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hello and welcome back to the nephrology
curriculum
today we're going to be talking about
nephrolithiasis or stones
so let's start out with a clinical case
a 44 year old gentleman
is seen in the emergency department for
acute onset left sided flank pain of two
hours duration
he rates the pain 10 out of 10 and he
can't sit still because of extreme
discomfort from the pain
hidden eyes fevers chills he's had some
nausea and association with the pain but
no diarrhea or other systemic symptoms
he does note taking high-dose vitamin c
supplements to prevent colds
and he drinks several glasses of iced
tea daily given that he's working
outside
in the heat as a construction manager
for several hours out of the day
on physical exam it's notable for left
cva or costo vertebral angle tenderness
to percussion
his labs show normal electrolytes and as
urine analysis shows greater than 40 red
blood cells per high power field
so the question is what is our next step
to diagnosing this gentleman
let's go back through our clinical
history and see if we've got some clues
he's complaining of acute onset of
colicky pain
that's very suggestive of a ureteral
stone
interestingly he's also taking very high
dose vitamin c and iced tea
both predisposed patients to
oxalate-based stones
working outside in the heat is also
going to predispose to stone formation
due to dehydration
and cba tenderness along with hematuria
very suggestive of stone
so our next step we want to image the
patient and see if in fact he does have
a stone
so that's exactly what we do we obtain a
ct non-contrast of the abdomen pelvis
and that's what's shown here in this
particular image this is an axial
section taken right through the kidneys
and you can see that arrow is pointing
in the left kidney to a bright hyper
density
that in fact is a stone
so the question is what is the etiology
of this patient's presentation
it's a stone so this patient has
nephrolithiasis
so let's talk a little bit more about
stones
stones are common in industrialized
nations
the lifetime risk of forming stones
varies between men and women so about
thirteen percent in men
and five percent in women the incidence
is about
one per one thousand persons per annum
and the peak incidence typically occurs
in the third and fourth decade of life
and increases with age until about 60 to
70 years
the u.s prevalence has increased in
stones
from 3.2 percent in the late 1970s to
about 8.8 percent in the first decade of
the 2000
and that increase in prevalence really
moves from the north to the south
so may have something to do with the
hotter climate
white populations are greater in terms
of stone formation than non-whites
stone types can also vary depending on
geographic location
for example in the mediterranean or
middle east
we typically will manifest with uric
acid stones
in the united states calcium oxalate or
calcium phosphate are most common
in the united kingdom magnesium ammonium
phosphate or struvite stones are most
common
and then there's cysteine stones which
are actually quite rare
if we look at the distribution by stone
type you can see in this pie chart
that clearly calcium based stones are
the highest
so typically calcium oxalate and calcium
phosphate make up
37 of all stones the next is calcium
oxalate making up 26 percent of stones
and then followed by struvite stones
making up about 22 percent of stones
then finally we have calcium phosphate
at seven percent uric acid at five
percent
and then cysteine only at two percent
so how do kidney stones form it occurs
when soluble material
super saturates in the urine
so let's go through that a little bit
more closely
free ion activities of a stone
components are going to be affected by
the following
the crystal component concentration
presence of inhibitors in the urine
these are things like citrate which
chelates calcium
and the urinary ph high urinary ph
may precipitate certain stone types
while low urinary ph precipitates others
the level of chemical free ion activity
where stones will neither grow nor
dissolve
is referred to as the equilibrium
solubility product
urine becomes supersaturated above that
level
and when that happens any stone present
is going to grow
in size how exactly does that happen
ions join together to form a stable
solid phase
and when homogeneous that results in
crystals or crystal urea
calcium oxalate crystals attach to
something called randall's plaques these
are plaques or areas of calcium
phosphate deposits in the renal papillae
shown here in the image on the right
when they do that it promotes stone
growth
and finally we have genetic
polymorphisms that are associated with
stone farmers
these are genes that code for proteins
that regulate tubular calcium and
phosphate reabsorption
proteins that prevent calcium salt
precipitation
or aquaporins in the proximal tubule
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