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Fellows Summer Lecture Series
Inpatient CKD and ESRD Management
Amanda Leonberg-Yoo, MD MS
July 25, 2019
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Outline & Points to review
The importance of being a good consultant
Management of inpatient CKD
• Metabolic derangements
– Hyperkalemia
– Metabolic acidosis
– Hyperphosphatemia
• Use of radiocontrast in CKD patients
• Drug dosing
• Transitions of care
Management of inpatient ESRD
• Metabolic derangements
• PICC Lines
• Transitions of care
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Case 1: Trauma and a CKD patient
44Y African American man with a history of CKD stage 3B (Cr 1.6-2), DM, HTN,
admitted after a motor vehicle accident.
Reason for consult: “CKD management”
127
7.2
101
20
45
2.67.8
351
eGFR 32
7.5
12.211.4
35.0207
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Metabolic Derangements in CKD
131
7.2
101
20
45
2.67.8
351
eGFR 32
7.5
12.211.4
35.0207
Hyponatremia
Reduced free
water excretion
Azotemia
Impaired excretion of
nitrogenous waste
Hyperkalemia
Impaired renal
K+ excretion
Metabolic Acidosis
Decreased ability to
excrete H+
Hypocalcemia
Increased PO4 leads
to calcium binding
Low vitamin D levels
Hyperphosphatemia
Decreased filtration of PO4
Anemia
Decreased EPO production
Chronic inflammation
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Inpatient management of hyperkalemia
Threshold for treatment – arbitrary
Serum potassium >= 6 mEq/L, compared to <=5.5
• OR Death: 33.4 among inpatients without CKD
• OR Death: 15.8 among inpatients with CKD
EKG changes – may not be sensitive enough, especially in CKD patients
• Sensitivity (K>5) = 34-43%
• Sensitivity (K>6.5) = 55-62%
• Specificity (all patients) = 85%
Montague B et al CJASN 2008;3:324
Wrenn et al Ann Emergency Med 1991;20(11): 1229
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Overview of current treatments for severe hyperkalemiaMechanism Intervention Onset/Duration Efficacy
Cardio-protection Calcium gluconate
Calcium chloride
Acts within 1 minute
Durable effect: 30-60 min
Does not affect serum K
Intracellular K+
Shift
Regular Insulin/
Glucose
Acts within 15 min
Peak ~ 30-60 min
Duration ~ 4-6 hrs
Reduces K ~ 1 mEq/L
Special population: Uremia, diabetics
Inhaled β2 agonists Acts within 30 min
Duration: 2 -6 hrs
Sodium bicarbonate Acts quickly if given quickly (2-3 hrs)*
*More effective if acidemic pt
50 mEq over 15 min = 0.5 mEq/L reduction
Reduces K by 2.1-3 mEq/L (in acidemic pts)
Potassium removal Loop diuretic
Fludrocortisone Acts within 3 hours Max dose 0.4 mg daily
K binding resins Kayexalate: 2 hr onset, peak at 4-6 hrs
Patiromer: 7 hour onset
ZS-9: 1 hour onset
Kayexalate: 0.9-1.7 mEq/L K
Patiromer: 0.23 mEq/L K within 7 hrs
ZS-9: 0.11 mEq/L within 1 hour
0.7 mEq/L in 48 hrs
Dialysis Caution: Serum-to-dialysate K gradient
Rebound post dialysis
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Acid-Base Derangement – Metabolic Acidosis
Risks of hypobicarbonatemia:
• Muscle wasting
• Bone disease progression
• CKD progression
• Increased mortality
Bicarbonate target > 22 mmol/L
• Bicarbonate deficit = HCO3 space X HCO3 deficit
= (0.5 x body weight) x (Goal bicarbonate – serum bicarbonate)
Treatment options:
Bicarbonate type Dose Amount of HCO3
Sodium bicarbonate tablet 650 mg 8 mEq
Sodium citrate 15 mL 15 mEq
Baking soda 1 tsp 54 mEq
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Inpatient management of CKD-MBD
Chronic Kidney Disease - Mineral Bone Disorders (CKD-MBD)
• Systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a
combination of the following:
1. Abnormalities of circulating mineral metabolites
○ Ca, Phosphorus, PTH, vitamin D
2. Abnormalities in bone structure
○ Turnover, mineralization, volume, linear growth or strength
3. Vascular or soft tissue calcification
○ Calciphylaxis
Reason for treatment in an inpatient setting:
1. Acute management: Calcium sequestration, may limit AKI recovery
2. Chronic management: Reduction in CVD and mortality
3. Tradeoff: Drug-drug interactions
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Wolf CJASN 2015;10(10):1875
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Hyperphosphatemia – Inpatient management
Usual treatment of CKD-MBD:
• Reduction in dietary phosphorus intake
• Use phos binders in close temporal proximity with meals
Practical considerations for inpatient management of hyperphosphatemia:
• NPO Status:
Composition of saliva:
• High in potassium (2-4 times higher than serum)
• High in phosphorus (>3x higher than serum) – increased in ESRD patients
• Total enteral nutrition:
– Use phos binders q4-6 hrs
My take: Treat only if excessively elevated. OK to continue if on as an outpatient.
