Buying and selling of Kidneys for transplant: The biggest ethical question in nephrology.


In India kidneys are widely available for purchse. This allows people with the means to get a kidney. The people with the means include Americans and Europeans as transplant tourists. organ tours.

JAMA published an article in 2002 showed that most of the donors are poor people in debt and a few years later they are still or again in debt and have experienced a decline in health. An essay in Lancet the following years details the global organ traffic and some of its negative consequences.

Despite these horrors they abysmal supply of organs makes the concept of buying and selling organs appealing. I have confidence that a well regulated market place for organs could improve the supply and avoid the horrors which result from the under-the-table, unregulated bazaar that currently exists.

Sally Satel outlines the pro argument in a couple of essays.

Giving patients good news

I was rounding at one of the rehab/sub-acute hospitals today. One of the patients was a 70 y.o. African American man who had undergone a kidney transplant 12 days ago. He had delayed graft function and so he had continued right along with his normal dialysis schedule. He had been on dialysis for 3 years.

Over the week-end, his kidney opened up (recovered renal function in his transplant kidney) and so we held his dialysis on Sunday (patients on the TTS schedule received the Saturday dialysis on Sunday due to a Thanksgiving schedule shift). Today his creatinine fell further and I told him he was done with dialysis.

He immediately began to cry and convulse. I wasn’t sure if these were tears of joy or a seizure. After a few minutes he was able to speak again and told me how happy and grateful he was to be off dialysis.

It was one of those moments the makes being a doctor special.

Renal Week 2008: CVD and CKD: Case 7

66 yo woman with ESRD due to analgesic nephropathy. Hx of Crohn’s Disease. Extended criteria deceased donor allograft transplant 1.5 yrs ago.

Now SBP of 160.

Next Speaker Ojo. Greatest name in Nephrology.

CVD and CKD in Transplantation

Progressive reduction of acute rejection since 2000 from 17.4 to 10.3% at one year. This should improve outcome of graft and patient; however post-transplant life-span has decreased from 14 in 1995 to 12.7 in ’06.

CVD is the explanation for this conundrum.

After the first year the most common cause of loss of graft is: death with a functioning graft (56%). This is twice as common as number 2, chronic rejection (21%).

43.5% die of CVD.

Hypertension, DM, hypercholesterolemia, obesity, and anemia are all more prevalent in transplant patients than transplant candidates or prevalent dialysis patients.

Focus on immunosupressant drugs

  • In HIV patients with lower cd4 have higher higher CVD death rate
  • Same relationship of CD4 to CVD is seen in patients with radiation exposure (Hiroshima) causing lower cd4 counts
  • also seen in transplant patients.

Rabbit data showing that increased cholesterol plaques with concurrent CSA, without change in lipid profile. Roselaar jci 1995 96 1389.

Steroids are dangerous even at low doses in the normal population.

CSA increase BP.

CSA also causes endothelial dysfunction.

Sirolimus is antiatherogenic, as seen in cardiac stents.
MMF also appears to reduce cholesterol plaque Romero Atherosclerosis 2000: 152:127-133.

Cr alone is a predictor of CVD independent of immunosupression and traditional risk factors.

Journal Club: Campath and ACE/ARB and AKI in CABG

The first article was an analysis of campath for induction with tacrolimus.

Patients were randomized to either

  • Methylpred 250 mg and Campath 20 mg immediately following surgery followed by Tacrolimus Group
  • Tacrolimus, prednisone, and MMF (no induction therapy)

Primary outcome was biopsy proven rejection at 6 months.
Secondary outcome was biopsy-proven rejection at 12 months, time to first rejection, patient and graft survival, incidence of corticosteroid resistant rejection.

n= 131 deceased donor, kidney transplant in patients with PRA ≤ 25%. All patients were receiving their first kidney. Age 18-65.


No episodes of humoral rejection was found in either group.

The figure above I think is particularly informative as it becomes obvious that all the difference is in the first month. This is a study of induction vs. no induction and they demonstrate a huge reduction in early rejection with induction.

Big picture: large reduction early reduction but no difference in serum creatinine at one year.

The second article was a retrospective analysis of the risk of acute kidney injury based the presence or absence of ACEi/ARB.

A VA study looking at chronic use of ACEi or ARB and the risk of acute kidney injury following cardiovascular surgery. SUNY Buffalo looked at 1,358 patients with CV surgery from 2001-2005. 50% were on ACE/ARB

  • 40% had AKI (essentialy all Modified RIFLE: Stage 1, Cr rise ≥0.3 or 50-100%)
  • 7 patients Stage 2 (Cr rise 2-3x the baseline)
  • 2 patients Stage 3 (Cr greater than 4 or >3x the baseline)

They found that use of ACEi/ARB had a 27.6% increase in risk of AKI.

Of note 18% of the patients who had AKI, their creatinine had not returned to baseline at 3 months post surgery and still qualified as AKI. This does not jive with the natural history of AKI, especialy relatively mild AKI. This makes me wonder if the baseline creatinine were abnormally low in some of the patients and the increase documented was not AKI but actually resolution of the creatine falling.

The primary concearn I have is that the study had 543 patients with AKI and only 9 had more than a doubling of creatinine. They used a very sensitive definition of AKI and like any test, when you increase the sensitivity you decrease the specificity. It is very possible that a large proportion of those patients defined as AKI didn’t actually have AKI, throwing the study into doubt.