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Post-Renal Acute Renal Failure
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urological problem (not in the domain of the
nephrologists)
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before a patient can be declared to have post-renal
failure, the doctor must be certain that the patient is
not obstructed; imaging studies are used to rule out
obstruction. Imaging studies include:
o
renal ultrasound – sonogram of the kidney
§
first step to rule out obstructive nephropathy
§
non-invasive, simple, affordable, no contrast, no
ionizing radiation
§
good
for showing size and echogenicity of kidney (abnormal
echogenicity implies an intrinsic renal disease)
§
if
patient is obstructed because of retrograde pressure in
the kidney (problems with urine outflow), hydronephrosis
(dilation of the renal pelvis because of accumulation of
urine) can occur which is visible on ultrasound
§
on
rare occasions an obstructed pt can have a normal
ultrasound (think of specificity and sensitivity issues
related to this test)
o
catscan
o
intravenous urogram – very popular prior to sonography,
radiocontrast is injected into vein and pictures are
taken at various stages as dye is sequentially excreted;
because of exposure to contrast and ionizing radiation,
test is only occasionally done
o
retrograde pyelogram – purest test, urologist enters
bladder through cystoscope, option to put scope in one
or both of the ureters, and dye can be injected to
outline anatomy of urinary tract – this is gold standard
for obstruction, but catscans are more commonly used
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intra-renal obstruction can cause post-renal failure
(very rare)
o
intratubular crystals:
crystals aggregating in urinary tract cause obstruction
– can be in excretory tubing of collecting system or
microscopically seen within the kidney parenchyma
o
intratubular protein deposition:
there can also be an aggregation/deposition of abnormal
proteins as is seen in multiple myeloma
Pre-Renal Acute Renal
Failure
-
no
problem with kidney, problem with delivery of blood to
the kidney
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causes of pre-renal Acute Renal Failure:
o
decrease in effective circulating plasma volume (if pt
has CHF, liver disease)
o
decreased cardiac output
o
severe renal vasoconstriction (decreased renal blood
flow; occurs with administration of IV radiocontrast
material)
o
mechanical occlusion of renal arteries
o
other non-renal factors include:
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gastrointestinal bleeding
§
high
protein diet
·
patient on very high protein diet
à
urea nitrogen is fate of dietary protein
à
patient’s blood urea nitrogen (BUN) may rise; creatinine
can also rise with high protein diet, but BUN rises much
more: high BUN/creatinine ratio is a good
indicator of pre-renal Acute Renal Failure
o
BUN
is a lousy renal function test because urea is freely
diffusible across the nephron and creatinine is not, so
reasons for a high BUN/creatinine ratio include volume
depletion, high absorptive abilities, or high protein
diets – the ratio doesn’t necessarily mean a problem
with renal function (hence why it is a good indicator of
the pre-renal non-kidney type of Acute Renal Failure)
§
administration of corticosteroids
·
medications such as corticosteroids can also make BUN
rise (anabolic steroids build muscle, but
glucocorticoids used as anti-inflammatories are
catabolic, and BUN once again rises because of the
destroyed musculature)
§
hypercatabolism
·
patients with massive trauma and resultant injured
musculature and patients with sepsis (endogenous muscle
is metabolized at a high rate in sepsis) also have high
BUN levels
Intrinsic Acute Renal Failure
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post
strep glomeronephritis, vasculitis, lupus, interstitial
nephritis (common b/c of many medicines that are used),
Wegener’s are all diseases intrinsic to kidneys that can
lead to Acute Renal Failure
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tests that can be done to diagnose intrinsic Acute Renal
Failure:
o
urine sediment is very important to look at to diagnose
these diseases – if you see red blood cells and red
blood cell casts in urine, these are signs of glomerular
injury usually because of a proliferative nephritic
process
o
protein in the urine is also an important indicator of
renal disease
o
serological markers in blood – such as ANA, ANCA,
hepatitis serologies, etc can clue you in to systemic
diseases affecting the kidneys
- subtype of intrinsic Acute Renal Failure –
Acute Tubular Necrosis (Acute Tubular Necrosis)
§
used
synonymously with Acute Renal Failure because it’s so
common, especially in ICU and with very ill patients
because of various illnesses (hemodynamic instability,
volume depletion, sepsis, hypotension, nephrotoxic
antibiotics)
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good
news: it’s reversible
§
there are two types of Acute Tubular Necrosis: ischemic
and nephrotoxic
·
there are pathological differences between the two, one
involves the basement membrane of tubular cells while
the other does not
·
both
types have potential to get better, so the nephrologists
must shepherd patient from when he/she has no kidney
function until the time he may potentially get kidney
function back
§
urinalysis shows ‘muddy cast’ – somewhat
characteristic of acute tubular necrosis
More
about Acute Tubular Necrosis
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necrosis means cellular death, but in Acute Tubular
Necrosis serial biopsies late in the course of the
disease shows tubular regeneration
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common clinical scenarios in which Acute Tubular
Necrosis occurs: volume depletion, septic patients,
radiocontrast, rhabdomyolysis (destruction of muscle
cells due to trauma, hypokalemia, CO, severe respiratory
alkalosis, statin medications, and others), nepthrotoxic
medications (for severe sepsis, nephrotoxic
aminoglycoside antibiotics are given; for cancer,
nephrotoxic cisplatnim is given – sometimes, the
patient’s condition requires treatment with a
nephrotoxic medication, so it should be used as
carefully as possible)
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some
fast facts: proximal tubule cells become necrosed,
injury can be nephrotoxic or ischemic, histologic
findings include vacuolization of proximal tubule, brush
border cells are blunted/shorted, regeneration possible
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Acute Tubular Necrosis is diagnosed clinically –
biopsies only done when patients are not getting better
after several weeks of treatment
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