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Living Donor Research Living Donor Risks Living Kidney Donor

How Many Living Kidney Donors Were Obese Pre-Donation?

47,705 adult living kidney donors as reported to OPTN from 1999 to 2011 were analyzed using their pre-donation BMI (body mass index)

  • 35.6% were normal weight.
  • 40.5% were overweight
  • 18.9% were mildly obese
  • 4.2% were moderate to morbidly obese
  • Overweight and mildly obese kidney donors have increased through time by 12% and 20% every 5 years, respectively
  • 63.6% of living kidney donors over the past thirteen years have spanned the overweight to obese categories

 

According to OPTN guidelines, having a BMI greater than 35 kg/m2 is considered a relative contraindication to be a living kidney donor. However, based on a 2007 survey, 20% of transplant centers surveyed excluded those with BMI greater than 40 kg/m2 , 52% excluded donors with BMI greater than 35 kg/m2 , 10% excluded those with BMI over 30 kg/m2 , 12% percent had no policy for exclusion, and 6% excluded based on BMI if they had other cardiovascular risks.

  • Short term outcomes of obese living kidney donors have shown increased wound related complications and longer operative times
  • At five year follow up, Kramer et al found that overweight and obese individuals had 20% and 40% risk of developing chronic kidney disease.
  • Having a higher baseline BMI can serve as an independent risk factor for end stage kidney disease.
  • The long term effects of obesity on the solitary kidney of a kidney donor are still uncertain. This risk factor increases the risk of developing other co-morbid conditions such as diabetes mellitus, hypertension, or even proteinuria which can together compromise the function of their solitary kidney
  • At a mean of 11 year follow up, obese donors had an increased risk of developing hypertension and dyslipidemia.

 

Read the entire article at the link (above). Take care of yourselves.

 
Sachdeva, M. (2015). Weight trends in United States living kidney donors: Analysis of the UNOS database World Journal of Transplantation, 5 (3) DOI: 10.5500/wjt.v5.i3.137

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Living Donor Risks Living Kidney Donor

Anemia and Kidney Function

A living kidney donor recently asked me if there was a connection between kidney donation and anemia. Because I’m not a walking encyclopedia, I put my google-fu to work and learned a lot along the way.

An analysis of NHANES III found that a GFR <60 was associated with a lower hemoglobin level and a higher prevalence of anemia.

(Note:Hemoglobin is the part of the red blood cell that carries iron and helps transport oxygen throughout the body.)

“The prevalence of anemia was 1.8% among those with an estimated GFR of 90 or higher, compared with 5.2% among those with an estimated GFR between 30 and 59, and 44.1% among those with an estimated GFR between 15 and 29.”

“Non-Hispanic black persons had a lower mean hemoglobin level than non-Hispanic white persons. Older age, female sex, and elevated CRP [C-reactive protein] level were also significantly associated with lower hemoglobin levels.”

This article has multiple tables and figures; go check them out.

 

A study of 5222 folks diagnosed with chronic kidney disease but not yet on dialysis (meaning they have not yet progressed to end-stage renal disease) found a higher prevalence of anemia as GFR declines.

“Percentage of patients with hemoglobin less than or equal to 12 g/dL [the cut-off for an anemia diagnosis] increased from 26.7% to 75.5% when glomerular filtration rate decreased from greater than or equal to 60 to < 15.”

“Prevalence of hemoglobin less than or equal to 10 g/dL increased substantially from 5.2% to 27.2% when glomerular filtration rate diminished from 60 to < 15.”

“Anemia was present in 47.7% of 5222 predialysis patients with chronic kidney disease”

 

Nurko states that most people “with chronic kidney disease eventually become anemic”.

“Factors likely contributing to anemia in chronic kidney disease include blood loss, shortened red cell life span, vitamin deficiencies, the “uremic milieu,” erythropoietin (EPO) deficiency, iron deficiency, and inflammation.”

“Deficiency of erythropoietin is the primary cause of anemia in chronic renal failure, but it is not the only cause. A minimal workup is necessary to rule out iron deficiency and other cell-line abnormalities.”

Erythropoietin is a protein excreted by the kidneys (yet another thing potential living kidney donors aren’t told prior to donating) which promotes the formation of red blood cells by the bone marrow. The kidney cells responsible for making erythropoietin are sensitive to oxygen levels in the blood, releasing erythropoietin when they drop too low. Red blood cells, as well, carry oxygen.

“Researchers postulate that the specialized peritubular cells that produce EPO are partially or completely depleted or injured as renal disease progresses, so that EPO production is inappropriately low relative to the degree of anemia”

 

“The consensus is that untreated anemia contributes to the large cardiovascular disease burden in [the CKD} population.”

“Left ventricular hypertrophy is closely linked to chronic kidney disease. The estimated prevalence in stage 3 and 4 is 39%, and it is even higher in patients with lower renal function”

If iron supplements don’t correct the issue, this author recommends the addition of an erythropoiesis-stimulating agent (ESA). “Studies suggest that treating anemia with a goal of raising the hematocrit to at least 36% improves quality of life, decreases the need for transfusions, improves muscle strength and cognitive function, and decreases rates of hospitalization and death”

Take care of yourself!

Categories
Informed Consent Living Donor Research Living Donor Risks Living Kidney Donor

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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Living Donor Research Living Donor Risks Living Kidney Donor

Living Kidney Donors Experience 37 Heart Changes After Donation

You’ve heard me harp on this before. How a 10% reduction in kidney function significantly increases the risk of cardiovacular disease and death. How most people who are diagnosed in with early stage CKD (chronic kidney disease), GFR 60-80, will die of a cardiovascular event before progressing to kidney failure. How 26% of kidney failure is due to hypertension, etc. etc.

Well.

Moody et. al. have found that only 12 months post-donation, living kidney donors experience 37 different cardiovascular changes. (yes, as compared to controls; see Figures 1 & 2 at the link)

The short version:

 

A modest reduction in GFR causes increased Left Ventricular mass, Left Ventricular systolic dysfunction, increased aortic stiffness and adverse changes to CV (cardiovascular) biomarkers. Reduced GFR should be regarded as an independent causative CV risk factor.

 

Below is one table from the study (click for full size). The other is too small to read, and can’t be accessed without a subscription.

 

moody-biochemical effects reduced GFR 2015

 

If you’re interested, you can read Moody’s rationale and design of the EARNEST study in The American Heart Journal from February 2014.

 

 

 

 

 

Moody, W., Ferro, C., Edwards, N., Chue, C., Lin, E., Cockwell, P., Steeds, R., Townend, J., & Taylor, R. (2015). 37 Cardiovascular Effects of Unilateral Nephrectomy in Human Kidney Donors Heart, 101 (Suppl 4) DOI: 10.1136/heartjnl-2015-308066.37

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Living Donor Research Living Donor Risks Living Kidney Donor

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