<Brief
History>
A 78-year-old man with hypertension for
20 years and benign prostate hyperplasia (BPH) for 6 years
suffered from a gradual onset of consciousness deterioration
one week prior to admission. Generally speaking, his blood
pressure had been well-controlled. Six months ago, he was
admitted to a local hospital for scheduled trans-urethral
resection of prostate (TURP). However, it was hold due to a
coincidental pneumonia. After completion of pneumonia
treatment, he led an uneventful life without undergoing the
operation. One week prior to admission, his family noticed
that he became drowsy and did not respond to external stimuli.
He had no fever, tarry or bloody stool, but a smell of urine
resulting from urine incontinence was noted. He also
complained of poor appetite during this period. He was then
brought to our emergency room (ER) for help. On arrival, the
Glasgow Coma Score was E3V4M4. Physical examination showed a
man of 169 cm height and 70 kg weight. His body temperature
was 37.2o
C, blood pressure
152/86 mmHg, and pulse rate was 122 bpm. No
focal neurologic deficit was detected. The other examinations
were unremarkable, except for a markedly distended low abdomen.
<Laboratory and Image
Study>
1.CBC/DC &
coagulation profiles:
Day after admission |
WBC K/μL |
RBC M/μL |
Hgb g/dL |
Hct % |
MCV fL |
Plt K/μL |
0 |
8.95 |
4.55 |
11 |
33 |
92.3 |
489 |
3rd |
8.54 |
4.71 |
11.3 |
33.7 |
92.2 |
423 |
7th |
8.66 |
4.75 |
11.4 |
32.6 |
92.2 |
421 | 2. Biochemistry
Day after admission |
BUN mg/dl |
Cre mg/dl |
Na mmol/l |
K mmol/l |
Cl mmol/l |
Ca mmol/l |
P mmol/l |
0 |
94 |
6.6 |
132 |
5.8 |
106 |
2.3 |
0.9 |
3rd |
74 |
4.0 |
138 |
4.6 |
|
|
|
5th |
50 |
2.3 |
133 |
4.8 |
101 |
2.2 |
1.2 |
7th |
30 |
1.4 |
137 |
4.5 |
|
|
|
|
GOT U/l |
T-Bil mg/dl |
LDH U/l |
CPK mg/dl |
0 |
34 |
0.8 |
190 |
85 |
3rd |
32 |
|
|
| 3. Urine analysis:
Day after admission |
Appearance |
Sp. gr |
pH |
Protein mg/dL |
Glu g/dL |
Ketones |
O.B |
Urobil EU/dL |
Bil |
0 |
Y;C |
1.005 |
6.0 |
- |
- |
- |
- |
0.1 |
- |
5th |
Y;C |
1.010 |
6.0 |
- |
- |
- |
- |
0.1 |
- |
Day after admission |
Nitrite |
WBC |
RBC /HPF |
WBC /HPF |
EpithCell /HPF |
Cast /LPF |
Crystal |
Bact |
0 |
- |
- |
3-5 |
0-1 |
3-5 |
- |
- |
- |
5th |
- |
- |
0-1 |
0 |
3-5 |
- |
- |
- |
Arterial blood gas: PH: 7.32, PaCO2: 36.4 mmHg, PO2: 41.4 mmHg, HCO3-: 18.3 meq/L
<Course and
Treatment>
At the ER, abnormal renal function was
noted, and the bedside ultrasonography showed a markedly
distended urinary bladder with prominent bilateral hydronephrosis. Under the impression of
obstructive nephropathy which was potentially reversible, hemodialysis was
not performed except that Kalimate was prescribed
to treat the hyperkalemia. A Foley catheter
was inserted at the ER and he was transferred
to the ward for further care. The initial
urine output was 4900 cc within 24 hours after admission and
then decreased gradually to around 1500 cc per day. His renal function
improved gradually and he regained consciousness paralleling decreasing serum
levels of blood urea nitrogen and creatinine. Throughout the hospitalization,
no hemodialysis was performed. The trans-rectal ultrasonography showed
an enlarged prostate, despite the fact that he had
a normal serum level of PSA.
A diagnosis of BPH-related obstructive nephropathy presenting
with acute renal failure (ARF) was made and
he was transferred to the urologic ward
for further TURP. After the operation, his renal function remained
within the normal range and he was discharged
in stable condition..
<Analysis>
The Patient was diagnosed as BPH-related obstructive
nephropathy presenting with acute renal failure and
consciousness disturbance. Clinically, obstructive uropathy
describes the structural or functional changes in the urinary
tract that hinder normal urine flow, whereas obstructive
nephropathy means obstructive uropathy with renal dysfunction.
The etiology of obstructive nephropathy can be divided into
three categories: 1. Mechanical obstruction within the lumen
of urinary tract 2. Functional or anatomical abnormalities 3.
External compression of urinary tract. The impediment of urine
flow will result in papillar and cortical pressure atrophy,
distal tubular and collecting duct defect and then impaired
Na, K, acid and water handling. It also increases
pyelocalyceal pressure (usually when reflux presented), and
urine backflow into renal tubules Furthermore, the enlarged
pelvis would stretch or kink renal vessels to induce the
collapse of medullar vessels, and finally ischemia develops.
The consequences after obstruction include renal fibrosis,
tubular atrophy, interstitial inflammation.
The clinical symptoms implying obstruction
uropathy/nephropathy are difficulty in voiding, frequency,
nocturia, flank pain/tender mass, ARF, anuria or widely
varying urinary output, chronic renal failure (CRF), fatigue,
anorexia, edema, renal tubular disorder, infection, renal
calculi, hypertension and polycythemia. Generally, ARF can be
divided into pre-renal, intrinsic and post-renal origin. The
post-renal origin, also the obstructive nephropathy, is the
first need to be excluded. The incidence of obstructive
nephropathy increases to around 9% in the elderly, and the
predisposing factors are simultaneous obstruction of both
ureters, unilateral ureteral obstruction with single kidney or
severe contra-lateral kidney disease. Obstructive nephropathy
should be considered in all causes of ARF especially in
patients with widely fluctuated urinary amount, rapid
deterioration in renal function unexplained by the primary
renal problem (normal urine sediment), relapsing urinary tract
infection or resistant urosepsis, single kidney, recent
surgery (genitourologic or retroperitoneal), elderly males.
So, bladder catheterization in unexplained ARF should be
considered in all elderly males.
Basically, the laboratory plays lesser important role in
the diagnosis of obstructive nephropathy than the imaging
study. Like this case, an easily accessed bedside
ultrasonography can make a diagnosis immediately. The initial
treatment needs to decide whether dialysis is needed and then
control the metabolic abnormalities, like hyperkalemia or
hypertension. However, the most important treatment is to
relieve the obstruction immediately either by bladder
catheterization or percutaneous nephrostomy. Then, specific
treatment for each etiology is mandatory.
<Reference>
- Harrison's principles of internal medicine 15
edition
- Comprehensive Clinical Nephrology 2nd edition
|