Farron Dozier aka I AM WDC aka WHATZ DA COUNT featured in this magazine for Sickle Cell Awareness Month 2015. #WDCRADIO #sicklecelltrait #whatzdacount
http://issuu.com/f.u.s.e./docs/final_september_issue

  • The Sports Lounge Live http://americatalklive.com/the-sports-lounge-live

  • WDC Radio Show http://americatalklive.com/wdc-radio-w-farron-dozier/

  • WDC DA MOVEMENT www.blogtalkradio.com/wdcdamovement

I am focusing on trait bc of my kids. They tend to act as if their ignoring me but I think THESE DEATHS AT AN ALARMINGLY FAST RATE BC OF SCD...YEA IT SHOOK US ALLL

@iamwdc has an awesome page that is focused on his life with trait...WDCONSCT.ORG so I suggest you go there to research. ‪#‎KNOWLEDGEISPOWER‬

IF YOU DON'T KNOW FARRON THEN LET ME BEGIN BY SAYING THIS...HE'S NOT AFRAID TO SPEAKUP FOR "ANYONE" IN NEED! I APPROACHED HIM BECAUSE OF HIS VAST KNOWLEDGE ABOUT SICKLE CELL TRAIT! HE WILL MOST DEFINITELY OPEN SOME EYES AND SAVE SOME LIVES...WELCOME HIM!!

Sickle Cell 'Trait' Linked to Chronic Kidney Disease: Just a single copy of the sickle cell gene may affect kidney function

Rakhi P. Naik, M.D.

Credit: JohnsHopkins MedicineSickle cell trait (SCT), an inherited condition
marked by having a single copy of the sickle
cell gene but not the two copies needed to
cause sickle cell disease (SCD), may raise the
risk of chronic kidney disease, according to
results of a large study led by researchers
from Johns Hopkins, the University of North
Carolina at Chapel Hill, the University of
Mississippi Medical Center, the Fred
Hutchinson Cancer Research Center and the
University of Washington School of Public
Health.

The finding may help explain some of the
disparity in rates of chronic kidney disease
between African-Americans — who account
for the vast majority of those with SCD and
SCT — and whites, the researchers say. And it
may eventually lead to new ways to prevent
this kidney disorder in susceptible
populations.

About 8 to 10 percent of African-Americans
have SCT, meaning they have inherited one
copy of the sickle cell gene from either parent;
other racial and ethnic groups carry this gene
mutation, but to far lesser extents. SCD, which
requires two copies of the gene — one from
each parent — causes red blood cells to
“sickle” or bend, creating anemia and often
extremely painful sickling “crises,” when the
misshapen blood cells become lodged in
small blood vessels.

The mutated gene is thought to have
developed in parts of the world where malaria
is endemic, as it offers some protection
against that disease. According to Rakhi P.
Naik, M.D., assistant professor of medicine in
the Division of Adult Hematology in the Johns
Hopkins University School of Medicine and
one of the study’s leaders, researchers have
begun to recognize a host of problems that
may accompany even a single copy of the
gene, or SCT, ranging from increased risk of
blood clots to sudden death.

Because researchers had previously linked
blood in the urine and kidney vessel damage
to SCT, Naik, along with Alexander P. Reiner,
M.D., an epidemiologist at Fred Hutchinson
Cancer Center and professor in the
Department of Epidemiology at the University
of Washington School of Public Health, and
their colleagues investigated whether SCT
might also play a role in chronic kidney
disease.

In the new research, they used data from five
large studies that followed populations of
adults over time: the Atherosclerosis Risk in
Communities Study, which ran from 1987 to
2013; the Jackson Heart Study, which ran
from 2000 to 2012; the Coronary Artery Risk
Development in Young Adults Study, which
ran from 1985 to 2006; the Multi-Ethnic Study
of Atherosclerosis, which ran from 2000 to
2012; and the Women’s Health Initiative,
which ran from 1993 to 2012.
Although the overarching purpose of these
studies was to better understand risk factors
for cardiovascular disease, the investigators
also collected other health data from
participants, including kidney function and
genetic information.

Mining this wealth of data, the researchers
carved out information on 15,975 self-identified African-American participants,
1,248 with SCT and the rest noncarriers of the
sickle gene. They looked specifically at how
many members of each group had developed
chronic kidney disease or other markers of
impaired kidney function, including poor
ability to filter blood through the kidneys and
the presence of protein in urine.

Their results, published in the Nov. 13 JAMA,
showed that the incidence of chronic kidney
disease was significantly higher in those with
SCT than in noncarriers: about 20.7 percent in
those with the trait, versus 13.7 percent of
those without it. The SCT carriers — who can
pass the gene on to offspring — were also
more likely to have impaired ability to filter
blood through the kidneys and to have protein
in their urine.

The researchers hypothesize that although
blood cells are less likely to sickle — or warp
into a sickle shape — as severely or frequently
in individuals with SCT as they do in patients
with SCD, they can still experience infrequent
and localized sickling that might affect certain
organs more than others, clogging blood
vessels and restricting oxygen to these areas.
This mild sickling may be enough to
eventually damage the kidneys, they say,
leading to chronic kidney disease and other
kidney problems.

Though variants in a gene named APOL1 have
recently been linked with increasing chronic
kidney disease risk, Naik says, it only explains
part of the risk in African-Americans, and it
cannot solely account for the high disparity of
chronic kidney disease between African-Americans and whites.

“Finding that SCT can influence kidney
disease is another piece of the puzzle to
explaining the higher risk of chronic kidney
disease in African-Americans,” she says.

“These findings may have implications for
more closely monitoring kidney function in
SCT carriers. The findings also highlight the
importance of large, population-based studies
to define the health consequences of SCT,”