Nephrology complications Flashcards
1
Q
Define pitting edema
A
press on a bony area of the leg (tibia), depression does not rapidly refill
-Rated depending on depth + how far it extends up the leg (semi-quantitative)
2
Q
Define pulmonary edema
A
increase in interstitial/alveolar water in the lung
- SOB + crackles (rales) upon auscultation (listening) of the lung
- Quantified by how far the rales extend from the dependent portion of the lung
3
Q
What are some non-pharms for edema?
A
Sodium restriction (less than 2000mg/day)
Dec Fluid intake
Compression stockings
Posture
- supine position, elevate legs
4
Q
T/F diuretics can impact had clinical outcomes (mortality, hospitilization)
A
False
5
Q
What are the purpose of diuretics
A
The purpose of using diuretics is for SYMPTOM relief (while balancing adverse effects of diuretics)
6
Q
What to do if asymmetrical swelling is present
A
Investigate for lymphatic obstruction, DVT or infection
7
Q
If patient has liver failure and edema what is the drug of choice?
A
Spironalactone
8
Q
If an edema patient has CrCl 50+ mL/min what is the drug of choice?
A
Hydrochlorothiazide
9
Q
If an edema patient has CrCl under 50mL/min, what is the drug of choice?
A
Furosemide
10
Q
What to add if furosemide is not effective? What lab value to monitor before adding?
A
If furosemide not effective and K<3.5:
- ADD Potassium-sparing diuretic
If furosemide not effective and K≥3.5:
- ADD thiazide/thiazide like
11
Q
What are ADRs common with all diuretics
A
Volume depletion (hypovolemia)
increased urea and creatinine
12
Q
What are loop diuretics and thiazides ADRs (4)
A
Hyponatremia
HYPOkalemia
metabolic ALKALOSIS
Hyperuricemia
13
Q
ADRs of potassium-sparing drugs
A
Hyponatremia
HYPERkalemia
metabolic ACIDOSIS
Hyperuricemia
14
Q
What does impaired renal function mean for diuretic drug delivery to kidneys
A
HIGHER doses of diuretic are needed to achieve the same response (CKD patients will often be on HIGH doses of diuretics)
15
Q
Define metabolic acidosis in CKD? What groups of patient? which drug?
A
impaired ability to excrete H+ (acid) and impaired abaility generate bicarbonate (base) -> Metabolic ACIDOSIS (blood pH >7.35-7.45)
CKD makes patients more prone to metabolic ACIDOSIS: in event of sudden acid load (ex. Lactic acidosis) or sudden bicarbonate loss (ex. Diarrhea)
eGFR in under 30mL/min
Potassium-sparing drugs
16
Q
What are ADRs associated with metabolic acidosis <22 bicarb? (7)
A
- increased risk of protein catabolism
- Muscle wasting
- Impaired cardiac function
- progression of CKD
- worsening of CKD-mineral and bone disease
- HYPERkalemia
- cognitive dysfunction
- increased mortality
17
Q
Are metabolic acidosis ADRs associative or causative
A
associated
- causality has not been shown yet
18
Q
When do we consider use of pharmacological treatment for MA in CKD patients
A
Bicarb <18 mmol/L
19
Q
What can over treatment for metabolic acidosis result in? (3)
A
- BP control
- K
- fluid status
20
Q
What did the BICARB trial tell us?
A
No better than placebo in treating patients with serum bicarb <22 for patients eGFR <30 not on dialysis
- no difference in physical performance outcome
- no difference in eGFR
- Bad QOL/cost in bicarb group
21
Q
What is the starting dose for MA of sodium bicarb?
A
500mg po BID
22
Q
ADRs of sodium bicarb
A
- GI intolerance and flatulence (gas)
- Sodium loading can cause hypertension. fluid loading, CHF
- HYPOkalemia
23
Q
DDI of sodium bicarb
A
Reduces stomach acidity which inc/dec absorption of some drugs
- space 2 hours from other meds
24
Q
Can a non-odb patient use 1/4 tsp of baking soda if cost is an issue
A
Yes
25
Will sodium bicarb inc BP or sodium retention in patients with dietary sodium restriction <2000mg?
No 500mg tab = 135mg sodium
- however under 2000mg is not always achieved
BICARB studies exluded patients with sodium sensitive conditions (CHF, uncontrolled HTN, edema)
26
T/F there is good evidence that correcting serum bicarb level is as important on clinical outcomes
False
27
What are the regulatory factors of potassium homeostasis?
