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Nephrotoxic drugs, Acid/base, Kidney failure Flashcards

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1
Q

What are the 3 definitions of acute kidney injury?

A
  1. Increase in SCr >= 0.3 within 48 hours
  2. Increase in SCr >=1.5x baseline of previous 7 days
  3. Urine output <0.5mL/kg/hour for at least 6 hours
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2
Q

What are the risk factors for acute kidney injury?

A

Pre-existing CKD (GFR<60)
Volume depletion (vomiting, diarrhea, poor fluid intake)
Nephrotoxic agents/medications
Obstruction

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3
Q

What are prerenal causes of AKI?

A

Hypoperfusion to kidney (hemorrhage, volume depletion)

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4
Q

What is intrinsic AKI?

A

kidney is damaged
typical identifiable insult, drug use, infections

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5
Q

What is postrenal AKI?

A

bladder outlet obstruction
-renal stones
-prostate enlargement

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6
Q

How to treat prerenal AKI?

A

correct hemodynamics
-normal saline if volume depleted
-pressure management
-remove offending agent if possible

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7
Q

How to treat intrinsic AKI?

A

Eliminate the causative abnormality or toxin
Avoid additional insults

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8
Q

How to treat postrenal AKI?

A

Relieve obstruction

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9
Q

When does acute tubular necrosis occur?

A

situations with reduced oxygen to kidneys

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10
Q

What are the ischemic causes of acute tubular necrosis

A

hypotension
sepsis
drugs
-radiocontrast dyes
-NSAIDs
-Cyclosporine

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11
Q

What are exogenous causes of ATN?

A

Radiocontrast dye
Aminoglycosides
Cisplatin
Amphotericin B

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12
Q

What causes functional AKI?

A

Decrease in intraglomerular pressure

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13
Q

Causes of functional AKI?

A

ACEs/ARBs
NSAIDs
Cyclosporine
Tacrolimus

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14
Q

By what mechanism do ACEs/ARBs cause functional AKI?

A

Cause vasodilation of the efferent arteriole leading to a decrease in glomerular hydrostatic pressure –> decrease GFR

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15
Q

What is the clinical presentation of functional AKI?

A

Minor increase of SCr of <30% is typical
Elevation of SCr occurs within 2-5 days and stabilizes within 2-3 weeks
SCr elevation is reversible on drug discontinuation

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16
Q

What are the risk factors for toxicity from ACEs/ARBs

A

Decreased effective renal blood flow (CHF, Cirrhosis)
Pre-existing renal disease

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17
Q

How to prescribe ACEs/ARBs to help with monitoring/prevention of functional kidney injury?

A

Start low and gradually titrate

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18
Q

What is the mechanism of NSAIDs causing functional AKI?

A

Occur when NSAID is taken in times of decreased kidney blood flow

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19
Q

What is the clinical presentation of NSAID functional AKI?

A

Within days of starting therapy
Low urine volume and sodium
Increased edema and weight
*treatment is usually rapid after discontinuing

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20
Q

What are some risk factors for functional AKI from NSAIDs?

A

Lupus
Diuretic therapy
Advanced age

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21
Q

What is the clinical presentation of functional AKI due to cyclosporine and tacrolimus

A

Within days of starting therapy
HTN

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22
Q

What is the use of biopsy in functional AKI due to tacrolimus and cyclosporine

A

used to distinguish drug-induced vs. acute allograft rejection

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23
Q

What are risk factors for toxicity from tacrolimus/cyclosporine

A

High initial cyclosporine dose
Kidney graft rejection
Infection

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24
Q

How to prevent toxicity from cyclosporine/tacrolimus

A

Monitor serum cyclosporine and tacrolimus concentrations
CCBs may help antagonize the vasoconstrictor effects of cyclosporine

