< Brief History
>
A 64-year-old man, a chronic
smoker, was admitted because of a worsening renal function. He
had had type 2 diabetes mellitus for 15 years. Usually, his
blood glucose levels before and after meals were around 130
and 200 mg/dl, respectively. The hemoglobin A1c (HbA1c) was
around 8%. He also had had hypertension for 10 years which had
been well-controlled with an angiotensin II receptor blocker.
Since 6 months earlier before this admission, he started to
develop exertional dyspnea, chest tightness or pain which
might radiate to the jaw or left shoulder. These symptoms
could be relieved by immediate resting. He visited another
hospital where nitroglycerin was prescribed. Three weeks prior
to admission, he experienced a sudden onset of chest pain with
cold sweating which could not be relieved by nitroglycerin.
Acute coronary syndrome was diagnosed at the emergency room,
and percutaneous balloon angioplasty with stenting was
performed immediately. During hospitalization, right flank
pain developed and one episode of microscopic hematuria was
detected by urine analysis. Two weeks after catheterization,
he was discharged. However, three more weeks after discharge,
worsening of renal function was detected. On admission,
physical examination showed a man of 167 cm in height and 60
kg in weight. His temperature was 37.2 oC, blood pressure
132/86 mmHg, and pulse rate 82 beats per minute. A systolic
murmur was heard over the cardiac apex, but there were no
obvious abdominal bruits in the periumbilical and back area.
The pulses in the four limbs were palpable, and there was no
blood pressure discrepancy between them. The other
examinations were unremarkable. Chest radiography showed
normal heart size and clear lung fields. Serologies for
autoimmune profiles were all negative. Other results of
laboratory and radiologic investigations are shown in tables
1-4.
Table 1. Results of
CBC/DC & coagulation profiles:
Day after 1st admission |
WBC K/μL |
RBC M/μL |
Hgb g/dL |
Hct % |
MCV fL |
Plt K/μL |
0 |
12.51 |
4.55 |
10.6 |
31.8 |
92.3 |
470 |
5 |
10.12 |
4.35 |
10.2 |
30.8 |
92.6 |
440 |
14 |
9.85 |
4.45 |
10.5 |
31.7 |
92.4 |
460 |
Day after 2nd admission |
WBC K/μL
|
RBC M/μL
|
Hgb g/dL
|
Hct % |
MCV fL |
Plt K/μL |
0 |
9.73 |
4.71 |
11.0 |
33.5 |
92.2 |
450 |
3 |
9.85 |
4.70 |
10.9 |
33.4 |
92.3 |
451 |
5 |
9.80 |
4.72 |
11.1 |
33.3 |
92.3 |
450 | Table
2. Results of blood
biochemistry
Day after 1st admission
|
BUN mg/dl |
Cre mg/dl |
Na mmol/l |
K mmol/l |
GOT U/l |
T-Bil mg/dl |
Alb g/dL |
0 |
28 |
1.4 |
141 |
3.8 |
34 |
1.0 |
4.3 |
3 |
36 |
1.5 |
138 |
4.1 |
53 |
0.8 |
|
7 |
36 |
1.4 |
|
|
56 |
|
|
14 |
35 |
1.5 |
|
|
66 |
1.0 |
|
Day after 2nd admission
|
BUN mg/dl |
Cre mg/dl |
Na mmol/l |
K mmol/l |
GOT U/l |
T-Bil mg/dl |
Alb g/dL |
0 |
65 |
2.6 |
138 |
4.5 |
40 |
0.9 |
4.2 |
3 |
71 |
2.9 |
136 |
4.4 |
42 |
|
|
5 |
65 |
3.0 |
136 |
4.4 |
41 |
|
|
7 |
60 |
2.9 |
137 |
4.3 |
43 |
|
|
Table 3. Results of
urine
nalysis
Day after 1st admission
|
Appearance |
Sp. gr |
pH |
Protein mg/dL
|
Glu g/dL |
Ketones |
O.B |
Urobil EU/dL
|
Bil |
0 |
Y;C |
1.02 |
7.0 |
>300 |
- |
- |
- |
0.1 |
- |
5 |
Y;TT |
1.02 |
7.0 |
>300 |
- |
- |
+ |
0.1 |
- |
14 |
Y;TT |
1.01 |
7.0 |
>300 |
- |
- |
+ |
0.1 |
- |
Day after 2nd admission
|
Appearance |
Sp. gr |
pH |
Protein mg/dL
|
Glu g/dL |
Ketones |
O.B |
Urobil EU/dL
|
Bil |
0 |
Y;C |
1.05 |
7.0 |
>300 |
- |
- |
- |
0.1 |
- |
1 |
Y;C |
1.04 |
7.0 |
>300 |
- |
- |
- |
0.1 |
- |
3 |
Y;C |
1.03 |
7.0 |
>300 |
- |
- |
- |
0.1 |
- |
Day after 1st
admission |
Nitrite |
WBC |
RBC /HPF |
WBC /HPF |
EpithCell /HPF
|
Cast /LPF |
Crystal |
Bact |
0 |
- |
- |
0-1 |
0-1 |
0-3 |
- |
- |
- |
5 |
- |
+ |
20-30 |
10-20 |
3-5 |
- |
- |
- |
14 |
- |
+ |
10-20 |
5-10 |
1-3 |
- |
- |
- |
Day after 2nd
admission |
Nitrite |
WBC |
RBC /HPF |
WBC /HPF |
EpithCell /HPF
|
Cast /LPF |
Crystal |
Bact |
0 |
- |
- |
5-10 |
0-1 |
0-3 |
- |
- |
- |
1 |
- |
- |
5-10 |
0-1 |
0-3 |
- |
- |
- |
3 |
- |
- |
0-1 |
0-1 |
0-3 |
- |
- |
- | 24 hour urine total protein: 1.5
g/d
Table 4. Results of renal sonography
Size |
Right kidney, 10.8 cm; left kidney, 11.0 cm |
Shape |
Bilaterally normal |
Cortical
thinkness |
