Posted on May 25, 2024 by Tom Wade MD
Today, I review, link to, and excerpt from Core IM‘s Cardiorenal Considerations: 5 Pearls Segment. Posted: May 13, 2024
By: Dr. Andrew Ling, Dr. Nayan Arora, Dr. Nicole Bhave and Dr. Shreya P. Trivedi
Graphic: Dr. Rahul Maheshwari
Peer Review: Dr. Larissa Kruger Gomes, Dr. Nisha Bansal
See Also
Prostate Cancer Staging Tnm - Ajcc cancer staging manual 7th edition pdf - It may grow slowly and it's typically treatable.Link To And Excerpts From "Ultrasound-guided Cricothyrotomy and a Novel 3-D Printed Training Model" - Tom Wade MDShoulder Multidirectional instability & surgical repair — Rayner & Smale🇵🇹 João Carvas, MD, PhD on LinkedIn: #worldthyroidday #thyroidhealth #nutritionmatters #hypothyroidism #tfi…All that follows is from the above resource.
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Time Stamp CME-MOC Show Notes Transcript References
Time Stamps
- 02:05Pearl 1:Make sure the renal dysfunction is not from something else
- 08:47Pearl 2:Practical tidbits on loop diuretics
- 18:08Pearl 3:Assessing diuretic response
- 27:35Pearl 4:Approaching diuretic resistance
- 35:08Pearl 5:Don’t be afraid of medical therapy because of CKD
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Show Notes
Pearl 1: Make sure the renal dysfunction is actually all cardiorenal!
- How do you define cardiorenal physiology?
- Classic Definition:
- Kidney dysfunction that is related to either a (1)low-flow state and/or (2) renal venous congestion
- BOTH can independentlylead to decreased intrarenal blood flow
- BOTH can lead to neurohormonal activation → Increased renin-angiotensin-aldosterone system (RAAS) activity
- These are compensatory mechanisms that initially preserve renal function but can become detrimental when kidney autoregulation can no longer compensate.
- NOTE:Renal venous congestion is thought to be a larger contributor to kidney dysfunction than low-flow states in most cases of cardiorenal syndrome.
- How should you think about the differential for a kidney injury in someone with heart failure?
- Be broad!Multiple processes can happen at the same time
- Urinalysis findings:
- Pure cardiorenal syndrome
- “Bland” with no protein, blood, granular or other cell casts
- May have hyaline casts
- No signs of intrinsic injury!
- NOTE:Screen for proteinuria in heart failure patients!
- Urine protein to creatinine ratio (UPCR)or
- Urine albumin to creatinine ratio (UACR)
- Dilute urine can falsely lower proteinuriaon a urine dipstick!
Pearl 2:Practical Tidbits on Loop Diuretics
- What is the “go-to” loop diuretic for someone who is hospitalized for volume overload?
- Intravenous therapy!
- Because gut edema may interfere with oral absorption
- Dosing:
- 2.5 times their equivalent daily oral home dose of diuretic
- Benefits of this dosing:
- Better decongestion at 72 hours
- Faster transition back to oral diuretics
- Compared tolowerIV doses
- Continuous vs. Bolus dosing?
- No difference in outcomes!
- NOTE:Patients being treated with bolusmayrequire more escalations in dosing during their hospitalization
- What are the differences between loop diuretics?
- IV formulations:
- Furosemide vs. Bumetanide
- No difference in outcomes demonstrated
- But not largely studied!
- Bumetanide Considerations:
- More potent
- Practitioners may be more comfortable with using higher equivalent doses since bumetanide doses are in the single digits
- Severe myalgiaswith IV bumetanide as a continuous infusion
- Especially with higher doses
- Unclear if unique to bumetanide or if purely dose-related given furosemide is not typically used at equally high equivalent doses
- PO formulations:
- Furosemide vs. Torsemide vs. Bumetanide
- Conversions (PO): Furosemide 40 mg = torsemide 20 mg = bumetanide 1 mg
- Considerations when choosing PO:
- Bioavailability
- Furosemide
- Torsemide & Bumetanide
- Duration of action
- Torsemide (6-16 hours) > furosemide (6-8 hours) > bumetanide (4-6 hours)
- NOTE:Torsemide can be dosedone daily,whereas
- Bumetanide should be dosed at leasttwice daily!
