Patients with concurrent heart failure and kidney disease are not getting proper GDMT

We have all seen the story play out before: a patient with heart failure with reduced ejection fraction (HFrEF) who is new to a hospital system is hospitalized for acute decompensated heart failure. A look at their complete metabolic panel shows a Cr of 2.0 mg/dL (with a corresponding eGFR of 35 mL/min/1.73m2), and despite diuresis, the Cr does not really budge. What was initially thought to be an acute kidney injury from possible renal vascular congestion or from renal hypoperfusion turns out to be a more longstanding chronic kidney disease (CKD). Because the medical team has only met the patient for the first time during this hospitalization and they “do not know where the kidney function is going to shake out,” the patient is perhaps started on a beta-blocker but no other guideline-directed medical therapy (GDMT). The patient is discharged from the hospital on only one guideline-recommended agent. Patients like this, with concurrent HFrEF and CKD, can easily get trapped in a vicious cycle in which they are recurrently hospitalized with heart failure exacerbations and varying degrees of kidney injury; their kidney function becomes an impediment to starting the crucial GDMT which will lower their mortality, reduce their likelihood of being hospitalized again, and even improve their quality of life.

This anecdotal experience is supported by data from a new study published in the Journal of the American College of Cardiology (JACC), “Kidney Function and Outcomes in Patients Hospitalized with Heart Failure.” This study utilized the Get With the Guidelines-Heart Failure (GWTG-HF) registry and analyzed over 365,000 hospitalizations with heart failure, including about 157,000 patients hospitalized for heart failure with a reduced ejection fraction (HFrEF, EF ≤40%). Hospitalized patients had kidney function all across the spectrum, ranging from those with a normal estimated glomerular filtration rate (eGFR) of ≥90 mL/min/1.73 m2 (10% of patients) to those on dialysis (5% of patients). As patients’ eGFR decreased (as kidney function worsened), in-hospital mortality rates for heart failure patients increased from about 1% for those with a normal eGFR to 4-5% for those with an eGFR <30 mL/min/1.73m2 or on dialysis.

Among patients with HFrEF, those with lower eGFR or on dialysis were less likely to be discharged on GDMT such as beta-blockers, mineralocorticoid receptor antagonists, angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs), or angiotensin receptor II blocker-neprolysin inhibitors (ARNI), than those with normal renal function. This pattern was consistent regardless of race/ethnicity and sex. Patients with worse renal function (measured as lower eGFR at time of discharge) were also less likely to have an appointment made after discharge.

These disparities in quality metrics for heart failure patients, particularly those with CKD, are disheartening because 1) many patients with heart failure also have concurrent chronic kidney disease and 2) hospitalized heart failure patients with worse kidney function already experience worse clinical outcomes, such as higher mortality (as shown in this and other studies). Though the use of evidence-based medical therapies is often suboptimal among all patients with HFrEF, patients with comorbid HFrEF and CKD are an especially vulnerable group who would especially benefit from treatment with medications that are proven to improve outcomes. Additionally, though they seem to less frequently have post-discharge outpatient appointments made, these patients would benefit from more (and not less) post-hospital monitoring.

This large contemporary study of patients from a major heart failure registry highlights a gap that we must address among heart failure patients at various stages of kidney disease. More work must be done to prevent or slow the progression of chronic kidney disease in heart failure patients. Finally, special attention should be given to the utilization of guideline-directed medical therapy in this vulnerable population of patients in order to help improve their outcomes, particularly when they are hospitalized for acute decompensated heart failure.

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What to expect at Joint Hypertension 2018 Scientific Sessions – Treating Hypertension in 2018

Two AHA Councils, the Council on HAHA|ASH Hypertension Scientific Sessions 2018ypertension and the Council on Kidney in Cardiovascular Disease, have joined forces with the American Society of Hypertension to make Joint Hyptertension 2018 Scientific Sessions (#Hypertension18) among the most impactful. Dr. Karen Griffin, FAHA Vice Chair for the Council on Hypertension Scientific Sessions Planning Committee calls it the “premier scientific meeting on hypertension in the world”. Understandably so; it boast experts from areas of cardiorenal disease, cardiovascular disease, stroke, and genetics to make for a vast cross-disciplianry session with the up-to-date information on hypertension. This year’s meeting received 439 abstracts in 37 categories, over 125 expert peer reviewers, and more than 20 countries represented.

There will be several interactive sessions that will target the established researcher/clinician, early career, and everything in between. With the addition of the new concurrent session D-Track, Clinical Practice Clinical Science and Primary Care tracks, a dimension will be added for elucidate the research science/clinical practice as it relates to patient care. In light of all the sessions that are available one should not have a problem reaching the milestones set by the program coordinators (infra vide).

