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PSBIM 2023 Nephro > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

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1
Q

Definition of AKi

A

the impairment of kidney filtration and excretory function over days to weeks, resulting in the retention of nitrogenous waste products normally cleared by the kidneys

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2
Q

Common causes of community-acquired AKI

A

Volume depletion
Heart failure
Adverse effects of medications
Obstruction of Urinary Tract
Malignancy

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3
Q

Common causes of hospital-acquired AKI

A

Sepsis
Major surgical procedures
Critical Illness involving heart or liver failure
Nephrotoxic medical administration

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4
Q

Classification of major causes of AKI

A
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5
Q

Most common form of AKI

A

Pre-renal azotemia

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6
Q

Decreased perfusion pressure in the presence of NSAIDS

A

loss of vasodilatory prostaglandins increases afferent resistance

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7
Q

Decreased perfusion pressure in the presence of ACE-i or ARB

A

loss of angiotensin II action reduces efferent resistance

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8
Q

Threshold of systolic blood pressure when renal autoregulation falls

A

80 mmHG

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9
Q

Type 1 Hepatorenal Syndrome

A

defined as >two-fold increase in SCr to >2.5 mg/dL within 2 weeks without alternate cause, persists despite volume administration and withholding of diuretics

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10
Q

Type 2 Hepatorenal Syndrome

A

less severe from characterized mainly by refractory ascites

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11
Q

Most common causes of intrinsic AKI

A

Sepsis
ischemia
Nephrotoxins

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12
Q

At risk to develop ischemia-associated AKI

A

limited renal reserve (older age),
Coexisting insults:
-Sepsis
-Vasoactive or nephrotoxic drugs
-Rhabdomyolysis
-Systemic inflammatory states associated with burns and pancreatitis

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13
Q

Procedures most commonly associated with AKI

A

Cardiac surgery with cardiopulmonary bypass,
Vascular procedures with aortic cross clamping,
Intraperitoneal procedures

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14
Q

Common risk factors for postoperative AKI

A

Underlying CKD
Older age
Diabetes Mellitus
Congestive heart failure
Emergency procedures

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15
Q

Risk factors for Nephrotoxin associated AKI

A

Older age
CKD
Pre renal azotemia
Hypoalbuminemia (in some)

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16
Q

Most common clinical course of contrast nephropathy

A

rise in SCr beginning 24-48h following exposure, peaking within 3-5 days, and resolving within 1 week

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17
Q

Most common findings in CI -AKI

A

low fractional excretion of sodium (FeNa) and relatively benign urinary sediment without features of tubular necrosis

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18
Q

Clinical features of amphotericin B nephrotoxicity

A

Polyuria
Hypomagnesemia
Hypocalcemia
Nongap metabolic acidosis

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19
Q

Chemotherapeutic drugs that accumulates in the proximal tubular cells and cause necrosis and apoptosis

A

Cisplatin and carboplatin

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20
Q

Ifosfamide nephrotoxicity

A

Cause hemorrhagic cystitis and tubular toxicity manifested as type II renal tubular acidosis (Fanconi’ syndrome), polyuria, hypokalemia, and a modest decline in GFR

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21
Q

Chemotherapeutic drugs that cause thrombotic microangiopathy

A

Bevacizumab
Mitomycin C
Gemcitabine

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22
Q

Tumor lysis syndrome

A

Hyperuricemia
Hyperkalemia
Hyperphosphatemia
Hypocalemia

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23
Q

Occurs when the normally unidirectional flow of urine is acutely blocked either partially or totally, leading to increased retrograde hydrostatic pressure and interference with glomerular filtration