Hormonal (insulin, catecholamines, aldosterone)
Acid base balance
28
How do the kidneys regulate potassium
In the distal collecting duct
- The kidneys release renin -> angiotensin II -> aldosterone -> potassium EXCRETION
- in response to aldosterone mediated Na+ reabsorption or hyperkalemia
29
What levels are mild, moderate, severe hyperkalemia
Mild: 5.1-5.9
Moderate: 6-7
Severe: Above 7
30
What are cause of pseudohyperkalemia?
Asymptomatic
- hemolysis of RBC (mechanical trauma_
- blood sample drawn when K+ infused
- Lab error
31
What are common drug causes of hyperkalemia
- RAAS blockers
- Aldosterone receptor blockers (spironolactone, eplerenone)
- Beta-blockers
- Cyclosporine (calcineurin inhibitors)
- NSAIDs
32
Presentation of hyperkalemia
Asymptomatic most of the times
May complain of heart palpitations or skipped heartbeats
weakness or paralysis
33
What ECG changes can you tell for hyperkalemia (3)
- Tall peaked T wave
- Tall peaked T wave + Loss of P wave
- Tall peaked T wave + Widened QRS wave
34
How to diagnose URGENT hyperkalemia
K+ over 6 mmol/L
and/OR
symptomatic (ECG changes)
35
How to treat urgent hyperkalemia (4)
1. Initiate cardiac stabilization
- IV calcium (does not change K levels)
2. Shift K into cells
- IV insulin/dextrose (prevent hypoglycemia)
- inhaled salbutamol if no IV access
- add sodium bicarb if MA
3. Remove potassium from body
- Loop diuretic (only if eGFR is good)
- Exchange resins/potassium binders
- Hemodialysis (for severe)
4. Follow measures to prevent recurrence
36
What is diagnosis of non-urgent hyperkalemia
K+ under 6 mmol/L
AND
Asymptomatic (no ECG changes)
37
What is 1st line, 2nd line, last resort for non-urgent hyperkalemia
1st line (address correctable factors)
- Stop non-RAASi meds (NSAIDs, trimethoprim, any herbal that has K+)
- Assess dietary intake
2nd line
- stop/reduce potassium sparing drugs
- start loop diuretic or thiazide (loop diuretic if 3GFR <30mL/min_
- optimize bicarb levels (make sure over 22)
- start potassium exchange resins/binders
3rd line
- D/C or reduce RASI or potassium sparing drugs (MRA)
- reassess later
38
What are the 3 potassium exchange resins/binders?
Which has the fastest onset?
Which has no sodium?
Least efficacy data?
Sodium polystyrene sulfonate (least efficacy)
Patiromir (no sodium)
Sodium zirconium cyclosilicate (fastest)
39
Why is sodium polysteyrene sulfonate still used if there is lack of efficacy data
Available and affordable
40
What is erythropoietin? How is it affected in CKD?
A glycoprotein (hormone) e released by kidneys (90%) in response to hypoxia
- EPO stimulates RBC production in bone marrow
- CKD -> less EPO -> less RBCs -> anemia
41
How does anemia present in CKD?
Usually eGFR under 30
normochromic, normocytic
42
What are symptoms of anemia of CKD? (non-specific)
- fatigue
- vertigo, faintness, headache
- pallor, sensitivity to cold
- shortness of breath
43
What are ADRs associated with anemia of CKD
- More rapid CKD progression
- Higher rate of hospitalization
- more MACE
- greater mortality
44
What is the Hgb target for anemia of CKD?
for non-dialysis and dialysis patient
90-115 g/L
45
What is the rationale for Hb above 115?
increased risk of
- stroke
- VTE
- death in patients with pre-existing malignancy
46
What does the Canadian erythropoietin study tell us
Group?
outcome?
In hemodialysis patients
- placebo <90 hb
- target 95-115
- target 115+
Outcome
- reduced need of blood transfusion vs placebo
- better symptoms (fatigue etc) than placebo
- HIGHER incidence of hypertension vs placebo
- HIGHER incidence of clotting of vascular access vs placebo
47
What did the TREAT trial tell us?
Group?
Target?
outcome? primary and secondary outcomes
Group
- non dialysis
- T2DM
Target
- High Hgb 120-135 vs Low (av 106)
- used darbopoetin
Outcome
No difference in primary outcomes (death/CV event or renal event)
Difference in secondary outcomes
- stroke
- VTE
- death in patients with pre-existing malignancy
48
What route of admin for ESA treatment is given to Non-dialysis, Peritoneal dialysis and Hemodynamic dialysis?