To point out a few conference highlights, there will be 24 oral sessions, 3 poster sessions, and travel award talks:

The Excellence Award for Hypertension Research (Saturday, September 8, 2018)

  • R. Clinton Webb, PhD, FAHA presents “A Study of the Innate Immune Response in Hypertension”
  • Paul K. Whelton, MB, MD, MSc, FAHA presents “Clinical Trials and Practice Guidelines: Evidence-Based Progress in Lowering Blood Pressure”

Conference Awards

  • 10 Council on Hypertension New Investigator Travel Awards
  • 10 Council on Kidney in Cardiovascular Disease New Investigator Awards
  • 4 New Investigator Travel Awards
  • 6 Hypertension Early Career Oral Award Finalists
  • 12 AFHRE Travel Award for Patient-Oriented or Clinical Research in Hypertension
  • 1 Clinical Science Investigator Award for Excellence in Translational or Clinical Hypertension Research
  • 3 New Investigator Awards for Japanese Fellows

25 Poster Presenters can potentially win the competition this year! Which has gone up significantly from the previous years.

I am excited to go to Chicago for #Hypertension18 this year. If there is anything you need to enhance your experience during your time at the conference contact the program officials (directions in the program book).

I look forward to meeting you all! If you see me around tweeting, introduce yourself. I love meeting new people and learning new things. After all, that is why we are all going, right? 🙂

#Hypertension18 Conference Learning Objectives:

  1. Discuss changes to the AHA/ACC guidelines for the management of hypertension and their clinical implications.
  2. Describe opportunities to improve blood pressure measurement in the clinical setting to provide more accurate results.
  3. Identify immune and inflammatory mechanisms that contribute to the development of hypertension and hypertension-related end-organ damage and discuss the research and clinical implications.
  4. Educate participants about medical approaches for the management of co-morbid obesity in patients with hypertension.
  5. Describe new and emerging strategies for treating resistant hypertension.
  6. Describe participants on the impact of value-based reimbursement on hypertension management and identify opportunities to improve its management.


Leave a comment or tweet @AnberithaT and @AHAMeetings if you have questions or are interested in something else specifically.

Follow me and @American_Heart @AHA_Research @AHAScience and @HyperAHA on twitter for more #HeartSmart information.

For meeting Tweets follow @AHAMeetings @HyperAHA @AHAScience #JAHAMeetingReports @JAHA_AHA for the latest on#Hypertension18!


Chronic Kidney Disease: The Silent Killer

“He felt well, so he didn’t follow up with his doctor.”

Our nephrology team was gathering history about a patient who had landed in the Emergency Department with advanced kidney failure and its consequences: confusion, severe anemia, metabolic acidosis, and a high blood potassium threatening to push him into cardiac arrest.  We asked the family: Did he have any known kidney problems?

“His doctor mentioned abnormal kidney function 3 years ago.  But he’s felt really healthy, and has been too busy to go back to the clinic.”

Convincing someone they have chronic kidney disease can be tough.  “But I feel fine!” is a common response along with a look of disbelief or suspicion (like they’re not sure if I’m trying to sell them something).  This is usually followed by: “What can I do to make my kidneys better?”  This part is a real downer because they find out I actually don’t have anything to sell – there isn’t any therapy that can regenerate kidney function.  It’s all about preventative measures to preserve the functioning nephrons – we focus on improving lifestyle practices and treating comorbidities so as to avoid further kidney injury.

World Kidney Day has been recognized on the 2nd Thursday of March every year since 2006 and tends to pass by with little fanfare.  Public awareness and media coverage of kidney disease is relatively low compared to conditions such as heart disease or cancer.   However, the statistics associated with chronic kidney disease are downright scary.  Chronic kidney disease doubles the risk of mortality from cardiovascular events or infection.  Every year, more Americans die from kidney disease than from breast cancer and prostate cancer combined.  End-stage kidney failure requiring dialysis has an average survival of 10-15 years.  If an individual transitioned to dialysis at the same time that he welcomed a baby to the family, he might not live to see his child graduate from high school.

person shruggingAbout 1 in 10 people worldwide, and >20 million in the US, have chronic kidney disease.

The functioning unit in the kidney is the nephron, and humans are born with 900,000 to 1 million nephrons per kidney (or less, if born premature).  No new nephrons form after birth.  We are actually born with more kidney function than we need to maintain electrolyte and fluid balance – evolutionary proof that the kidneys are so important!

In most cases of progressive kidney disease, the body is remarkably adept at adjusting to the buildup of toxins.  The person “feels well” until the kidney function falls below 15% at which point the “crash” happens and they feel terrible.

