chronic kidney disease (CKD) and atrial fibrillation (AF)

In patients with chronic kidney disease (CKD), atrial fibrillation (AF) occurs frequently. The British physician Richard Bright first described the link between albuminuria in urine and kidney disease in 1827. For many years, kidney disease was called Bright’s disease. Currently, the prevalence of CKD ranges between 8% and 16%, rising to approximately 36% in individuals aged 64 and older. In South Korea, the prevalence of CKD is 13.8%.

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Atrial fibrillation is a common cardiac arrhythmia that ranges from harmless palpitations to severe complications like stroke and death.

Key Clinical Features of Atrial Fibrillation:

• ECG findings typical of AF
• Symptoms include palpitations and irregular heartbeats.

Causes of Atrial Fibrillation in CKD Patients

The occurrence of AF in CKD patients is multifactorial. The major contributing factors include inflammation, activation of the renin-angiotensin system (RAS), electrolyte imbalance, anemia, and uremia.

1. Inflammation
   • In CKD, inflammatory markers such as C-reactive protein, interleukin-6, and fibrinogen are elevated, increasing the risk of AF.
   • Activation of the NLRP3 inflammasome, a cytoplasmic protein complex triggered by cellular damage, induces inflammation. NLRP3 activation is also associated with reactive oxygen species (ROS), which can cause further cellular damage.
   • Systemic inflammation in CKD promotes atrial fibrosis, leading to the onset of AF.
2. Renin-Angiotensin System Activation
   • The renin-angiotensin system regulates water and sodium balance to maintain blood pressure.
   • Increased plasma renin leads to RAS activation, causing fluid overload and cardiac stress. This overload can impair cardiac structure and function, leading to AF.
3. Anemia
   • Anemia results in reduced oxygen delivery, which decreases myocardial activity. This can lead to impaired cardiac contraction and relaxation, causing a reduction in left ventricular afterload and subsequent risk of AF.
4. Calcium Deposition in Myocardium
   • In CKD patients, calcium may accumulate in myocardial cells, disrupting cellular function.
   • Prolonged calcium release from the sarcoplasmic reticulum increases the likelihood of AF.
5. Electrolyte Imbalance
   • Electrolyte imbalances, particularly hypokalemia, are common in CKD and contribute to the development of AF.

Key Studies Linking CKD and AF

1. Nelson et al. (2012)
   • Study Type: Retrospective cohort (Medicare)
   • Population: 55,962 participants
   • Focus: AF occurrence across CKD stages.
2. Watanabe et al. (2009)
   • Study Type: Prospective cohort (Japanese general population)
   • Population: 234,818 participants
   • Findings:
     • eGFR 30-50 ml/min: AF risk ratio 1.32 (1.08–1.62)
     • eGFR <30 ml/min: AF risk ratio 1.47 (0.89–2.77)
     • CKD in AF patients: Risk ratio for CKD development 1.77 (1.50–2.10)
     • Proteinuria in AF patients: Risk ratio 2.20 (1.92–2.52)
3. Piccini et al. (2013)
   • Study Type: Cohort (ROCKET trial data)
   • Population: 13,559 participants with non-valvular AF.
4. Guo et al. (2013)
   • Study Type: Cohort
   • Population: 617 participants
   • Findings: eGFR measured at baseline, 6 months, and 12 months to assess clinical outcomes like stroke, major bleeding, and mortality.
5. Airy et al. (2018)
   • Population: 62,459 CKD patients
   • Findings:
     • AF increased mortality risk by 23% (18–29%).
     • AF increased cardiovascular risk by 45% (31–61%).

(Source: Cureus, 2022;14(8): e27753)

Key Conclusions

1. The incidence of AF increases with CKD progression.
2. Renal dysfunction elevates AF risk, while AF can exacerbate CKD progression.
3. Impaired renal function is a strong predictor of stroke and systemic embolism.
4. Worsening kidney function increases the risk of stroke in AF patients.
5. CKD patients with AF face higher mortality and cardiovascular risks.