Evaluation and Management of Kidney Dysfunction in Advanced Heart Failure

Authors, Journal, Affiliations, Type, DOI

• Tang WHW (Vice Chair), Bakitas MA, Cheng XS, Fang JC, Fedson SE, Fiedler AG, Martens P, McCallum WI, Ogunniyi MO, Rangaswami J, Bansal N (Chair); on behalf of AHA Council on the Kidney in Cardiovascular Disease and multiple additional AHA councils
• Circulation, 2024;150:e280–e295
• Multi-institutional (Cleveland Clinic, Stanford Medicine, University of Washington, University of Utah, Tufts Medical Center, Emory University, UCSF, Washington DC VA, University of Alabama Birmingham)
• AHA Scientific Statement
• DOI: 10.1161/CIR.0000000000001273

Overview

This AHA Scientific Statement provides a comprehensive framework for evaluating and managing kidney dysfunction throughout the trajectory of advanced heart failure. It proposes a multi-domain kidney assessment model emphasizing reversibility testing, introduces the Heart-Kidney Profile classification (A/B/C) for clinical trajectory guidance, and details perioperative kidney management for both LVAD implantation and heart transplantation. Palliative care integration and shared decision-making are addressed for patients with concomitant advanced HF and kidney disease who are ineligible for surgical therapies.

Keywords

AHA Scientific Statements, heart failure, heart-assist devices, kidney diseases, kidney transplantation, renal replacement therapy

Key Takeaways

Conceptual Framework: Holistic Kidney Assessment

• eGFR via serum creatinine is unreliable in advanced HF due to sarcopenia (low muscle mass); cystatin C preferred where muscle mass is a concern; serum creatinine (not eGFR) preferred for day-to-day changes during hospitalisation
• Multi-domain assessment recommended: glomerular function, tubular function, endocrine function, solute/volume homeostasis, and reversibility potential
• Staged reversibility assessment: alleviate hemodynamic factors (congestion, kidney hypoperfusion, intra-abdominal hypertension) → objectively quantify kidney response in multiple domains
• Transkidney perfusion pressure (MAP − CVP) goal >60 mmHg as a reasonable hemodynamic target to optimise kidney perfusion
• Creatinine rise >1.5× baseline or >50% eGFR drop (especially with rising NT-proBNP or elevated lactate) → consider pulmonary artery catheter for hemodynamic profiling

Identifying Irreversible Intrinsic Kidney Disease

• Markers of irreversibility: microscopic hematuria, acanthocytes, cellular casts; proteinuria/albuminuria; echogenic kidneys with cortical thinning or small kidney size on ultrasound; kidney biopsy showing fibrosis/atrophy burden (invasive; weigh risk vs. benefit)
• Kidney venous flow ultrasonography may identify congestion-driven eGFR decline (venous congestion may have greater but reversible impact on eGFR than low cardiac output); not yet standard of care

Neurohormonal and Hemodynamic Reversible Dysfunction

• RAAS and sympathetic upregulation → eGFR decline, electrolyte disturbances, diuretic resistance
• BUN:creatinine elevation (via AVP-stimulated urea reabsorption) independently associated with higher mortality
• Hyponatremia and hypochloremia both independently predict adverse outcomes; hypochloremia → reduced chloride delivery to macula densa → juxtaglomerular renin release → worsens sodium retention
• Urinary sodium <50–70 mEq/L after loop diuretics = inadequate natriuresis / heightened sodium avidity
• Pharmacological eGFR decline with RAAS inhibitors or SGLT2i is paradoxically renoprotective (reduced intraglomerular pressure → attenuated nephron loss); do NOT discontinue GDMT solely for eGFR decline

Heart-Kidney (H-K) Profiles

• Profile A: No kidney dysfunction
• Profile B: Transient HF-related kidney dysfunction — reversible with hemodynamic and medical optimisation
• Profile C: Persistent kidney dysfunction despite vasoactive drugs or temporary MCS — requires kidney replacement therapy (KRT)
• Profile classification aids timely referral for appropriate medical or surgical treatment options

LVAD — Preoperative Kidney Considerations

• Preoperative kidney dysfunction strongly predicts: postoperative KRT need, post-LVAD mortality, thrombosis, bleeding, and infections
• Patients on chronic KRT before LVAD: median post-implantation survival ~3 weeks
• No validated protocol for pre-LVAD kidney optimisation; temporary MCS/inotropes/vasodilators to test reversibility is reasonable before LVAD in patients with questionable kidney function
• Key challenge: differentiating hemodynamic-driven dysfunction (potentially reversible) from irreversible nephron loss — significant inter-centre variability in tolerance of preoperative kidney dysfunction

