or nephrotoxins
Kidney injury molecule-1 (KIM-1)
| p. 1808
62
Biomarker for AKI with the role of conferring phagocytic properties to tubular cells, enabling them to clear debris from tubular lumen after injury
Kidney injury molecule-1 (KIM-1)
| p. 1808
63
Biomarker for AKI which is also known as lipocalin-2 or siderocalin
Neutrophil gelatinase associatied lipocalin (NGAL)
| p. 1808
64
Biomarker for AKI which can bind to iron siderophore complexes and may have tissue-protective effects in the proximal tubule
Neutrophil gelatinase associated lipocalin (NGAL)
| p. 1808
65
Biomarker for AKI which can be detected in the plasma and urine within 2 hours of cardiopulmonary bypass-associated AKI
Neutrophil gelatinase associated lipocalin (NGAL)
| p. 1808
66
Biomarker for AKI that may mediate ischemic proximal tubular injury and L-type fatty acid binding protein
Interleukin-18
| p. 1808)
67
Fluid solution that is contraindicated in AKI secondary to prerenal azotemia
Hydroxyethyl starch solutions
| p. 1809
68
True or false: Albumin may prevent AKI in those treated with antibiotics for spontaneous bacterial peritonitis
True
| p. 1810
69
Definitive treatment of the hepatorenal syndrome
Orthotopic liver transplantation
| p. 1810
70
Treatment for AKI due to scleroderma (scleroderma renal crisis)
ACE-inhibitors
| p. 1810
71
Treatment for idiopathic TTP-HUS
```
Plasma exchange
(p. 1810)
```
72
Initial fluid resuscitation requirement for rhabdomyolysis
10 liters of fluid per day
| p. 1810
73
True or false: In decompensated heart failure, stepped diuretic therapy is superior to ultrafiltration in preserving renal function
True
| p. 1810
74
According to KDIGO guidelines, patients with AKI should achieve a total energy intake of ____.
20-30 kcal/kg/day
| p. 1810
75
According to KDIGO guidelines for patients with AKI, what is the protein intake requirement per day in non-catabolic AKI without the need for dialysis?
0. 8-1 g/kg/day
| p. 1810
76
According to KDIGO guidelines for patients with AKI, what is the protein intake requirement per day in patients on dialysis?
1 - 1.5 g/kg/day
| p. 1810
77
According to KDIGO guidelines for patients with AKI, what is the protein intake requirement per day if hypercatabolic and receiving continuous renal replacement therapy (CRRT)?
Up to a maximum of 1.7 g/kg/day
| p. 1810
78
True or false: Anemia seen in AKI is improved by erythropoiesis-stimulating agents
False
| p. 1810
79
Why is erythropoiesis-stimulating agents not helpful for anemia in AKI patients?
1) Delayed onset of action
2) Presence of bone marrow resistance in critically ill patients
(p. 1810)
80
Uremic bleeding may respond to what medications?
Desmopressin or estrogens
| p. 1810
81
Risk factors for CKD
1) Small for gestational age birth weight
2) Childhood obesity
3) Hypertension
4) Diabetes mellitus
5) Autoimmune disease
6) Advanced age
7) African ancestry
8) Family history of kidney disease
9) Previous episode of AKI
10) Presence of proteinuria, abnormal urinary sediment, or structural abnormalities of the urinary tract
(p. 1811)
82
Allelic versions of what gene contribute to the several-fold higher frequency of certain common etiologies of non-diabetic CKD?
APOL1
| p. 1811
83
True or false: Mean GFR is lower in women than in men
True
| p. 1812
84
What is the normal annual mean decline in GFR with age?
~1 ml/min per year per 1.73 m2
| p. 1812
85
True or false: Microalbuminuria is a good screening test for early detection of renal disease
True
| p. 1813
86
True or false: Albuminuria is a major risk factor for cardiovascular disease
True
| p. 1813
87
Leading cause of CKD
Diabetic nephropathy
| p. 1813
88
What is the pathophysiology of the uremic syndrome?
1) accumulation of toxins
2) loss of other kidney functions
3) progressive systemic inflammation and its vascular and nutritional consequences
(p. 1814)
89
True or false: Hyponatremia is not commonly seen in CKD patients
True
| p. 1814
90
What is the mechanism of action of metolazone?
Inhibits the sodium chloride co-transporter of the distal convoluted tubule
(p. 1814)
91
How does metabolic acidosis occur in CKD?
Patients produce less ammonia thus cannot excrete the normal quantity of protons
(p. 1814)
92
Acid-base abnormality found in early CKD (specific)
Non-anion gap metabolic acidosis
| p. 1814
93
Acid-base abnormality seen in late stages of CKD (specific)
Anion-gap metabolic acidosis
| p. 1814
94
Alkali supplementation for CKD patients is recommended when the serum bicarbonate concentration falls below what level?
20-23 mmol/L
| p. 1814
95
What is the classic lesion of secondary hyperparathyroidism?
Osteitis fibrosis cystica
| p. 1815
96
Bone changes in CKD start to occur when the GFR falls below what level?
60 ml/min
| p. 1815
97
In CKD, how does FGF-23 defend normal serum phosphorus levels?
1) increased renal phosphate excretion
2) stimulation of PTH --> increases renal phosphate excretion
3) suppression of the formation of 1,25(OF)2D3 --> diminished phosphorus absorption from the GI tract
(p. 1815)
98
True or false: high levels of FGF-23 is an independent risk factor for LVH and mortality in CKD, dialysis, and renal transplant patients.
True
| p. 1815
99
Osteitis fibrosa cystica is also known as what?
Brown tumor
| p. 1815
100
What disorder seen in CKD is associated with high bone turnover with increased PTH levels?
