網路內科繼續教育
有效期間:民國 95年10月16日 95年10月31日

    Case Discussion

<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>

  1. Harrison's principles of internal medicine 15 edition
  2. Comprehensive Clinical Nephrology 2nd edition

繼續教育考題
1.
(D)
會造成acute renal failure原因如下,何者為正確?
APre-renal origin
BIntrinsic origin
CPost-renal origin
DAll of above
2.
(B)
在老年男性病患中,常見的obstructive nephropathy病因為何? 
AAtonic bladder
BProstate disorder
CUreteral stone
DBladder tumor
3.
(E)
常見引起雙側obstructive nephropathy病因可能包括?
ABenign prostate hyperplasia
BBladder neck transitional cell carcinoma
CUrethral stricture
DReflux of urine
EAll of above
4.
(A)
在obstructive nephropathy最有效益的診斷方式為何?
AUltrasonography
BComputer tomography
CKUB
DUrine analysis
5.
(C)
一般治療obstructive nephropathy中最重要的治療為何?
ADiuretics
BDialysis
CRelief of the obstruction
DTreat coincidental infection
6.
(D)
何者不會是obstructive nephropathy的臨床表現?
APolyuria
BOliguria
CAnuria
DGlucosuria

答案解析 

  1. (D ) Generally, acute renal failure can be divided into pre-renal, intrinsic and post-renal origin. In them, the post-renal origin is the first to exclude.
  2. (E )  Obstructive nephropathy can occur in men or women. Men with enlarged prostates or prostate cancer are at a higher risk for developing obstructive nephropathy.
  3. (E ) Generally, bilateral obstruction implies that the obstruction origin exists below the orifices of bilateral ureters. So, abnormalities in bladder or bilateral renal reflux all predispose to bilateral obstructive nephropathy.
  4. (A ) 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. 
  5. (C) 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.
  6. (D ) 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.


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