Good opportunity to check CKD-MBD labs (although not likely cost effective)
Eknoyan JASN 2009;20(3): 460
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Table for phos binding agents
Name Brand Name Dose Pro Tips
Calcium carbonate aka “Tums”
Calcium Acetate PhosLo 667 mg = 1 tablet Blue & White pill
Sevelamer Renvela
Renagel
800 mg = 1 tablet White pill
Aluminum hydroxide Amphojel
Alternagel
320 mg/5mL
5 mL TID x 3 days
- Not used as an outpatient
- Generally reserved for severe
hyperphosphatemia with NGT
- Long-term use associated with
cognitive disturbances, osteomalacia,
& anemia
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Case continued -
The patient has undergone bilateral fasciotomies for treatment of rhabdomyolysis.
Life-threatening electrolyte abnormalities have been corrected with non-dialytic
measures, although his AKI has not yet resolved. He has had persistent
transfusion-dependent anemia following surgeries.
He develops new onset hypoxia on hospital day 4, and primary differential is a
pulmonary embolism.
Reason for consult: Risk of IV contrast exposure
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CKD and contrast-induced nephropathy
KDIGO Clinical Practice Guideline definition:
• Rise in SCr ≥ 0.5 mg/dL OR ≥ 25% increase from baseline
• 48-72 hrs after IV contrast exposure
Risk factors for CIN
• CKD status
• Diabetes mellitus
• Periprocedural hemodynamic instability
• Anemia
• Contrast – volume and osmolar content
Risk score for CIN after PCI can be used to estimate risk
• Mehran Risk Calculation
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Prevention Strategies Reduction in dose and osmolality of IV contrast
• Volume of contrast can be calculated by the following equation:
Risk of CIN ratio = volume of contrast (mL)/CrCl
Ratio < 3.7, lower risk of CIN
• Low osmolar contrast administration
Optimization of volume status
• Inpatient IV hydration protocol: 1 mL/kg/hr NS 6-12 hrs pre- , intra-, and post-procedural
• LVEDP-guided therapies reduced risk of CIN and major adverse events (volume overload)
• RenalGuard
Interventions that target “bad humors”
• Remote ischemic preconditioning
• N-acetylcysteine
• HMG-CoA Reductase inhibitors
• RAAS blockade
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Prevention Strategies
Removal of contrast medial by extracorporeal treatment
• Methodologically flawed by definition of CIN
• HD can remove 60-90% of contrast from blood
Intermittent HD: Not supported for CIN prevention
Continuous renal replacement therapy: Not supported for CIN prevention
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Case 2: Medication dosing in CKD
39YM with a history of gunshot wound resulting in paraplegia, suprapubic catheter,
multiple infectious complications with multidrug resistant infection, admitted with
osteomyelitis. Baseline SCr 1.19 mg/dL, BMI 14. In the past, he has developed AKI
in the setting of IV colistin use.
Reason for consult: Pharmacy clearance for colistin use
The real renal consult question:
1. CKD diagnosis and management
2. Estimation of true kidney function
3. Drug dosage adjustments
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Principles of drug dosing
Pharmacodynamics: Study of how a drug affects an organism
Pharmacokinetics: Study of how the organism affects the drug
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Drug dosing and estimated GFR
Considerations for our patient:
• Reduced Cr generation may bias all creatinine-based eGFR calculations
• Individualize based on body surface area (BMI 14) – generally not recommended for drug dosing
• Biologic readouts are better than pharmacokinetic surrogates
– Examples: INR, BP measurement, vanco troughs
Matzke et al. Kidney Intern 2011;80:1122
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Conclusions for Drug Dosing
We are the experts for estimating (and measuring) kidney function
Drug dosing trials are primarily performed using the CG estimation and have
generally excluded CKD individuals
• mGFR should really be the standard for renal function
• CG equation over-estimates GFR
If able to, use biologic markers to assess efficacy of drugs (eg Vanco levels)
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Specific drugs to monitor with CKD patients
Neuropsychiatric meds
• Narcotics – Think of active metabolites (morphine)
• Antidepressants
Antibiotics
• Aminoglycosides
• Cephalosporins – neurotoxicity
• Acyclovir
• Fluoroquinolones – Drug-drug interactions and dosing strategies
Direct oral anticoagulants
Oral hypoglycemic agents
• Sulfonylureas
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Case continued: Transition of care
The patient is ready for discharge. He unfortunately developed an acute kidney
injury in the setting of IV colistin use and IV contrast exposure.
His primary team is ready for discharge and asks you if the patient needs to follow-
up post-discharge
What do you tell them?
