Abstract
There are numerous interactions between the cardiac and renal systems important to the management of heart failure. These interactions are bidirectional, in that acute or chronic dysfunction of either the heart or kidneys can then induce acute and chronic changes in the other organ as well. Mortality is increased in patients with heart failure who have reduced renal function. Likewise, cardiovascular disease is responsible for up to 50% of deaths in patients with renal failure. An incomplete understanding of the intricate partnership between these two organs can lead to limitations in heart failure guideline-directed medication therapy and worsening patient outcomes. Primary care serves as a hub for patient communication, collection of test results, and overall collaboration among specialty providers, including cardiology and nephrology making primary care providers a key link to the management of heart failure and cardiorenal disease. In this chapter, we will summarize the interactions between heart failure and renal dysfunction and the clinical management thereof focusing on both heart failure patients with cardiorenal syndrome and those with chronic renal insufficiency, ending in two separate case studies that highlight the bidirectional considerations necessary for the care of each group.
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Appendices
Case Study 1: Cardiorenal Syndrome Type II and Diuretic Resistance
Subjective: Ms. Jones is a 68 year-old female with the following past medical history/problem list: Heart failure with reduced ejection fraction, NYHA Class II; status post-ICD implant for primary prevention of sudden cardiac death; dilated, ischemic cardiomyopathy; coronary artery disease, status post-coronary artery bypass grafting >10 years ago; hypertension; diabetes mellitus, type 2.
Family history: Coronary artery disease in her father and paternal grandmother.
Social history: She lives at home with her husband. They have three grown children. Homemaker. Denies alcohol, tobacco, and illicit drug use.
Medications: Carvedilol 3.125 mg BID; Sacubitril/Valsartan 24/26 mg BID; Spironolactone 25 mg daily; Furosemide 80 mg BID; Metformin 1000 mg BID; Aspirin 81 mg daily; Atorvastatin 80 mg QHS.
Allergies: NKDA.
1.1 Case Scenario
Chief complaint: The patient called requesting an appointment due to worsening shortness of breath and her “fluid pill not working anymore.”
HPI: Ms. Smith returns for episodic visit complaining of increased shortness of breath with mild activity, 11 lb weight gain in 1 week, and lower extremity edema. She has recently returned from a vacation with her grandchildren where she admits she did not watch her sodium intake and ate out almost every day. She states, “I’ve been taking my furosemide, but it just doesn’t seem to be working as well as it used to.” She normally limits sodium intake to 2 g daily and fluid intake to 2 l daily and reports taking all medications as prescribed. She admits to bloating, early satiety, 3-pillow orthopnea, and less than expected urinary output. She denies any recent ER visits, hospitalizations, chest pain, or palpitations. No fever, dark or foul-smelling urine, frequency, urgency, frank hematuria, or hesitation.
1.2 Objective
Vital signs: BP 102/65; HR 89; oxygen saturation 97% on room air; Temp 98.2°. Weight 172 lbs (last recorded office weight was 161 lbs)
Physical exam: JVD 10 cm. Normal S, S2 without S3 or murmur. Normal work of breathing at rest. Lung sounds decreased in bilateral bases. Abdomen distended but still soft and non-tender. 1 + bilateral lower extremity pitting edema to mid-calves
1.3 Labs
Today—Sodium 134; Potassium 4.6; BUN 32; Creatinine 1.8; Pro BNP 3560
2 months ago—Sodium 137; Potassium 3.9; BUN 22; Creatinine 1.2; Pro BNP 540
1.4 Diagnostics
The most recent echo 2 months ago showed a stable EF of 35%.
1.5 Assessment
Ms. Jones is having a mild acute chronic heart failure exacerbation with NYHA Class III symptoms complicated by an acute decrease in renal function with a rise from baseline creatinine from 1.2 to now 1.8 over the last 2 months. Her pro-BNP is also elevated much higher than baseline. On exam, she appears to have increased abdominal pressure and congestion which is likely causing diuretic resistance to her furosemide and associated lab fluctuations.
1.6 Plan
Change furosemide 80 mg BID to bumetanide 4 mg in the morning and 2 mg in the afternoon for the next week starting today. Repeat visit with BMP in 5–7 days. Call in 1–2 days if urinary output does not increase with medication change or if shortness of breath or swelling continues to worsen.
Check weight daily upon waking after emptying the bladder and before eating or drinking. Call for further weight gain of 2 lbs overnight or weight loss greater than 10 lbs in 1 week.
Resume a low sodium diet and reduce fluid intake to 1.5 L/day until symptoms improve.