A

Post-renal AKI

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24
Q

Common cause of postrenal AKI which impacts both kidneys

A

Bladder neck obstruction

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25
Definition of AKI
-elevation in the SCr concentration or reduction in urine output -a rise from baseline of at least 0.3 mg/dL within 48h or 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 6h
26
Key differences from CKD
Clues suggestive of CKD: 1. Radiologic studies -small shrunken kidneys with cortical thinning on renal ultrasound -evidence of renal osteodystrophy 2. Laboratory findings -normocytic anemia in the absence of blood loss -secondary hyperparathyroidism with hyperphosphatemia and hypocalcemia
27
Clinical and laboratory features of prerenal azotemia
28
Clinical and laboratory features of sepsis-associated AKI
29
Clinical and laboratory features of ischemia-associated AKI
30
Clinical and laboratory features of endogenous nephrotoxin-associated AKI
31
Clinical features of exogenous nephrotoxin associated AKI
32
Clinical features of other causes of intrinsic AKI
33
Urinary sediments in AKI
34
Definition of Oliguria
defined as <400 ml/24h
35
AKI conditions that may present with complete anuria
Complete urinary tract obstruction, Renal artery occlusion, Overwhelming septic shock, Severe ischemia, Severe GN or vasculitis
36
AKI conditions that may present with preserved urine output
Nephrogenic DI (longstanding urinary tract obstruction), Tubulointerstitial disease, Nephrotoxicity from cisplatin or aminoglycosides, etc/
37
Characteristic urine sediment of AKI from ATN (sepsis, ischemic injury, or certain nephrotoxins)
pigmented "muddy brown" granular casts and tubular epithelial cells
38
Causes of disproportionate BUN elevation compared to creatinine
Prerenal azotemia UGIB Increased tissue catabolism Glucocorticoid use
39
the fraction of filtered sodium load that is reabsorbed by the tubules, and is a measure of both the kidney's ability to reabsorb sodium as well as endogenously and exogenously administered factors that affect tubular reabsorption
FeNa
40
Diagnostic and therapeutic in prerenal azotemia
Response of urine output to crystalloid or colloid fluid administration
41
Conditions with urinary tract obstruction that can present without radiologic abnormalities
Volume depletion, Retroperitoneal fibrosis, Encasement with tumor, Early in the course of obstruction
42
CKD conditions with normal kidney size on radiologic evaluation
Diabetic nephropathy, HIV-associated nephropathy, Infiltrative disease
43
AKI conditions with enlarged kidneys
Acute interstitial nephritis Infiltrative diseases
44
A rare but serious complication seen most commonly in patients with ESRD and severe AKI undergoing MRI with gadolinium based-contrast agents
Nephrogenic system fibrosis
45
Provide definitive and prognostic information about AKI and CKD
Kidney biopsy
46
Renal failure indices
BUN Crea FeNa Urine osmolality
47
Can be used as a prognostic test for Oliguric AKI
urinary flow rate in response to bolus IV furosemide 1.0-1.5 mg/kg UO <200 ml over 2h post furosemide ->higher risk for progression to more severe AKI and the need for RRT
48
a type 1 transmembrane protein that is abundantly expressed in proximal tubular cells injured by ischemia or nephrotoxins such as cisplatin
Kidney injury molecule-1 (KIM-1)
49
a novel bioimarker that is highly upregulated after inflammation and kidney injury and can be detected in the plasma and urine within 2h or cardiopulmonary bypass-associated AKI
Neutrophil gelatinase associated lipocalin (NGAL) aka Lipocalin-2 or siderocalin
50
Predictive biomarkers for higher risk of the development of moderate to severe AKI in critically ill patients
Insulin-like growth factor binding protein 7 (IGFBP7), Tissue inhibitor of metalloproteinase 2 (TIMP-2)
51
Hallmark of AKI
Build of nitrogenous waste products , manifested as an elevated BUN concentration
52
Polyuric phase of recovery from AKI
may be due to an osmotic diuresis from retained urea and other waste products as well as delayed recovery of tubular reabsorptive functions
53
Fluid contraindicated in AKI
Hydroxyethyl starch solutions
54
Management of AKI - general principles
55
Definitive treatment of hepatorenal syndrome
Orthotopic liver transplantation
56
Bridge therapies that have shown promise in HRS
Terlipressin (a vasopressin analog), Combination tx with octreotide (A somatostatin analog), Midodrine (an a1 adrenergic agonist), and norepinephrine in combination with IV albumin (25-50 g, max 100 g/d)
57
Treatment for scleroderma renal criis
ACE inhibitors
58
Treatment for idiopathic TTP-HUS
plasma exchange
59
Treatment for rhabdomyolysis
Early and aggressive volume repletion , may initially require 10L of fluid per day - alkaline fluids may be beneficial
60
Management in severe cases of volume overload
Furosemide may be given as a bolus (200 mg) followed by an intravenous drip(10-40 mg/h), with or without a thiazide diuretic
61
General threshold of treatment of metabolic acidosis
Severe metabolic acidosis: pH< 7.20 serum hco3 <15 mmol/L
62
Total energy intake of patients with AKI
20-30 kcal/kg per day
63
Protein intake of noncatabolic AKI without the need for dialysis
0.8-1.0 g/kg/day
64
Protein intake of patients with AKI on dialysis
1.0-1.5 g/kg/day
65
Protein intake of patients with AKI with hypercatabolic state receiving continuous renal replacement therapy
1.7 g/kg/day
66
Indications for dialysis in AKI
When medical management fail to control volume overload, hyperkalemia, or acidosis; in some toxic ingestions; and when there are severe complications of uremia (asterixis, pericardial rub or effusion, encephalopathy, uremic bleeding)
67
Small solutes are removed across a semipermeable membrane down thier concentration gradien
"Diffusive clearance"
68
Solutes are removed along with the movement of plasma water
"Convective clearance"
69
Conditions when CRRT is preferred in patients with AKI
Severe hemodynamic instability Cerebral edema Significant volume overload

PSBIM 2023 Nephro (8 decks)

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