Osteitis fibrosa cystica
| p. 1815
101
What disorder/s seen in CKD is associated with low bone turnover with low or normal PTH levels?
Adynamic bone disease
Osteomalacia
(p. 1815)
102
What is "tumoral calcinosis"?
When calcium precipitate in the soft tissues into large concretions
(p. 1815)
103
True or false: There is a strong association between hyperphosphatemia and increased cardiovascular mortality rate in patients with CKD
True
| p. 1815
104
What condition seen almost exclusively in patients with advanced CKD is heralded by livedo reticularis and then advance to patches of ischemic necrosis?
Calciphylaxis
| p. 1816
105
True or false: Warfarin treatment is a risk factor for calciphylaxis
True
| p. 1816
106
What is the optimal management of secondary hyperparathyroidism and osteitis fibrosa cystica?
Prevention
| p. 1816
107
According to KDOQI, the recommended target PTH level is ____.
Between 150 and 300 pg/ml
| p. 1816
108
What is the leading cause of morbidity and mortality in patients at every stage of CKD?
Cardiovascular disease
| p. 1816
109
What are the CKD-related risk factors for ischemic vascular disease?
```
Anemia
Hyperphosphatemia
Hyperparathyroidism
Increased FGF-23
Sleep apnea
Generalized inflammation
(p. 1816)
```
110
True or false: Cardiac troponin levels are frequently elevated in CKD without evidence of acute ischemia
True
| p. 1817
111
True or false: Consistently elevated levels of cardiac troponin is an independent prognostic factor for adverse cardiovascular events in CKD patients
True
| p. 1817
112
True or false: The absence of hypertension in CKD patients may signify poor left ventricular function
True
| p. 1817
113
True or false: In dialysis patients, low blood pressure has worse prognosis than those with high blood pressure
True
| p. 1817
114
Goal BP in CKD patients with diabetes or proteinuria > 1 g per 24 hours (according to Harrison's)
130/80
| p. 1817
115
Classic ECG abnormalities seen in pericarditis
PR interval depression
Diffuse ST segment elevation
(p. 1817)
116
Anemia is universal at what stage of CKD?
Stage 4
| p. 1818
117
What is the primary cause of anemia in CKD patients?
Insufficient production of EPO
| p. 1818
118
True or false: The susceptibility to bacterial infections is increased in CKD patients on IV iron therapy
True
| p. 1818
119
What is the target hemoglobin concentration in CKD patients (according to Harrison's)?
100-115 g/L
| p. 1818
120
Subtle clinical manifestations of uremic neuromuscular disease usually become evident at what stage of CKD?
Stage 3
| p. 1818
121
Peripheral neuropathy usually become clinically evident by what stage of CKD?
Stage 4
| p. 1819
122
What is the pattern of peripheral neuropathy in CKD?
Sensory > Motor
Lower extremities > Upper extremities
Distal > Proximal
(p. 1819)
123
What is the "restless leg syndrome" seen in CKD?
Ill-defined sensations/debilitating discomfort in the legs and feet relieved by frequent leg movement
(p. 1819)
124
True or false: In CKD patients, evidence of peripheral neuropathy without another cause (ex. Diabetes mellitus) is an indication for starting renal replacement therapy
True
| p. 1819
125
Assessment of protein-energy malnutrition should begin by what stage of CKD?
Stage 3
| p. 1819
126
Imaging/diagnostic test that is widely used to estimate lean body mass versus extracellular fluid volume (ECFV)
Dual-energy X-ray absorptiometry
| p. 1819
127
Pregnancy is associated with a high rate of spontaneous abortion when the GFR has declined to what level?
~40 ml/min
| p. 1819
128
True or false: Pregnancy may hasten the progression of CKD
True
| p. 1819
129
What is nephrogenic fibrosing dermopathy?
Progressive subcutaneous induration (especially on the arms and legs) seen in CKD patients who have been exposed to gadolinium contrast
(p. 1819)
130
What is the skin condition seen in CKD patients who have been exposed to gadolinium contrast?
Nephrogenic fibrosing dermopathy
| p. 1819
131
True or false: Liver disease is a risk factor for nephrogenic fibrosing dermopathy
True
| p. 1819
132
What is the most useful imaging study for CKD?
Renal ultrasound
| p. 1820
133
Etiologies of CKD which may present as normal to large-sized kidneys
```
Diabetes mellitus
Amyloidosis
HIV nephropathy
Polycystic kidney disease
(p. 1820)
```
134
What diagnostic/imaging test can be done if reflux nephropathy is suspected in CKD patients?
Voiding cystogram
| p. 1820
135
What are contraindications to renal biopsy?
1) Bilaterally small kidneys
2) Uncontrolled hypertension
3) Active UTI
4) Bleeding diathesis
5) Severe obesity
(p. 1820)
136
Why is renal biopsy contraindicated in patients with bilaterally small kidneys?
1) Technically difficult and has greater likelihood of causing bleeding
2) So much scarring that the underlying disease may not be apparent
3) Window of opportunity to render disease-specific therapy has passed
(p. 1820)
137
The renoprotective effect of antihypertensive medications is gauged through what laboratory finding?
Proteinuria
| p. 1820
138
What is the effect of ACE inhibitors and ARBs in the renal vasculature?
Inhibits the angiotensin-induced vasoconstriction of the efferent arterioles
(p. 1821)
139
True or false: ACE inhibitors and ARBs are effective in slowing the progression of renal failure in patients with advanced stages of BOTH diabetic and nondiabetic CKD
True
| p. 1821
140
Which calcium channel blockers exhibit superior anti-proteinuric and renoprotective effects?
Diltiazem
Verapamil
(p. 1821)
