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Cardiorenal syndrome (CRS) describes a spectrum of disorders where acute or chronic dysfunction in the heart or kidneys leads to dysfunction in the other organ. This bidirectional relationship involves complex hemodynamic, neurohormonal, and inflammatory interactions, resulting in a vicious cycle of progressive organ damage.

Classification

CRS is classified into five subtypes based on the primary organ affected and disease acuity:

Type	Name	Primary Dysfunction	Secondary Dysfunction	Example
1	Acute cardiorenal	Acute heart injury	Acute kidney injury	Cardiogenic shock
2	Chronic cardiorenal	Chronic heart disease	Progressive CKD	Chronic heart failure
3	Acute renocardiac	Acute kidney injury	Acute heart injury	Post-glomerulonephritis arrhythmia
4	Chronic renocardiac	CKD	Chronic heart disease	LV hypertrophy in ESRD
5	Secondary CRS	Systemic disease	Combined heart-kidney dysfunction	Sepsis, diabetes, lupus

Pathophysiology

The mechanisms involve hemodynamic and non-hemodynamic factors:

• Hemodynamic: Reduced cardiac output and elevated central venous pressure impair renal perfusion, while kidney dysfunction exacerbates fluid retention and hypertension.
• Neurohormonal: Activation of the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system drives sodium retention, vasoconstriction, and inflammation.
• Inflammatory: Cytokines and oxidative stress contribute to endothelial dysfunction in both organs.

Clinical Features

Patients typically present with:

• Cardiac symptoms: Shortness of breath, peripheral edema, and fatigue.
• Renal symptoms: Elevated creatinine, reduced urine output, and electrolyte imbalances.
• Volume overload: Jugular venous distension, pulmonary congestion, and hypertension.

Risk Factors

Key predisposing conditions include:

• Pre-existing heart failure or chronic kidney disease.
• Diabetes mellitus, hypertension, and advanced age.
• Use of nephrotoxic drugs (e.g., NSAIDs) or cardiotoxic agents.

Management

Treatment focuses on breaking the cardiorenal cycle:

1. Volume control: Loop diuretics (e.g., furosemide) for fluid overload, with thiazides or ultrafiltration for refractory cases.
2. RAAS inhibition: ACE inhibitors/ARBs to reduce afterload and proteinuria, but requires careful monitoring in advanced CKD.
3. Inotropes: Dobutamine or milrinone in acute decompensated heart failure with low cardiac output.
4. Palliative care: For end-stage disease to manage symptoms and reduce hospitalisations.

Despite advances, CRS remains associated with high mortality due to the interplay of multi-organ dysfunction. Emerging therapies targeting inflammatory pathways and novel biomarkers for early detection are under investigation.

Citations:

1. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000664
2. https://www.ncbi.nlm.nih.gov/books/NBK542305/
3. https://www.ekjm.org/journal/view.php?number=25298
4. https://en.wikipedia.org/wiki/Cardiorenal_syndrome
5. https://synapse.koreamed.org/upload/synapsedata/pdfdata/0119jkma/jkma-63-20.pdf
6. https://journals.lww.com/cjasn/fulltext/2023/07000/cardiorenal_syndrome_in_the_hospital.16.aspx