- Torsemide is preferred over furosemide since it is more predictable!
- Caveat:TheTRANSFORM-HF trialdid not show significant difference in outcomes between torsemide and furosemide
- However, there are many criticisms of the trial!
- Significant crossover
- Use of mortality as the primary outcome rather than other metrics
Pearl 3: Assessing Diuretic Response and Renal Function
- How to assess diuretic response?
- Traditional assessment:
- Weights
- Exam findings
- Urine output
- Challenges with relying on these:
- Inaccurate documentation and/or
- Delay in diuretic titration
- In case of inadequate response
- Alternative assessment:
- Spot urine sodium (UNa) level
- Measures diuretic responsiveness
- Quick assessment 1-2 hours after administering loop diuretic
- Interpretation:
- UNa < 50-100 mEq/L → poor responseto the current dose of loop diuretic
- GOAL:>70 mEq/L
- For an appropriate response
- Causes offalsely highspot UNa:
- Low volume of urine
- Metabolic alkalosis
- Medications (ex. piperacillin-tazobactam)
- Causes offalsely lowspot UNa:
- Cirrhosis
- High volume of urine
- NOTE:Using a spoturine sodiumAND6-hour urine output-guided protocolto escalate loop diuretic dosing was feasible
- What do you do if the response to diuretic is not adequate?
- Double your loop diuretic dose
- Start a drip (if at maximum dose)
- Reassess initial diagnosis or if new insult!
- What happens to creatinine during diuresis?
- Generally safe to see up to 30% rise in from baseline levels with active decongestion
- Known as “rise in serum creatinine” (RSC)or”worsening renal function” (WRF)
- Usually does NOT reflect true renal tubular injury
- Even though this threshold is how acute kidney injury (AKI) is defined
- Rise is a result of:
- Hemodynamic or functional change in glomerular filtration
- Hemoconcentration of creatinine
- Alone, should NOT be a reason to stop diuresing a volume overload patient
- NOTE:Mortalityactually worse for patient’s whose serum creatinine “improved”from baseline compared to those who had “worsening” levels.
- The rise has nopredictive value for rehospitalization or mortalityunless patients also had other signs of congestion at discharge
- Still, always still do the due diligence each day!
- Volume assessment
- Urine output monitoring
- Consider need to evaluate for another cause of rising serum creatinine
- Consider more sophisticated and/or invasive measures of volume status
- Point-of-care ultrasound (POCUS)
- Venous Excess Ultrasound (VExUS)
- Right heart catheterization
Pearl 4: How to approach diuretic resistance
- What is diuretic resistance?
- Failure to achieve therapeutically desired congestion reliefdespite using appropriate or escalating doses of diuretics.
- Consider…Is something else going on?
- Diuretics cannot work if they are not reaching the kidney!
- Some factors to consider:
- Shock
- Low-flow state
- Elevated intra-abdominal pressure (ascites)
- How can you augment your diuresis?
- Sequential nephron blockade!
- Thiazide or Thiazide-Like Diuretics:
- PO Metolazone vs. IV Chlorothiazide (or Diuril)
- Metolazone
- Less expensive
- Metolazone has amuch longer half-life and duration of actioncompared to chlorothiazide
- Chlorothiazide
- More expensive (cost is starting to come down)
- NOTE:Many clinicians anecdotally prefer chlorothiazide because of faster onset and IV administration
- Effect:
- No significant difference between twoin terms of urine output measured at 24-48 hours.
- Alternative adjusts:
- Hydrochlorothiazide or Chlorthalidone
- Reasonable options though more in outpatient setting
- Commonly used as antihypertensives
- Acetazolamide
- Achievessuccessful decongestion and shortening length of stay
- Without any differences in safety outcomes!
- In practice:Considered especially in cases of worsening metabolic alkalosis or in COPD
- Caution when using if there is acidosis or serum bicarbonate is low!
