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Cardiovascular Changes in Living Kidney Donors After 12 Months

The data continues to mount.


“We hypothesized that the reduction in GFR in living kidney donors is associated with increased left ventricular mass, impaired left ventricular function, and increased aortic stiffness.”

” At 12 months, the decrease in isotopic GFR in donors was -30±12 . In donors compared with controls, there were significant increases in left ventricular mass (+7±10 versus -3±8 g/mL) and mass:volume ratio (+0.06±0.12 versus -0.01±0.09 g/mL), whereas aortic distensibility (-0.29±1.38 versus +0.28±0.79×10-3 mmHg-1) and global circumferential strain decreased (-1.1±3.8 versus +0.4±2.4%). Donors had greater risks of developing detectable highly sensitive troponin T and microalbuminuria. Serum uric acid, parathyroid hormone, fibroblast growth factor-23, and high-sensitivity C-reactive protein all increased significantly. ”

These findings suggest that reduced GFR should be regarded as an independent causative cardiovascular risk factor.


Moody, W., Ferro, C., Edwards, N., Chue, C., Lin, E., Taylor, R., Cockwell, P., Steeds, R., & Townend, J. (2016). Cardiovascular Effects of Unilateral Nephrectomy in Living Kidney Donors Hypertension DOI: 10.1161/HYPERTENSIONAHA.115.06608

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Cardiovascular Changes Shown in Living Kidney Donors

It’s well established that a reduction in kidney function (GFR) significantly increases one’s risk of cardiovascular disease and death. It’s all known that folks in all stages of chronic kidney disease are at risk for heart troubles.

Finally, a few researchers got together and decided to look at how living kidney donor’s hearts change post-nephrectomy.


“We hypothesised that the reduction in GFR associated with nephrectomy causes increased left ventricular (LV) mass, impaired LV function and increased aortic stiffness.”


“Compared to controls, nephrectomy in donors was associated with increases in [left ventricular] mass ; [left ventricular] mass-volume ratio and [carotid-femoral pulse wave velocity] PWV ; and reductions in aortic distensibility [flexibiity; ie. more stiffness] and global circumferential strain”


“Change in GFR independently predicted the change in LV mass (R2=0.26; P<0.01).”


“Nephrectomy causes concentric LV remodelling and dysfunction, increased aortic stiffness and adverse changes in[cardiovascular]  CV biomarkers. These findings suggest reduced GFR is an independent causative CV risk factor and that donors should be under long-term CV review.”

Moody, W., Ferro, C., Edwards, N., Chue, C., Lin, E., Taylor, R., Cockwell, P., Steeds, R., & Townend, J. (2015). EFFECTS OF NEPHRECTOMY ON CARDIOVASCULAR STRUCTURE AND FUNCTION IN LIVING KIDNEY DONORS Journal of the American College of Cardiology, 65 (10) DOI: 10.1016/S0735-1097(15)62150-7

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Arterial Stiffness and Hyperfiltration

After a kidney is removed, the remaining kidney often adapts (NEVER grows) to compensate for the missing nephrons. This process is known as hyperfiltration or hypertrophy.

One of the problems with hyperfiltration is that no one knows exactly how much function someone’s remaining kidney will pick up. That’s why we talk about losing 20-40% of pre-donation function or regaining approximately 70% of pre-donation function. No one knows for sure, and there is no guarantee (We do know, however, that folks over 50 years of age tend to hyperfiltrate less, as do folks with high pre-donation BMI).


These researchers looked at pre-donation blood pressure and two measures of arterial stiffness for their effect on hyperfiltration. They found that blood pressure seemed not to be a significant factor, but greater arterial stiffness resulted in less post-donation hyperfiltration.

Arterial stiffness refers to the elasticity of the arteries. Arteries, of course, being the blood vessels that deliver the blood away from the heart. Stiffness (lack of elasticity) is strongly related to strokes or other cardiovascular events.


Since potential kidney donors aren’t tested for arterial stiffness during their evaluation, I don’t know if this information will have much short-term impact. Hopefully, other researchers will expand on these results.


For more on arterial stiffness:


Aortic Stiffness: Current Understanding and Future Directions – 2011

Role of arterial stiffness in cardiovascular disease – 2012


Fesler P, Mourad G, du Cailar G, Ribstein J, & Mimran A (2015). Arterial stiffness : an independent determinant of adaptive glomerular hyperfiltration after kidney donation. American journal of physiology. Renal physiology PMID: 25568135

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Urine Toxins Related to Heart Disease Found in Living Kidney Donors

Indoxyl Sulfate (IS) and p-cresyl sulfate (PCS) are two toxins that accumulate in the urine of folks with impaired renal function, and may contribute to the development of cardiovascular disease.

Rossi et al. found a significant and sustained increase in both IS and PCS in living kidney donors two years post-donation. The levels of these toxins were associated with other markers of cardiovascular disease. They were also found to be predictors of reduced kidney function from pre-donation levels.

Read here: