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 2 hours duration.
He rates the pain 10 out of 10 and he can't sit
still because the extreme discomfort from the pain.
He denies fevers, chills, he's had some nausea in 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 of the day.
On physical exam, it's notable for left CVA or
costocertebral angle tenderness to percussion
His labs showed normal electrolytes and his 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.
So 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 predispose patients to oxalate-based stones
Working outside in the heat is also gonna
predispose to stone formation due to dehydration
and CVA tenderness along with
hematuria, very suggestive of stone.
So our 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 and pelvis
and that's what 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 hyperdensity,
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
there is between men and women,
so about 13% in men and 5% in women.
The incidence is about 1 per 1000 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 US prevalence has increased in stones from 3.2% in
the late 1970s to about 8.8% in the first decade of the 2000
and that increas 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 the 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 the most common
and then there are 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.
Sol typically, calcium oxalate and calcium
phosphate make up 37% of all stones.
The next is calcium oxalate
making up 26% of stones,
and then followed by struvite
stones making up about 22% of stones.
Then finally, we have calcium phosphate at
7%, uric acid at 5% and then cysteine only at 2%.
So how do the kidney stones form?
It occurs when soluble materials
supersaturates in the urine.
So let's go through that a little bit more closely.
Free ion activities of the stone components
are gonna be affected by the following:
the crystal component concentration,
presence of inhibitors in the urine - these
are things like to treat which chelates calcium,
and the urinary pH.
High urinary pH may precipitate certain stone
types while a 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 joined together to form a stable solid phace and
when homogenous, that results in crystals or crystalluria.
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 formers.
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.