Return to the clinic for a recheck of symptoms in about 1 week. Would consider the addition of an SGLT2 inhibitor at the next visit for heart failure, diabetes, and renal protective benefits and decrease bumetanide to 2 mg BID (once the goal is reached) with an additional 2 mg PRN for a weight gain of 2 lbs overnight or 5 lbs in 1 week.
1.7 Clinical Pearls
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Although this patient is experiencing acute symptoms of both cardiac and renal symptoms, she does not need to be treated as an inpatient or go to ER for IV diuretics unless oral medications do not help or symptoms worsen.
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Changing furosemide to bumetanide should improve diuretic resistance and drug absorption. Increasing the dose temporarily will also be beneficial.
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SGLT2 inhibitor benefits heart failure, diabetes, and renal function.
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Lab monitoring expectations—creatinine will likely rise slightly at the next visit from increased diuretic use, but symptoms and BNP should improve. Renal function will then return to baseline over the next few weeks. Would trend labs every 2 weeks. If creatinine does not return to baseline in the next 1–2 months would consider a nephrology referral.
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Monitor NT pro-BNP while taking sacubitril/valsartan.
Case Study 2: The Complex Interaction of CKD, HF, and Anemia
Subjective: Mr. Greene is a 55 year-old male with a past medical history/problem list: poorly controlled hypertension 20+ years; microscopic hematuria 10 years; nephrolithiasis; depression, obesity
Family history: Hypertension
Social history: Tool and dye maker. Divorced with 2 grown children. Denies current alcohol, tobacco, and illicit drug use. History of 1 ppd smoker for 30 years.
Medications: Lisinopril 20 mg daily, amlodipine 5 mg daily, hydrochlorothiazide 25 mg daily, sertraline 20 mg daily
Allergies: NKDA
1.1 Case Scenario
Chief complaint: Increased shortness of breath, swelling in ankles, and a metallic taste in the mouth for 2 months.
HPI: Since his last visit 9 months ago, the patient has noticed shortness of breath with walking short distances, swelling in the ankles, and a metallic taste in the mouth for about 2 months. He has checked his BP at home a couple of times and says it averages 150s/90s. He has also noted weight gain of about 15 lbs, bloating, and poor appetite. He states, “I just feel so tired all the time now.” He denies any missed doses of medications, lightheadedness, chest pain, or palpitations. No recent illness or hospitalizations.
1.2 Objective
Vital signs: BP 145/100; HR 102; oxygen saturation 96% on room air; Temp 98.0°. Weight 258 lbs
Physical exam: JVP elevated 12 cm; displaced apical beat (mid-axillary line); loud S3; lung fields clear, dull at both bases; liver edge 6 cm below costal margin; No ascites; 2+ Ankle edema
Labs: Serum creatinine 2.8 mg/dl; BUN 30; eGFR 26%; Potassium 4.0; Total CO2 28; Hemoglobin 10.3; (add diff showing anemia). Total cholesterol 216, LDL 146, triglycerides 362; fasting glucose 122; Albumin-creatinine ratio >300; Urinalysis 3+ protein, 5–10 rbc, No rbc cast–trace granular cast
No prior labs for comparison in the last 12 months.
Assessment: This patient has labs indicative of chronic renal insufficiency and anemia. He also has signs and symptoms of new-onset heart failure.
Plan: The patient needs an echocardiogram to better assess for LV dysfunction and referral to cardiology for management. He also needs a nephrology referral for CKD stage IV based on GFR. Would stop HCTZ and begin furosemide 80 mg BID for better diuresis. Would decrease lisinopril and begin hydralazine 100 mg TID for tighter BP control. Needs iron levels checked and replaced if indicated for anemia. Reduced sodium diet. A renal US for secondary hypertension workup and assessment of intrinsic kidney disease. Avoid nephrotoxins including NSAIDs.
1.3 Clinical Pearls
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Diuresis is less effective with low-dose thiazide-like diuretics alone in the setting of CKD; he will need a higher dose loop diuretic to break the threshold and begin diuresis.
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Current guidelines recommend reducing, not discontinuing ACE/ARB, with isolated elevated creatinine reading. Would add hydralazine for blood pressure coverage while further evaluation takes place. Would add isosorbide dinitrate if the echo reveals HFrEF.
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Stabilization including appropriate diagnosis of renal disease, aggressive HTN management, and fluid volume likely to improve cardiac symptoms and quality of life.
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Parker, M.M., Wigger, M. (2023). Cardiorenal Syndrome, Chronic Kidney Disease, Anemia, and Heart Failure. In: Hayes, K.M.S., Dellise, N.R. (eds) Managing Heart Failure in Primary Care: A Case Study Approach. Springer, Cham. https://doi.org/10.1007/978-3-031-20193-6_11
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