LVAD — Post-implantation Kidney Outcomes

• INTERMACS data: early eGFR improvement in 85% of patients; sustained improvement in only 3.3%; sustained worsening in 10.1%
• AKI incidence: 11–45% post-LVAD; meta-analysis (n>63,000): 37%; 13% require KRT
• Younger patients in cardiogenic shock: more sustained kidney recovery (larger preserved nephron mass)
• RV failure prevention critical: target CVP <10–12 mmHg; up to 24% develop RV failure post-LVAD
• Perioperative AKI risk factors: cardiopulmonary bypass duration, bleeding/transfusion, intraoperative hypotension, RV failure, venous congestion, nephrotoxins, intra-abdominal hypertension

Dialysis Modalities in Advanced HF

• Hemodialysis: High ultrafiltration rates cause hemodynamic instability; platelet and endothelial dysfunction → paradoxical bleeding + thrombosis risk; central catheter infection risk; logistically challenging for LVAD patients (need for trained dialysis units); hemodynamic disturbance 3–4×/week
• Peritoneal dialysis: Preferred for LVAD patients — smaller hemodynamic shifts, no vascular access needed, no heparin, home-based, preserves residual kidney function, associated with hospitalization reduction in LVAD case reports; current-generation intrapericardial LVADs have lower peritonitis/driveline infection risk than earlier models
• Table 2 practical volume management options for advanced HF patients ineligible for surgical therapies: subcutaneous/IV loop diuretics, hemodialysis, or peritoneal dialysis — each with distinct advantages/disadvantages

Heart Transplantation — Kidney Considerations

• Screen all HTx candidates with eGFR <45 mL/min/1.73m² for simultaneous heart-kidney transplantation (sHKTx), especially with intrinsic kidney disease evidence
• UNOS threshold for sHKTx eligibility: eGFR ≤30 mL/min/1.73m²; eGFR fluctuation in advanced HF complicates accurate estimation → nephrologist–cardiologist co-evaluation essential
• Retrospective data: eGFR <30 or KRT-requiring → sHKTx superior survival vs HTx alone
• Post-HTx kidney failure requiring dialysis: 13.4% within 90 days; independent predictors include ECMO, IABP, ventilator use, longer ischemia time
• Delayed kidney graft function: 27–37%; primary kidney nonfunction: 14–33% in sHKTx recipients
• CNI nephrotoxicity: CNI-delaying induction protocols reasonable; long-term CNI minimisation recommended; avoid nephrotoxins and limit contrast (use PET for CAV surveillance instead of coronary angiography)
• Safety net policy: priority deceased donor kidney access for HTx recipients meeting KTx eligibility criteria at 60–365 days post-HTx; <10% of carefully selected sHKTx recipients experience kidney failure requiring KRT at 5 years

Palliative Care and Shared Decision-Making

• Early palliative care integration from the time of advanced HF + kidney disease diagnosis (COR 1)
• Core elements: patient/family engagement, information sharing, goals of care clarification, adaptation to social determinants of health
• Conservative non-dialysis approach ("conservative care" in nephrology) should be presented alongside intensive treatment options
• Decision aids specific to concomitant advanced HF + kidney disease do not yet exist — identified as a key research gap

Social Determinants and Health Equity

• Underrepresented races/ethnicities bear higher burden of chronic HF + CKD but receive fewer referrals to advanced HF/transplantation centres
• Race and gender bias results in delayed referral and lower acceptance into LVAD and HTx programs
• Interdisciplinary team-based approach may help address SDOH inequities

Limitations of the document

• Scientific statement; most evidence for specific management decisions is based on retrospective data, registry analyses, or small case series rather than RCTs
• No validated pre-LVAD kidney optimisation protocol exists; major inter-centre variability
• Kidney Failure Risk Equation and standard prediction models not validated in advanced HF
• sHKTx evidence predominantly retrospective; limited prospective data
• Decision aids specific to concomitant advanced HF + kidney disease absent from current practice
• Social equity interventions in this population understudied

Key Concepts Mentioned

• concepts/Cardiorenal-Syndrome — central pathophysiological framework for HF-kidney interaction
• concepts/HFpEF — context for kidney dysfunction in preserved EF HF

Key Entities Mentioned

• entities/Heart-Failure — primary disease context throughout

Wiki Pages Updated

• Created: wiki/sources/AKI-HF-AHA-2024.md
• Created: wiki/concepts/Cardiorenal-Syndrome.md
• Updated: wiki/entities/Heart-Failure.md — added Kidney Dysfunction in Advanced HF section
• Updated: wiki/wikiindex.md
• Updated: wiki/sourceindex.md