Right kidney, 10 mm; left kidney, 11 mm (within
normal limits) |
Central sinus |
No hydronephrosis |
Solid or cystic
lesion |
Nil
|
< Course and Treatment
>
On admission, angiotensin II
receptor blocker was discontinued because of acute renal
failure. Renal biopsy was performed 3 days after admission,
which revealed a cleft at the glomerular hilum, capillary wall
thickening and wrinkling due to ischemia. Acute tubular
necrosis and concentric fibrosis were also seen. Because of
the clinical presentations and renal biopsy, cholesterol
embolism- related acute renal failure was diagnosed which
might have resulted from previous cardiac catheterization.
Because of the stable general function, this patient was
discharged at 10th day after admission. During follow-up at
the outpatient clinic, his renal function improved gradually
two months later. However, serum creatinine levels remained
elevated compared with those at first discharge from this
hospital.
< Analysis
>
Cholesterol atheroembolic kidney
disease results when cholesterol crystals and other debris
separate from atheromatous plaques, flow downstream, and lodge
in small renal arteries, producing luminal occlusion,
ischemia, and kidney dysfunction. Depending on the source and
distribution of emboli, kidney disease might be the sole or
predominant manifestation or simply one feature of a systemic
illness characterized by multi-organ ischemia or infarction.
Atheroembolism is now recognized as a cause of occult or
reversible declines in kidney function. Recovery of function
may follow extended survival on renal replacement therapy.
Embolization might be spontaneous, particularly with severe
aortic disease, but mechanical disruption of plaque during
angiographic or surgical procedures usually precedes it.
Irrespective of the area primarily targeted for imaging,
passage of a catheter alone the ascending or descending aorta
proximal to the renal arteries confers a risk of embolization
to the kidneys. Our patient ever underwent cardiac
catheterization five weeks before detection of abnormal renal
function which is a major risk for cholesterol embolization.
However, what needs to differentiate is contrast nephropathy
and cholesterol embolization related kidney disease. Contrast
nephropathy usually occurs immediately 24 to 48 hours after
contrast media exposure; however, cholesterol embolization
related kidney disease usually shows a protracted clinical
course which might take weeks to months. Other risk factors
include smoking history, male and old age. The mean age at
diagnosis is in the mid-seventh decade. Furthermore, high
C-reactive protein, HTN, multi-vessel coronary disease, and
acute coronary syndrome are also suggestive.
The typical clinical presentations
are either constitutional symptoms, such as fever, abdominal
or flank pain, tachycardia or specific organ ischemia or
infarction. Many organs or systems could be involved, such as
brain, lung, kidney, intestine, muscular system, and endocrine
system. Laboratory findings are usually non-specific. However,
microscopic hematuria in renal involvement might be seen. In
renal biopsy, the pathologic presentations are similar to what
we saw in this case. The size of affected artery is typically
around 200 μm. The typical lesion is cholesterol cleft, a
space which is occupied by cholesterol crystal but lost during
specimen preparation. Besides, ischemic changes of glomeruli
with glomerular collapse and basement wrinkling will be seen.
Because cholesterol embolization
is so rare, there's no available data from controlled trials
for prevention or treatment. Whereas vasodilator prostaglandin
infusions have also been used to increase blood flow and use
of statins has been reported to improve survival, monitoring
basic electrolytes and urine output is essential. Although
most patients will show a gradual improvement later, patients
with pre-existing renal impairment will be at higher risk of
renal replacement therapy or mortality.
< Reference
>
- Harrison's principles of internal medicine 15th edition
- Comprehensive Clinical Nephrology 2nd edition
- Primer on Kidney Disease 4th edition.
- eMedicine, Cholesterol embolism. Last
Updated: August 5,
2005
|