Uremic Cardiomyopathy: Pathogenesis, Diagnosis and Treatment

I. Overview

Uremic cardiomyopathy refers to myocardial damage secondary to renal failure, predominantly caused by chronic kidney disease (CKD), though acute kidney injury may also contribute.

II. Etiology

While primary renal diseases initiate CKD, systemic conditions like diabetic nephropathy, hypertensive nephropathy, and rheumatic disease-related kidney injury concurrently damage the heart. Key pathogenic factors include:

1. Hemodynamic Factors

• Volume overload
• Renal anemia
• Arteriovenous fistula
• Hypertension
• Valvular disorders

2. Non-Hemodynamic Factors

• Ischemic heart disease
• Electrolyte imbalances (hypocalcemia, hyperparathyroidism)
• Metabolic acidosis
• Toxin accumulation (aluminum, β2-microglobulin amyloidosis)
• Nutritional deficiencies (vitamin B1, carnitine)

3. Non-Uremic Factors

• Aging, smoking, dyslipidemia, genetics

III. Clinical Manifestations

Cardiac complications manifest as:

1. Congestive Heart Failure (CHF)

Major causes: Hypertension, anemia, hypoalbuminemia, and fluid retention.
Symptoms: Edema, oliguria, dyspnea. CHF accounts for high mortality in end-stage renal disease (ESRD).

2. Arrhythmias

Driven by electrolyte disturbances or conduction system calcification. Common types: sinus tachycardia, premature contractions, heart block.

3. Ischemic Injury

Mismatched coronary perfusion leads to angina or infarction.

4. Severe Anemia

Linked to erythropoietin deficiency (Hb inversely correlates with creatinine).

5. Other Complications

• Valvular calcification (70% prevalence)
• Infective endocarditis
• Pericarditis (7%)

IV. Diagnostic Workup

1. Labs: Normocytic anemia, elevated BUN/creatinine, metabolic acidosis, hyperparathyroidism.
2. Imaging:
   • CXR: Cardiomegaly (CTR >60%), pulmonary congestion.
   • Echo: LV dilation, reduced EF.
   • Nuclear scan: Abnormal LHR/CMR ratios predict prognosis.
3. Biopsy: Myocyte hypertrophy, fibrosis, calcium/oxalate deposits.

V. Treatment Strategies

1. Heart Failure & Arrhythmias: ACE inhibitors reduce mortality; antiarrhythmics tailored to rhythm disturbances.
2. LV Hypertrophy Control: ACEi/CCBs to reverse fibrosis.
3. Dialysis: Removes uremic toxins, corrects fluid/electrolyte imbalances. Initiate early if cardiac dysfunction appears.
4. Mineral Bone Disease: Phosphate binders, vitamin D analogs to lower PTH.
5. Anemia Management: Erythropoiesis-stimulating agents (ESAs) improve cardiac output.
6. Transplantation: Definite cure; reverses cardiac remodeling when dialysis fails.