|
A
23-year-old woman, previously healthy, presented to the
hospital with intermittent fevers, malaise, and lower leg
edema for 1 month, for which she sought medical attention at
an outside clinic. She received treatment for upper
respiratory tract infection with a 3-day course of an oral
antibiotic and the fever responded to the treatment. However,
the fever recurred intermittently after discontinuation of the
prescribed antibiotic. Because the temperature was in low
grade with an average of 37.8oC, she only took acetaminophen
without seeking further medical attention. Other than the
intermittent fevers, she also complained of general malaise
and weight loss, but without gastrointestinal symptoms. Ten
days prior to this admission, she felt mild shortness of
breath while climbing stairs and noticed lower leg edema, for
which she visited our outpatient clinic. At the clinic, she
appeared ill but with clear consciousness. The blood pressure
was 136/76 mmHg, the pulse rate was 88 beats per minute, the
respiration was 22 breaths per minute, and the temperature was
37.7oC. The conjunctiva was
mildly pale and the sclera was anicteric. Lungs were
symmetrically expanded with clear breath sounds. The heart
rhythm was regular and no cardiomegaly was detected. A
pansystolic murmur (Grade 2/6) at the apex of the heart with
radiation to the left axillary region was heard on
auscultation. No thrill or heave was noted. Examination of the
abdomen was normal. Mild pitting edema of the lower
extremities was noted. No lymphadenopathy was found at the
neck, axillary and inguinal regions. There was no skin lesion
or needle track. Based on the history and physical findings,
infective endocarditis was suspected and she was admitted for
further management.
< Laboratory and Imaging
Study >
Table 1. CBC and differential count
| Date |
WBC
(K/μL) |
Hgb
(g/dL) |
Hct
(%) |
Plt
(K/μL) |
Band
(%) |
Seg
(%) |
Eos
(%) |
Baso
(%) |
Lym
(%) |
| Hospital day 1 |
13.5 |
10.0 |
30.1 |
142 |
1 |
82 |
0.1 |
0.3 |
3 |
| Hospital day 5 |
10.6 |
10.8 |
34.2 |
150 |
0 |
78 |
0.2 |
0.2 |
2 |
| Hospital day 15 |
8.2 |
11.8 |
35.1 |
179 |
0 |
72 |
0.4 |
0.3 |
2 |
Table 2. Biochemistry
| Date |
BUN
(mg/dl) |
Cre
(mg/dl) |
Na
(mmol/l) |
K
(mmol/l) |
AST
(U/l) |
ALT
(U/l) |
Bil (T)
mg/dL |
Albumin
(g/dl) |
Glucose
(mg/dl) |
| Hospital day 1 |
38 |
2.7 |
137 |
5.0 |
56 |
38 |
0.7 |
3.9 |
Not Available
(N/A) |
| Hospital day 5 |
32 |
2.2 |
136 |
4.0 |
N/A |
N/A |
N/A |
N/A |
N/A |
| Hospital day 15 |
24 |
1.5 |
138 |
4.1 |
36 |
N/A |
N/A |
N/A |
N/A |
Table 3. Urine analysis
| Date |
Appearance |
Specific
gravity |
pH |
Protein
(mg/dl) |
Glucose |
Ketone |
Occult
blood |
| Hospital day 1 |
yellow, clear |
1.012 |
6.8 |
100 |
-- |
1+ |
2+ |
| Hospital day 15 |
yellow, clear |
1.013 |
7.1 |
30 |
-- |
-- |
1+ |
| Date |
Urobilinogen |
Bilirubin |
RBC |
WBC |
Epithelial cells |
Cast |
Bacteria |
| Hospital day 1 |
0.1 |
-- |
50 |
10 |
1-3 |
RBC cast |
-- |
| Hospital day 15 |
0.1 |
-- |
10 |
-- |
-- |
-- |
--
|
4. C3: 42 (80 to 178 mg/dl), C4: 30 (12 to 42 mg/dl); ANCA:
negative; rheumatoid factor: negative
5. 24-hour urine total protein: 1.87 g
6. CXR: Normal heart size and clear lung field.
7. Renosonography: Normal kidney size; bilateral
parenchymal renal disease without
hydronephrosis.