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25
What differentiates acute vs chronic tubulointerstitial disease?
systemic symptoms like fever and rash in acute, not systemic
26
What meds cause tubulointerstitial disease - acute allergic interstitial nephritis
B-lactams -penicillin (1-2 weeks after starting therapy) NSAIDs -onset is more delayed (6ish months)
27
Treatment of tubulointerstitial disease - acute allergic interstitial nephritis
Stop offending drug and consider steroid therapy initiation
28
Cause of postrenal nephropathy
Obstruction of urine flow after glomerular filtration
29
How to prevent postrenal nephropathy
pretreatment hydration
30
What does nephrolithiasis not affect?
GFR
31
What is the hallmark sign of glomerular disease?
Proteinuria -may occur with or without a decrease in GFR
32
What are drug related causes of glomerular disease
NSAID Heroin Parenteral gold
33
What medication classes need renal dosing adjustments?
Antimicrobials Cardiac meds Lipid lowering agents Pain meds Antipsychotic/antiepileptic agents Hypoglycemic agents
34
Which antimicrobials require renal dose adjustments?
Most all antibiotics Except: -clindamycin -Metronidazole -Azithromycin Antiretrovirals that do: -tenofovir -acyclovir -valacyclovir -foscarnet -fluconazole
35
Which cardiac meds require renal dose adjustments?
ACE inhibitors Digoxin Potassium sparing diuretic loop diuretic thiazides Enoxaparin
36
Which lipid lowering agents require renal dose adjustments
most statins
37
What pain meds require renal dose adjustments
codeine morphine tramadol
38
Which antipsychotic meds require renal dose adjustments?
gabapentin pregabalin lithium
39
Which hypoglycemic agents require renal dose adjustments?
insulins metformin
40
Which miscellaneous meds need renal dose adjustments?
allopurinol colchicine H2 receptor agonists -famotidine -ranitidine Avoid all NSAIDs in CKD
41
Normal pH range
7.35-7.45
42
What anion gap is related to metabolic acidosis?
metabolic acidosis considered if anion gap >12 mEq/L
43
What are the most common causative medications/chemicals for metabolic acidosis?
biguanides salicylates cyanide
44
What is the mechanism of drug induced metabolic acidosis?
Increased exogenous ingestion acidic precursors that are converted into strong acids Loss of alkali from kidney or GI tract Increased endogenous production of strong organic acids Compromised renal net acid excretion by inhibition of the RAAS, impaired proximal tubule, or distal tubule H+ secretion
45
Which meds most common cause lactic acidosis?
Acetaminophen Biguanides (Metformin) Cocaine Propofol
46
What is the hemodynamic consequence of lactic acidosis?
reduction of cardiac contractility and reduced vascular hypo-responsiveness to vasopressors
47
What happens in metabolic alkalosis?
alkalosis leads to hypoxemia
48
What are the most common drugs associated with metabolic alkalosis?
Loop and thiazide diuretics Penicillin Aminoglycosides Laxative abuse (chloride depletion metabolic alkalosis)
49
Pharmacologic causes for induced hyperventilation (respiratory alkalosis)
Salicylates Nicotine
50
What is the definition of CKD?
more than 3 months structural or functional abnormality of the kidney +/- decreased GFR Abnormalities in composition of blood or urine or imaging tests OR GFR <60 mL/minute with or without kidney damage
51
What is the significance of albuminuria with CKD?
marker of kidney damage suggesting increased glomerular permeability Normal ACR is <10mg/kg
52
What are two measurement scales for CKD
KDIGO KDOQI
53
What is the etiology of CKD?
Diabetes (40%) HTN (25%)
54
CKD general management
treat reversible causes of renal failure Slow progression of renal disease Treat complications Adjust drug dosing for GFR Adequate preparation for patient for patient indicated for dialysis
55
CKD complications
Uremia (waste backs into blood stream) Anemia (low RBC) Renal osteodystrophy (abnormal bone growth or development)
56
How is anemia a complication of CKD
decreased EPO production Blood loss during dialysis
57
Describe epoetin alfa
An ESA that has the same molecular structure as human EPO SubQ or IV
58
Describe Darbepoetin alfa?
Modified molecular structure of human EPO less frequent dosing SubQ or IV
59
Adverse effect of ESAs
Increased risk of cardiovascular events
60
Recommendations for ESAs?
Only initiate if hgb <10 and individualize risk/benefit
61
Dose adjustments for ESAs?
Do not make a dose adjustment increase more often than every 4 weeks Downward adjustments occur at any time Dose adjustments are made in 25% intervals (up or down)
62
What is renal osteodystrophy?
Complication of end-stage renal disease that weakens bones Seen with GFR <60
63
What serum levels are affected by osteodystrophy?
calcium PTH Vit D
64
What plays a major factor in development of renal osteodystrophy?
secondary hyperparathyroidism
65
What are phosphate binders?
used to manage high phosphate levels Aluminum (not often used) Calcium Sevelamer
66
What patient education should be offered with phosphate binders?
Take with meals to bind phosphorus in the gut Calcium products should be taken before meals Avoid calcium binders in patients who have both hyperphosphatemia and hypercalcemia because of the risk of calcification
67
Calcium carbonate
widely used phosphate binder because of its low cost and efficacy Hypercalcemia concerns with use
68
Sevelamer
nonabsorbable phosphate binder Primary therapy in CKD stage 5
69
What is the mechanism of vit D and vit D analogs
suppress PTH synthesis and reduce PTH concentrations Ergocalciferol Cholecalciferol Calcitriol (analog) All have oral and parenteral formulations
70
Ergocalciferol
Recommended for CKD stages 3-5 in presence of an elevated PTH and documented vit D deficiency (levels <30)
71
Calcimimetic agent
cinacalcet HCL attaches to the calcium receptor and reduces PTH do not initiate if serum calcium is less than 8.4

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