- Acute SGLT2i
- Not well-established adjunct
- (though beneficial in general andmay be safe to add during heart failure hospitalizations post-AKI)
- Hypertonic saline
- Not well-established adjunct
- What should be monitored during diuresis?
- Electrolytes, particularly hypokalemia
- More common with augmentation
- Hypokalemia is an independent risk factor fordevelopment of diuretic resistance
- Add potassium-sparing diuretics early!
- Long-term benefit
- Rapid Volume Depletion
- What about ultrafiltration (UF)?
- CARRESS-HF Trial
- Stepped diuretic algorithm was superior to starting with ultrafiltration
- Preserved renal function
- Lower rates of adverse events
- Criticisms:
- May not be realistic (diuresis was not attempted in UF group)
- Unclear if ideal rate of UF was used
- In practice: UFonlyafter a failing maximal medical therapy
- Due to concerns about future renal function when starting HD and dialysis access complications
Pearl 5:Don’t be afraid of medical therapy because of CKD
- Guideline-directed medical therapy (GDMT) for heart failure
- Also arekey medical therapies that slow progression of CKD!
- Benefit of medications seen in patients with:
- Proteinuric CKD (estimated albuminuria > 300 mg/day) with or without diabetes
- GDMT meds areheavily underutilizedin patients with concomitant heart failure and CKD
- Despite worse outcomes!
- Percent of patients of GDMT (RAAS inhibition, MRA, beta blocker) by eGFR at discharge
- eGFR 30-45 →only15% of patients!
- eGFR < 30→only5% of patients!
- NOTE:Data from 2014-2019 heart failure registry
- Before SGLT2 inhibitors became an established pillar in heart failure and CKD
- How should you start GDMT in advanced CKD?
- Expect an initial decline in eGFR based on creatinine
- When starting RAAS inhibitors and/or SGLT2 inhibitors
- But don’t panic!
- Decline is usually reflective of:
- Glomerular hemodynamic changes
- Reduction of pathologic hyperfiltration
- Decline is associated with:
- Better outcomes
- Slower annual eGFR decline afterwards
- SGLT2i studies
- General Advice:Tolerate up to a 30% reduction in eGFRafter initiation as declines in eGFR larger than 30% are unusual with these agents!
- RAAS Inhibitors
- Tips & Tricks
- RAAS inhibitors shouldNOTbe stopped solely because of declining eGFR
- STOP-ACE Trial –no significant difference in trajectory of GFR decline or number of patients started on RRTwhen stopping vs. continuing RAS inhibitors at eGFR < 30
- Signal towards worse cardiovascular outcomes, however, when these agents are stopped.
- Hyperkalemia IS more of a reason to pause – but consider trying to treat the potassium first!
- SGLT2 inhibitors are also protective against hyperkalemia – even more reason to have them on board if not already!
- Consider adding potassium binders (see our episode onhyperkalemia in CKD).
- SGLT2 Inhibitors
- Tips & Tricks
- Currently approved forinitiation at eGFR > 20
- EMPA-CKD Trial
- Subgroup analyses of DAPA-CKD Trial
- There are ongoing trials where people are being safely continued on these agents even through dialysis!
- SGLT2 inhibitors can likely be continued safely even if eGFR eventually declines to < 20!
- Mineralocorticoid Receptor Antagonists (MRA)
- Tips & Tricks
- All MRAs:
- Improved cardiovascular outcomes and mortality
- At leastobservational data that they may improve renal outcomesover the long-term
- NOTE:It is stillextremely important to closely monitor for dangerous potassium issuesand kidney function especially when initiating any MRA!
- Finerenone:
- New agent on the block!
- Slows CKD progressionin patients with type 2 diabetes and proteinuric CKD in randomized setting (FIDELIO-DKD)
- Non-steroidal mineralocorticoid receptor antagonist
- More selective for the mineralocorticoid receptor
- Compared to more familiar agents like spironolactone or eplerenone (which are steroidal MRAs)
- Reduced rates of hyperkalemia
- Compared with steroidal MRAs
- Also improves cardiovascular outcomes like the other MRAs (primarily by reduced heart failure hospitalizations)
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