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Transitions of care for our patients – Practical Points
Acute kidney injury – Goal is for a 2-week follow-up (can be made by clinic staff with
facilitation by renal inpatient team)
Communicate with patient re: need to follow-up
Review medication reconciliation prior to discharge
Provide information for labwork frequency and follow-up
Communicate with Renal Clinic (PPMC, HUP) and outpatient provider re: patient
synopsis
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Case 3: Inpatient ESRD management
88 year-old woman with ESRD on HD (TTS) via LUE AVG, atrial fibrillation, frequent
falls, pseudogout, admitted with acute onset abdominal pain and nonbloody
diarrhea.
Physical Exam: BP 141/106, HR 150. Elderly woman, in distress. + diffuse
tenderness to palpation. No rebound or guarding
Labs: Lactate 13.4, K 4.8, Hgb 11.7
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Question 1: Can this patient receive IV contrast?
Contrast exposure in maintenance dialysis patients is generally OK
• Cautious use for individuals that rely on residual renal function
– Peritoneal dialysis
• Cautious use for individuals that may have very tenuous volume status
– Isovue 370 = 796 mOsm/L
– For a 70 kg person, extracellular volume expansion ~ 330 mL
• HD in individuals on chronic maintenance HD can be safely delayed for >24 hrs
• CTA: Patent mesenteric arteries and veins. No e/o bowel ischemia
Bahrainwala, Leonberg-Yoo, Rudnick. Seminars in Dialysis, 30(4): 290-304
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Question 2: Special considerations for dialysis?
Heparin use:
• Rationale: Reduces dialyzer clotting rate better clearance less risk for dialyzer blood loss
• Con: Surgeries, risk of bleeding, HIT, hyperkalemia
• Method: Hourly bolus dosing (500-1000 units IV)
• Alternatives: High BFR or periodic saline rinse
Vitamin D receptor analogs:
• Rationale: If prolonged hospitalization, would benefit from continued inpatient mineral bone
disease management
• Con: Creates confusion among inpatient teams, contributes to higher Ca/Phos
• Method: Paricalcitol (Zemplar) vs Calcitriol vs Doxercalciferol (Hectorol)
Epogen use:
• Rationale: Maintain consistent ESA exposure
• Con: If very sick, may be ESA unresponsive
• Method: IV ESA during HD
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Question 2: Special considerations for dialysis?Ordered by
renal fellow
Medications ordered Rationale Downside
HD prescription Yes
Heparin Yes • Heparin bolus = 500-
1000 units
• Heparin 500-1000 units
q 1 hour
• Reduce dialyzer clotting
• Better Clearance
• Less risk for dialyzer
blood loss
• Surgeries
• Risk of bleeding
• HIT
• Hyperkalemia
Activated
Vitamin D
Yes/No • Paricalcitol/Zemplar* 2-
5 mcg IV with HD
• Calcitriol PO/IV*
*Conversion Calcitriol 1 = zemplar 4
• Maintain consistent MBD
management as inpatient
• Confusing for
inpatient teams
• Higher Ca/Phos
inpatient
ESA Yes • Epoetin 50-100 units/kg
IV with HD
• Maintain consistent ESA
exposure
• May be ESA
unresponsive
Antibiotics No • No antibiotic needs to be given during HD
• You should know which abx can be given at outpatient HD
Blood
transfusions
No • Call team and discuss if you feel PRBC is necessary
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Anemia
Minimize blood draws
Iron replacement therapy
ESAs
US Pharm 2014;39(8) 56-60
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Question 3: We can’t get IV access. Can this patient have
a midline?
The answer is almost always no
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Case 4: ESRD Management
38 year-old man with ESRD on HD (MWF) via tunneled HD catheter, who presents to
the ED with dyspnea, bilateral LE edema. Target weight is 74 kg. Due to catheter
malfunctioning, several treatments have been truncated.
Admission Vitals: BP 141/89, SpO2 96% on room air, Weight = 87.2 kg
Admission Labs: K 5.3, HCO3 30, pH 7.32 (VBG)
CXR: Moderate pulmonary edema with small right and trace left pleural effusion
Questions:
1. Does this patient need emergent dialysis?
2. Do you need additional clinical information?
3. Do you need to evaluate the patient in the ED to make this decision?
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ESRD Management – Consult Policy
Fellows must discuss all after hour decisions with the responsible attending
nephrologist throughout the entire academic year
Established patients on maintenance HD and may require after-hour treatments
should be seen by the fellow and discussed with the attending on call prior to
initiation of treatment unless clinical circumstances necessitate more urgent
initiation
In non-emergency situations, exceptions to this may be made on a case-by-case
basis under the following circumstances:
• Patient is hemodynamically stable
• Fellow has reviewed relevant clinical information remotely and has discussed with attending on-
call who agrees that treatment may be initiated without patient being seen until the next morning
For the first 3 months, fellows are expected to see patients initiating HD after hours.
Subsequently, need is determined by the attending on call
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