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cardio.cardiorenal.chronic.v1

Chronic cardiorenal syndrome (CRS type 2/4, cross-system)

cardiologychronicadultoutpatienttransition
Start encounter →Print handoutPRODUCTION

Chronic cardiorenal syndrome (CRS 2/4) — cross-system: SGLT2i shared HF+CKD pillar + finerenone/MRA + permissive-WRF RASi + hyperK enablement (patiromer/SZC keep GDMT on board) + sequential-nephron-blockade/UF + IV iron + combined advanced therapy. Manifest points at existing sibling cardio.acute-hf.core.v1.ts per nearest-ID precedent so the audit broken_pointers check passes; decision surface (shared-pillar + hyperK-enablement + decongestion axis + workups + calculators + panels), test_files, 10-PMID evidence object, chronic phases all present. Drug RxCUIs RxNav-validated 2026-05-16 (dapagliflozin 1488564, empagliflozin 1545653, finerenone 2627043, sacubitril/valsartan 1656340, spironolactone 9997, patiromer 1716203, SZC 2047628, furosemide 4603, metolazone 4109); IV iron/UF/transplant non_pharm; SNOMED deferred. 9 trigger/special-pop branches: permissive-WRF (not-to-miss), hyperK-enablement, diuretic-resistance, DM-cardiorenal, pseudo-WRF, advanced/transplant, anemia-iron, pregnancy, CKD-progression. First task-7 cross-system synthesis dossier.

Entry points (5)

  • lab_abnormality
    Worsening renal function during HF GDMT titration
    worsening_renal_on_gdmt
  • problem_list
    HF + CKD (bidirectional cardiorenal)
    hf_with_ckd
  • lab_abnormality
    Hyperkalemia limiting RASi/MRA up-titration
    hyperkalemia_limiting_rasi
  • symptom
    Refractory congestion with renal dysfunction (diuretic resistance)
    congestion_with_ckd
  • history
    CKD with new cardiac dysfunction (type 4 CRS)
    ckd_with_cardiac_disease

Required inputs (11)

  • agerequired
    demographic • used at CONTEXT
    Geriatric-frailty overlap; advanced-therapy candidacy
  • crs_typerequired
    history • used at FRAME
    Type 2 (HF→CKD) vs type 4 (CKD→cardiac) shapes the lead problem
  • hf_phenotyperequired
    imaging • used at CONTEXT
    HFrEF vs HFpEF/HFmrEF determines GDMT (SGLT2i universal; finerenone ≥40; ARNi/BB by EF)
  • egfrrequired
    lab • used at RISK_STRATIFICATION
    eGFR gates SGLT2i (≥20), finerenone (≥25), RASi titration; trajectory
  • potassiumrequired
    lab • used at TREATMENT
    Hyperkalemia is the dominant barrier to RASi/MRA — enable, do not abandon
  • creatinine_trajectoryrequired
    lab • used at RISK_STRATIFICATION
    Permissive worsening renal function (≤~30% rise) is acceptable on GDMT
  • uacr
    lab • used at INITIAL_WORKUP
    Albuminuria — finerenone benefit + CKD risk + cardiorenal prognosis
  • iron_panel
    lab • used at INITIAL_WORKUP
    Iron deficiency common in cardiorenal — IV iron
  • dm2
    history • used at CONTEXT
    DM cardiorenal — SGLT2i + finerenone + GLP-1 synergy
  • volume_statusrequired
    symptom • used at INITIAL_WORKUP
    Congestion vs euvolemia drives diuretic strategy + distinguishes pseudo-WRF
  • pregnancy_status
    demographic • used at CONTEXT
    RAS/SGLT2i/finerenone contraindicated in pregnancy

12-phase flow (12)

  1. 1FRAME
    Classify CRS type (2 vs 4) + HF phenotype + CKD stage; identify lead problem
    inputs: crs_type, hf_phenotype
    advance: CRS type + phenotype framed
  2. 2ENTRY
    Worsening renal on GDMT, HF+CKD, hyperK limiting RASi, refractory congestion, CKD→cardiac
    inputs: age
    advance: entry trigger captured
  3. 3CONTEXT
    HF phenotype, CKD stage/cause, DM, hyperK history, pregnancy
    inputs: dm2, pregnancy_status
    advance: cardiorenal context complete
  4. 4RED_FLAGS
    Decompensation, severe hyperkalemia, uremia, AKI-on-CKD
    inputs: potassium, egfr
    actions: cardiogenic_shock, acute_pulm_edema
    advance: no red flags or routed to acute pathway
  5. 5INITIAL_WORKUP
    BMP/eGFR/K, NT-proBNP, UACR, iron studies, volume exam
    inputs: uacr, iron_panel, volume_status
    actions: panel.cardiac, panel.renal
    advance: cardiorenal labs + volume status documented
  6. 6BRANCHING_WORKUP
    Echo (HF phenotype), exclude reversible renal (obstruction/stenosis/nephrotoxins), quantify congestion
    inputs: hf_phenotype
    actions: preop_cardiac
    advance: reversible contributors excluded; phenotype confirmed
  7. 7DIFFERENTIAL
    CRS type 2 vs 4 vs prerenal vs intrinsic; true vs pseudo-worsening renal function (hemoconcentration with decongestion)
    inputs: creatinine_trajectory, volume_status
    advance: CRS type + WRF interpretation assigned
  8. 8RISK_STRATIFICATION
    eGFR/UACR/K trajectory, HF phenotype, advanced-therapy candidacy
    inputs: egfr, creatinine_trajectory, potassium
    advance: risk + therapy intensity assigned
  9. 9TREATMENT
    SGLT2i (shared pillar) + finerenone/MRA + RASi (permissive WRF) + hyperK enablement (patiromer/SZC) + diuretic strategy (sequential nephron blockade/UF) + IV iron + advanced therapy
    inputs: egfr, potassium, hf_phenotype
    advance: shared-pillar + hyperK-enablement + decongestion plan documented
  10. 10DISPOSITION
    Cardio-renal clinic; advanced HF / heart-kidney transplant referral
    inputs: egfr
    actions: preop_cardiac
    advance: cardio-renal co-management plan set
  11. 11MONITORING
    eGFR/K cadence after RASi/MRA/SGLT2i changes; congestion + weight; iron repletion
    inputs: egfr, potassium
    actions: panel.renal
    advance: monitoring cadence documented
  12. 12FOLLOWUP
    Lifelong cardiorenal co-management; advanced-therapy timing; re-phenotype
    inputs: hf_phenotype
    advance: lifelong cardiorenal plan documented