Research is ongoing to develop saliva tests that quantify levels of toxins that have diffused from the blood, as a measure of kidney function.  These are yet to be validated and commercialized.  For now, periodic blood tests (inconvenient and painful, but necessary) are the only way we can reliably monitor chronic kidney disease to guide treatment recommendations.

Wei Ling Lau Headshot
Wei Ling Lau, MD is Assistant Professor in Nephrology at University of California-Irvine, where she studies vascular calcification and brain microbleeds in chronic kidney disease. She is currently funded by an AHA Innovative Research Grant, and has been a speaker for CardioRenal University and the American Society of Nephrology.


Back To Square One: Normal Saline For Prevention Of Contrast-Associated Kidney Injury

I was in medical school when the JAMA paper came out that reported superiority with sodium bicarbonate IV fluids over normal saline in preventing contrast-induced acute kidney injury.  This was a Big Deal.  Kidney injury is associated with prolonged hospital stays and increased risk of death.  I recall carefully making a note of the exact sodium bicarb formulation and pre- and post-contrast infusion rates, carrying this index card around in my coat pocket.  Later during residency, I would diligently order the sodium bicarb fluids for high-risk patients pending contrast procedures and spell out the protocol in my chart notes.
A barrage of studies followed the JAMA report but the robust benefit in preventing kidney injury was not replicated.  While some investigators were able to detect a modest benefit with sodium bicarb fluids (for urine alkalinization) or oral N-acetylcysteine (NAC, for scavenging of reactive oxygen species) other groups reported no difference, and small cohort sizes with low outcome rates was a prevailing limiting factor.
The PRESERVE trial (Prevention of Serious Adverse Events Following Angiography) definitively lays to rest all the uncertainties surrounding sodium bicarb and NAC.  In a very anti-climactic fashion.  Sodium bicarb was no better than normal saline, and NAC was no better than placebo.  The study was funded by the Veterans Affairs Cooperative Studies Program and included about 5,000 high-risk patients with stage 3-4 chronic kidney disease (80% were diabetic) from 53 medical centers in the US, Australia, New Zealand and Malaysia.  (I was born and raised in Malaysia, and am simultaneously impressed and bemused that Malaysia was the only Asian country involved in PRESERVE.)  Rates of acute kidney injury were ~9% and death by 90 days ~2.5% across all treatment groups.  PRESERVE trial findings were published in NEJM to coincide with Dr. Weisbord’s presentation at the #AHA17 late-breaking clinical trials session.
I chatted with Dr. Pastor-Soler, a nephrologist from University of Southern California who was the discussant at the media briefing session, expressing my disappointment that we don’t have more effective prevention strategies for contrast-induced kidney injury.  In pragmatic fashion, she pointed out that the PRESERVE trial is important since sodium bicarb fluids often have to be prepared to-order by hospital pharmacies, and there are intermittent shortages plus increased cost.  Based on the PRESERVE trial findings, we can confidently proceed with normal saline which is readily available, with more efficient patient care.  (I’ll make a plug here for Women In Nephrology (WIN) where Dr. Pastor-Soler is President-Elect… if you’re a female in the field of nephrology, consider joining!)
So how much normal saline should we give?  The PRESERVE investigators allowed a great deal of flexibility to participating medical centers: “1 to 3 ml per kilogram of body weight per hour during a period of 1 to 12 hours for a total volume of 3 to 12 ml per kilogram before angiography, 1 to 1.5 ml per kilogram per hour during angiography, and 1 to 3 ml per kilogram per hour during a period of 2 to 12 hours for a total volume of 6 to 12 ml per kilogram after angiography… In patients with a BMI of more than 30, we capped fluid-administration rates on the basis of a weight of 125 kg.”  It sounds like if you give some NS before, during and after, you’re a winner!
To end on a sobering note, the PRESERVE statistics indicate that in high-risk stage 3-4 chronic kidney disease patients who require IV contrast procedures, about 1 in 10 will develop acute kidney injury and 1 in 40 will not survive past 90 days.  Medical necessity for IV contrast should always be carefully weighed.  And normal saline hydration – yes, definitely! – while keeping in mind that 1 liter of NS contains 3.5 grams of sodium and it is prudent to avoid excessive salt/water loading (volume overload being another key predictor of poor hospital outcomes).

Wei Ling Lau Headshot

Wei Ling Lau MD is Assistant Professor in Nephrology at the University of California-Irvine, where she studies vascular calcification and brain microbleeds in chronic kidney disease. She is currently funded by an AHA Innovative Research Grant, and has been a speaker for CardioRenal University and the American Society of Nephrology.