Uremic Cardiomyopathy

Synonyms:
Uremic heart disease, uremic myocardial disease

Etiology

(1) Causes
Chronic renal failure (CRF) stems from primary kidney diseases or systemic conditions like diabetic nephropathy, hypertensive nephrosclerosis, and rheumatic disorders, which concurrently damage the heart. Key contributing factors include:

1. Hemodynamic Factors: Volume overload, renal anemia, arteriovenous fistula, hypertension, and valvular lesions.
2. Non-Hemodynamic Factors: Ischemic heart disease, autonomic dysfunction, hypocalcemia, myocardial calcification, elevated PTH, metabolic acidosis, aluminum toxicity, β₂-microglobulin amyloidosis, vitamin B₁/carnitine deficiency, malnutrition, and infections.
3. Non-Uremic Factors: Age, smoking, hyperlipidemia, and genetics.

(2) Pathogenesis
The exact mechanism remains unclear but involves:

1. Toxin Accumulation: Urea, creatinine, and guanidine compounds impair myocardial energy metabolism, reducing contractility.
2. Lipid Dysregulation & Carnitine Deficiency: Elevated triglycerides/LDL and low HDL accelerate atherosclerosis and apoptosis. Carnitine deficiency disrupts fatty acid oxidation, worsening cardiac function.
3. Secondary Hyperparathyroidism (SHPT) & Calcium-Phosphorus Imbalance:
   • PTH promotes myocardial fibrosis and left ventricular hypertrophy (LVH) via calcium overload.
   • Vascular/valvular calcification restricts blood flow and causes arrhythmias.
4. Pressure/Volume Overload: Hypertension and anemia induce concentric LVH or ventricular dilation, impairing systolic/diastolic function.
5. Hemodialysis Toxicity: Inadequate toxin clearance (e.g., PTH, β₂-MG), carnitine loss, and acetate dialysate exacerbate myocardial injury.
6. Myocardial Ischemia: Even with normal coronaries (27% cases), anemia, tachycardia, and endothelial dysfunction reduce oxygen supply.
7. RAAS & Endothelin: Angiotensin II and aldosterone drive hypertrophy/fibrosis; endothelin elevates afterload.
8. Malnutrition & Anemia: Protein-energy wasting, infections, and micronutrient deficits (e.g., zinc, cobalt) worsen cardiomyopathy.

Pathology:

• Interstitial fibrosis dominates, with disproportionate collagen deposition versus cardiomyocyte loss.
• Common findings: Increased heart weight (men 96%, women 86%), LVH (66%), atherosclerosis (86%), pericardial effusion (31%), and valvular calcification (28%).

Symptoms

1. Congestive Heart Failure (CHF):
   • Present in 30–52.9% of end-stage renal disease (ESRD) patients, often fatal.
   • Manifestations: Edema, oliguria, dyspnea, and fatigue due to volume/pressure overload.
2. Arrhythmias:
   • Tachycardia, premature beats, or conduction blocks from electrolyte shifts or calcific conduction system damage.
3. Ischemic Injury:
   • Angina or infarction despite normal coronaries, driven by LVH-microvascular mismatch.
4. Anemia:
   • EPO deficiency leads to hemoglobin decline correlating with creatinine rise.
5. Other:
   • Valvular calcification (70%), infective endocarditis, pericarditis (7%), or thromboembolism.

Diagnosis: Clinical history of CRF with cardiac symptoms + imaging/lab confirmation.

Diet & Nursing

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Treatment

Multimodal Management:

• Nutrition: High-quality protein, essential amino acids, vitamins (B/C), and micronutrients. Restrict sodium/fluid for volume control.
• Metabolic Correction:
  • Lipid-lowering agents, anemia treatment (EPO/iron), and calcium-phosphate balance.
• Dialysis Optimization:
  • Adjust dialysate to minimize hypotension/carnitine loss.
• Comorbidity Control:
  • Tight BP management, infection prevention, and avoidance of nephrotoxic drugs.

Diagnostic Tests

1. Labs:
   • Normocytic anemia ↑ urea/creatinine/uric acid; metabolic acidosis; dyslipidemia (↑VLDL/LDL, ↓HDL).
   • Elevated PTH.
2. Imaging:
   • EKG: LVH/arrhythmias.
   • CXR: Cardiomegaly (CTR >60%), pulmonary congestion.
   • Echocardiogram: LV dilation (23%), systolic dysfunction (15%), valvular calcification.
   • Nuclear Imaging (99mTc-MIBI): Abnormal LHR/CMR ratios predict prognosis.
3. Biopsy:
   • Hypertrophy, fibrosis, calcification, or oxalate deposits.

Differential Diagnosis

1. Hypertensive Heart Disease: Early cardiac involvement + retinopathy/cerebrovascular disease. Echo shows less myocardial mass vs. uremic cardiomyopathy.
2. SLE/Amyloidosis: Systemic signs (e.g., fever, anti-nuclear antibodies) or organomegaly with amyloid deposits.
3. Primary Cardiomyopathy: No severe anemia/renal dysfunction; improves with heart failure therapy.

Complications

1. CHF: From hypertension, anemia, or pericarditis.
2. Arrhythmias: Due to fibrosis, electrolyte imbalances, or calcific conduction blocks.
3. Dialysis Hypotension: Impaired myocardial compensation during ultrafiltration.