ND-CKD and PD
- Subc ONLY
HD
- Subc or IV
49
When is iron indicated in terms of TSAT and Ferritin in CKD patients?
TSAT 20% or under
and/OR
Ferritin 100 ng/mL or under
50
When are blood transfusions in CKD patients used? (3)
- Used when rapid Hgb is needed (acute hemorrhage, unstable, MI, surgery)
- If ESA therapy is not effective
- signs where risks of ESA may outweigh benefits (cancer, history of malignancy, history of stroke)
51
What are risks of blood transfusions in CKD patients
- Human Leukocyte antigen (HLA) sensitization -> makes it harder to find match for transplant
- Volume overload, hyperkalemia, citrate toxicity
- Fever/allergic reaction, hemolytic reaction
52
Which route of admin can cause iron overload? oral or IV
IV
53
When is IV iron indicated in non-dialysis patients? (4) TSAT and Hb level?
- TSAT <0.12 or Hb <70
- If risk of ongoing blood loss
- side effects to oral iron that limit adherence
- history of inadequate response to oral iron
54
What are the IV iron products used?
Iron sucrose
Sodium ferric gluconate
Iron isomaltoside
55
ADRs of IV iron
- Hypersensitivity rxns,
- flushing/hypotension, fatigue/dizziness/weakness,
- N/D,
- infection risk from IV,
0 Iron overload (monitor closely!)
56
What are ADRs of ESA (darbepoetin, epoetin)? What is lack of consensus based of?
- Hypertension
- Seizures
- increased risk stroke
- increased risk vascular access thrombosis
- increased risk of mortality pre-existing malignancy
we are not sure if ADRs are due to Hgb target or ESA therapy
57
Which ESA has a longer half life? How to dose adjust? How long do you have wait?
Darbopoietin
ESA dose adjustment (must wait at least 4 weeks between each adjustment)
- If Hgb <90g/L: INCREASE dose by 25%
I- f Hgb >115g/L: HOLD until Hgb is <115g/L, then DECREASE dose by 25%
58
Parathyroid hormone regularly inhibited by? stimulated by? (2)
Inhibited by:
Ca2+
Calcitriol (activated Vit D)
Stimulated by:
Phosphate
59
What is production of calcitriol stimulated by? inhibited by?
Stimulated by PTH
Inhibited by FGF-23
60
What is the pathogenesis of CKD- Mineral and bone disorders?
Reduced phosphate excretion (inc PO4)
- stimuates PTG
- PO4 precipitates with Ca resulting in hypocalemia
- Reduced Vit D activation
- Loss of negative feedback (persistent high PTH)
61
What does PTH do in renal impairment? what does it NOT do
Stimulates osteoclasts and bone resorption
- inc Ca and inc PO4
DOES NOT
- stimulate calcium reabsorption
- inhibit phosphate reabsorption
- does not stimulate production of calcitriol
62
Causes of the following diseases
Adynamic bone disease
OSteitis fibrosis cystica
Osteomalacia
Adynamic bone disease
- Over-suppressed PTH levels
- treatment induced due to calcitriol
Osteitis fibrosis cystica
- high PTH -> increased bone resorption
Osteomalacia
- soft bones due to mineralization defect
63
What are the 2 types of metastatic calcification
deposits of calcium salt in otherwise normal tissue due to high serum Ca levels
Soft tissue calcification
Vascular Calcification
Calciphylaxis (in the arterioles -> leads to ischemia, SC necrosis): happens in 1-5% of dialysis patients, has a 80% mortality rate
64
What numbers is increased mortality associated with for
Calcium
Phosphate
PTH
Calcium: 2.6+ mmol/L
Phosphate: 1.8 mmol/L
PTH: 62 mmol/L
65
Which value do you need target 2-9 times the upper normal limit in dialysis patients?
PTH
66
What does it mean if calcium and albumin (protein bound to calcium) are both low
Ca is higher than it appears
67
What is the MOA of phosphate binders?
Counselling points?
DDI?
MOA phosphate binders?
- bind PO4 molecules in GI to form insoluble complex to be excreted in feces
Counselling points?
- take with first bite of meal
- if over 30 min since end of meal, skip dose
DDI?
- Separate 1 hour prior or 3 hours after
68
What is first line for high phosphate?
Calcium based phosphate binders
- TUMS
69
What are the non-calcium phosphate binders?
Sevelamer
Lanthanum
Sucoferric oxyhydroxide
70
What is the exclusion criteria for sucoferric oxyhydroxide?
