Association between AF and kidney disease
NIIGATA, JAPAN. The main function of the kidneys is to remove excess water and waste products from the blood. The kidneys process about 200 liters of blood and produce about 2 liters of urine every day. An indication of the health of the kidneys can be obtained by evaluating their filtration capacity. An estimated glomerular filtration rate (GFR) above 60 mL/min is usually considered a sign of good kidney function, while a rate below 45 mL/min may indicate chronic kidney failure (CKF). The calculation of GFR is primarily based on the serum creatinine level, but also takes into account results of urine tests, age, gender, and other factors. An adequate kidney function is particularly important for afibbers supplementing with potassium and magnesium since any excess of these vital electrolytes are excreted by the kidneys.

In 2008 Japanese researchers reported a significant inverse correlation between AF and GFR. Now another group of Japanese researchers from Niigata University reports that AF is associated with an increased risk of developing chronic kidney disease, while chronic kidney disease is associated with an increased risk of developing AF. Their study included over 220,000 individuals participating in the annual health examinations in the Niigata Association for Comprehensive Health Promotion and Research.

During a mean follow-up of 6 years (over 1 million person-years) 1.3% of participants developed afib. The incidence of afib was significantly higher in participants with a baseline GFR less than 60 mL/min per 1.73 sq m than in those with a higher GFR (0.52%/year vs. 0.22%/year). Similarly, during the same 6-year period, 3.3% of participants experienced a decline in kidney function. Among patients with no AF at baseline, the annual incidence of kidney disease was 0.68%, while among those with AF at baseline, it was 1.8%.

The researchers also noted that the development of proteinuria (protein in the urine, a common forerunner of kidney disease) was higher among participants with AF at baseline than in those without. For afibbers without hypertension or diabetes at baseline, the incidence of proteinuria was 2.5%/year as compared to only 0.8%/year in those without AF at baseline. The researchers conclude that systemic inflammation, oxidative stress and an overactive renin-angiotensin-aldosterone system (RAAS) may be common factors in the development of both AF and chronic kidney disease. They also point out that treatment with ACE inhibitors and angiotensin receptor blockers (ARBs) slows progression of kidney disease and reduces the risk of developing AF.

Watanabe, H, et al. Close bidirectional relationship between chronic kidney disease and atrial fibrillation. American Heart Journal, Vol. 158, October 2009, pp. 629-36

Editor's comment: The Japanese study, unfortunately, did not report the incidence of cardiovascular disease at baseline, so it is not possible to deduce whether the risk of developing kidney disease also applies to lone afibbers. However, since the suggested common risk factors systemic inflammation, oxidative stress and inappropriate RAAS activation likely also apply to LAF; it is possible that declining kidney function could accompany long-term LAF. Thus, it would be prudent to include a creatinine test and urine analysis in one's annual medical check-up. This would be particularly important for afibbers who rely on magnesium and potassium supplementation to keep their afib under control.

During the 14-year follow-up period, 747 women developed AF (94% lone AF). The researchers found a clear correlation between elevated inflammation markers at baseline and the risk of developing AF. Assigning 1 point each for CRP level above 3.4 mg/L (0.34 mg/dL), slCAM-1 level above 373 ng/mL, and fibrinogen level above 382 mg/dL, the researchers observed that women with 1 point had a 22% increased risk of developing AF compared to women with 0 points (none of the inflammation markers above the cut-off points). Women with a 2-point score had a 32% increased risk, and those with a 3-point score had a 59% increased risk after adjusting for possible confounding variables including smoking, blood pressure, body mass index, diabetes, hypercholesterolemia, exercise, alcohol consumption, and race/ethnicity. The actual number of newly diagnosed afibbers per 1000 person-years was 1.66 for an inflammation score of 0, 2.2 for a score of 1, 2.73 for a score of 2, and 3.25 for a score of 3.

The researchers conclude that, "markers of inflammation were independently associated with incident AF in initially healthy, middle-aged women, even after controlling for traditional risk factors. These findings suggest that inflammation may be involved in the pathogenesis of AF."
Conen, D, et al. A multimarker approach to assess the influence of inflammation on the incidence of atrial fibrillation in women. European Heart Journal, May 25, 2010 [Epub ahead of print]

Editor's comment: There is overwhelming evidence of an association between systemic inflammation and atrial fibrillation. The Harvard study clearly supports the hypothesis that inflammation causes AF rather than vice versa. Although this study in no way proves that existing afib can be reduced or eliminated by eliminating systemic inflammation, it certainly would be advisable to do so, preferably through the use of such natural anti-inflammatories as curcumin, bromelain, ginger, beta-sitosterol, boswellia, fish oil, Zyflamend or Moducare.