<
Course and Treatment >
Upon admission, under
the impression of infective endocarditis (IE), IE-associated
glomerulonephritis and acute kidney injury, she was treated
with vancomycin administered intravenously and oral
furosemide. Subsequently, the blood cultures revealed
methicillin-sensitive Staphylococcus aureus (MSSA)
two days after admission, and vancomycin was changed to
oxacillin administered intravenously. Gentamicin was also used
in the first five days of oxacillin therapy. Renal sonography
did not show urinary tract obstruction and transthoracic
echocardiography revealed a vegetation about 0.6 cm in size on
the mitral valve. No other metastatic infection focus was
identified during the hospitalization. Her general condition
responded to 4-week intravenous oxacillin therapy promptly and
she did not develop signs and symptoms suggestive of heart
failure throughout the hospitalization. Her renal function
improved gradually and she was discharged and followed up at
our nephrology clinic as an
outpatient.
< 病例分析
>
Infective endocarditis
(IE)常對腎臟引起immune-mediated及embolic renal
diseases。由於腎臟接受的血流佔心輸出的25%，因此當有IE時，腎臟自然有相當高的機會受到emboli的影響，而產生embolic
renal disease。在fungus或Haemophilus
spp.所引起的IE較易產生較大的emboli，病患常以突發性的flank pain、血尿(gross
hematuria)及renal
dysfunction表現。當然較小的emboli在臨床上是不一定會有症狀的，但有時這些microvascular
emboli會引起renal infarction及cortical
microabscesses，進而導致所謂的flea-bitten kidney。有時embolic renal
disease的尿液培養會呈陽性或可靠超音波幫忙診斷。有報告指出，臨床上IE的病患，是以immune-mediated的IE-associated
glomerulonephritis (GN)較為常見，約有20%的IE病患會產生IE-associated
GN。不過也有報告指出是以embolic renal disease居多(Nephrol Dial
Transplant.
2000;15(11):1782-7)。此落差或許來自於並不是每個懷疑IE-associated
GN的病患都會接受renal biopsy，因此或許會遺漏可能的embolic renal
disease，尤其當emboli較小時。
S. aureus為IE-associated
GN最常見的致病菌。IE造成GN的原因被認為有四種：帶有病原體抗原的immune
complex沈積、cryoglobulin的immune
complex沈積、由super-antigen造成的polyclonal
gammopathy或病原體抗原直接活化complement的alternative
pathway。病理變化以diffuse或focal proliferative
GN為主要表現，通常在微血管壁上可見到IgG、IgM及C3的沈積，另外以電子顯微鏡則可在subendothelium及mesangium處發現immune
complex沈積。輕微的GN或只見mesangial proliferative
GN，而嚴重的則甚至可見到crescent形成。IE-associated GN的臨床表現包括microscopic
hematuria、non-nephrotic proteinuria及acute kidney
injury，不過極少見到以nephrotic syndrome表現的。實驗室方面，可見到rheumatoid
factor、cryoglobulin及低下的補體(C3,
CH50)。而本病患檢驗之結果，hypocomplementemia、RBC cast、non-nephrotic
proteinuria都是GN的典型表現。不過即使腎臟未被影響的IE病患，有時也可能出現這些檢驗結果，因此並不能光憑檢驗結果做診斷。另外，也曾有報告過在IE-associated
GN的病患身上偵測到ANCA。雖然本例並未接受腎臟切片，但依病史、相關症狀及檢查結果，因此認為是IE-associated
GN的機會較高，但是並無法完全排除embolic renal
disease，不過基本上兩者的治療大致相同。在治療IE-associated
GN方面，最重要的是適當的抗生素治療並加上支持性治療。IE-associated
GN的預後通常都不錯，即使IE造成rapidly progressive
GN，但在適當的抗生素治療後，腎功能仍可能恢復正常。另外曾有報告以steroid或plasmapheresis來治療IE-associated
GN，但都缺乏大規模的臨床證據支持。至於本例的mitral valve vegetation，由於臨床上並無明顯的heart
failure症狀、且對抗生素治療反應良好及vegetation小於一公分，因此並未以手術治療而是繼續在門診追蹤。另外需注意的是，曾有報告指出，有約15至20%的IE病患是先因腎臟功能的異常才進而診斷出IE，因此，在診斷需特別注意。
< References
>
- Comprehensive clinical nephrology,
3rd edition.
- Harrison’s Primciples of Internal
Medicine. 16th edition
- Nephrol Dial Transplant.
2000;15(11):1782-7
| 
Case Discussion
繼續教育考題