Patients with hemochromotasis or any other iron accumulation disorders
- however does not increase iron levels (contradictory)
71
What is the EAP criteria for ODB coverage of phosphate binders
Has to be on dialysis
Sustained PO4 over 1.8 AND Ca over 2.65
OR
Sustained PO4 over 1.8 AND calciphylaxis (SC necrosis) and/OR evidence of coronary artery calcification
72
What is the non-pharm option for secondary hyperparathyroidism? Indication?
Parathyroidectomy (partial or total removal of parathyroid gland)
Indicated for:
- persistently high PTH levels with hypercalcemia (+/- hyperphosphatemia) due to medical therapy
73
What is "hungry bone syndrome"
Sudden drop in PTH --> rapid increase in bone production
- post-operative low Ca, PO4, Mg, due to all being absorbed in the bone
74
What is the efficacy of Vit D supplement?
Meta-analysis shows improvement in VitD levels, decreased PTH (without hypercalcemia or hyperphosphatemia)
75
Which Vit D is more effective, cholecalciferol vs ergocalciferol?
Check Vit D levels before starting?
Recomended dose?
cholecalciferol
Check Vit D levels before starting? No
Recommended dose?
- 2000 IU daily
76
When is calcitriol indicated?
For dialysis patients
- can use in non-dialysis if needed
77
MOA of calcitriol (3)
ADRs (3)
MOA
- bind Vit D receptors
- inhibits PTH synthesis
- stimulates Ca and PO4 absorption by intestinal cells
ADRs
- GI
- hypercalcemia (dose-limiting)
- hyperphosphatemia (dose-limiting)
78
Alfacalcidol vs calcitriol
Alfacalcidol
- ineffective in end stage liver failure (requires activation by liver first)
comparable efficacy
- Alfacalcidol is cheaper
79
Cinacalcet MOA
ADRs
MOA
- binds to Calcium-sensing receptor on Parathyroid gland -> suppresses PTH synthesis
- PTH release is inhibited
ADRs
- GI
- HYPOcalcemia
80
When do we recommend a statin right away for CKD patient? When do we add on?
eGFR
Age
Add on?
50+ and eGFR <60
Add on ezetimibe for G3 (<60) - G5 (<15)
81
When do we give statins for 18-49 years CKD patient (4)
If one of the following risk factors apply
- Known CAD
- DM
- Prior stroke
- CV risk over 10% using tool
82
When should we get a lipid profile in CKD? Why?
Initial
- to diagnose severe hypertriglyceridemia and/or severe hypercholesterolemia and
to rule out any secondary causes of elevated lipids (liver disease)
Ongoing lipid profile is not recommended
83
Which CVD risk calculator is for eGFR <30? What does it tell you?
Advanced CKD risk tool
- 2 and 4yr risk of ESKD, CV disease, and death
84
Which risk calculator predicts 10-year atherosclerotic CV disease?
PCE ASCVD Risk with GFR + ACR
- no hard outcomes
85
Which risk calculator predicts 10-year MI, stroke, CVD mortality (hard outcomes)?
Score2 CV risk with eGFR + ACR
86
What does the 4D trial tell us?
Group
Intervention
Results
Group
- T2DM
- Hemodialysis
- No MI past 3 months
Intervention: Atorva 20mg
Results
- no difference in primary and secondary outcome
- no difference in ADRs
DO NOT INITIATE STATIN FOR DIALYSIS for primary prevention
87
What did the AURORA trial tell us?
Rosuva 10mg in hemodialysis patients have no difference in primary and secondary outcomes and ADRs vs palcebo
88
What did the SHARP trial tell us
Group
Intervention
Results?
Group
- G3-G5 patients
- no prior ischemic CVD
Intervention: Simva 20 + Ezetimibe 10
Results?
- Fewer outcomes of major atherosclerotic events in SE group than placebo
- effect primary by non-dialysis patients
ADRs no difference
89
KDIGO guidelines for statins in
Dialysis patients already on statin from before?
Primary prevention in dialysis?
Secondary prevention in dialysis?
Dialysis patients already on statin from before?
- continue therapy (eGFR dosing)
Primary prevention in dialysis?
- Do not initiate
Secondary prevention in dialysis?
- Initiate (previous MI, stroke etc..)
90
Which statin needs renal dosing? What is it?
Which do not?
Rosuva CrCl <30 GFR
- 5-10 mg daily
Simva + Atorva = no renal adjustment
91
T/F Statins increase risk of AKI
False
92
ASA in CKD
Use in secondary prevention
do not use in primary prevention with CKD
