Case Report

Portal Hypertension Secondary to Benign Prostatic Hyperplasia


  • Mustafa Küçükyangöz
  • Emrullah Söğütdelen
  • Sebahat Gücük
  • Adnan Gücük

Received Date: 22.05.2021 Accepted Date: 23.09.2021 J Urol Surg 2022;9(1):74-75

Benign prostatic hyperplasia (BPH) obstructs the bladder outlet. Patients with BPH frequently present with lower urinary tract symptoms. However, patients with BPH can present with serious fatal complications unless diagnosed and treated sufficiently. In this case report, we present the case of a 63-year-old male patient with renal insufficiency, generalized edema, and portal hypertension due to chronic obstructive uropathy secondary to BPH. To the best of our knowledge, this is the first report to present portal hypertension secondary to BPH as a rare complication.

Keywords: Prostate, BPH complications, generalized edema, portal hypertension


Benign prostatic hyperplasia (BPH) is defined as the enlargement of the prostate gland that obstructs the bladder outlet. BPH is an important cause of lower urinary tract symptoms (1,2). Patients with BPH usually present with voiding and storage symptoms (1,3,4). Complications such as recurrent or persistent urinary tract infections, macroscopic or microscopic hematuria, bladder stones, acute or chronic renal failure, incontinence, erectile dysfunction, and electrolyte imbalance are observed. Moreover, patients with chronic obstruction could present with hypertension secondary to hypervolemia (5,6).

Portal hypertension (PH) is defined as an increase in blood pressure between the inferior vena cava and portal veins mainly due to cirrhosis. Furthermore, diseases such as portal vein occlusion, primary biliary cholangitis, alcoholic hepatitis, hepatic vein thrombosis, and chronic right heart failure are possible causes of PH (7).

Renal insufficiency frequently occurs in chronic obstructive uropathies (8). Chronic kidney insufficiency further triggers right heart insufficiency (9). These diseases can cause PH depending on the volume load (10). In this report, we present the case of a patient with generalized edema, renal insufficiency, and PH secondary to BPH.

Case Report

A 63-year-old male patient admitted to the department of urology outpatient clinic of our institution for the swelling of the legs, lower abdomen, and genital area (Figure 1a). The patient had no history of PH or heart failure previously. After taken an informed consent, n the physical examination, a diffuse bilateral pedal, scrotal, penile, and lower abdominal edema was observed. In the deep abdominal palpation, we observed a mass effect of the overfilled bladder in the suprapubic region due to urinary retention.

Furthermore, the patient had the following laboratory results: white blood cell, 12,200/uL; hemoglobin, 6.39 g/dL; blood urea nitrogen, 225 mg/dL; creatinine, 12.45 mg/dL; aspartate aminotransferase, 9 u/L; alanine aminotransferase, 11 u/L; total prostate-specific antigen, 6.66 ng/mL; and free prostate-specific antigen, 1.63 ng/mL. The patient was consulted with the department of nephrology and was decided not to dialyze since all electrolytes were in the normal range and had no uremic complications.

To further explore renal insufficiency, abdominal ultrasound (US) (GE Healthcare, Chicago, IL, USA) was performed, revealing bilateral grade 3 hydroureteronephrosis with a 74 mL prostate volume, 37 mm ureteral stone, and 1.250 mL residual urine in the bladder. Furthermore, a color Doppler US of the portal system was performed, revealing dilatation of the hepatic veins as well as of the splenic vein and hilum.

A 16-French two-way urethral catheter was inserted into the patient to drain residual urine when significant residual urine was observed. The urine output of the patient was 1.500 mL in 10 min after catheterization. The patient was hospitalized to correct the hemoglobin deficit and monitor renal function. In the control kidney function tests, creatinine level decreased to 5.7 mg/dL and blood urea nitrogen to 167 mg/dL by day 5 of admission.

After histopathological confirmation of the prostate by transrectal US-guided biopsy with BPH, an open suprapubic transvesical prostatectomy and cystolithotomy was performed. The patient was discharged on postoperative day 3 with a urethral catheter, which was taken on postoperative day 7.

Physical examination on postoperative day 7 revealed the complete regression of a generalized edema (Figure 1b). In the control laboratory tests, creatinine was at 4.24 mg/dL and blood urea nitrogen at 111 mg/dL. Postvoiding residual urine was not observed on US. A control doppler US revealed that PH findings like a dilatation in the splenic and portal veins were completely regressed. The patient was followed up for one year and had normal renal function.


Chronic urinary retention is characterized by the accumulation of urine in the bladder slowly and paimless with volumes ranging between 450 and 4.500 mL. In chronic retention, high pressure in the bladder causes an increase in the pressure of the pelvicalyceal system, leading to bilateral hydronephrosis. Subsequently, this may result in different degrees of renal failure (6).

PH is asymptomatic until severe complications, such as gastrointestinal bleeding from varices, ascites, and hepatic encephalopathy develop (11). In this study, bilateral grade 3 hydronephrosis, renal insufficiency, generalized edema, and PH secondary to BPH were observed. To the best of our knowledge,

there was no PH presentation secondary to BPH. Thus, although a patient may be hospitalized for chronic urinary retention, PH and its complications should be considered.


BPH is the most common cause of obstructive uropathy with rare fatal complications. Its presentation ranges from no symptoms to much more morbid situations like end-stage renal disease, right heart failure, and PH. Thus, if a patient presents with chronic urinary retention and generalized edema, PH should be checked although it is rare.


Informed Consent: Informed consent was obtained.

Peer-review: Externally peer-reviewed.

Authorship Contributions

Surgical and Medical Practices: M.K., A.G., Concept: M.K., E.S., Design: M.K., A.G., Data Collection or Processing: M.K., Analysis or Interpretation: E.S., S.G., Literature Search: E.S., S.G., Writing: M.K., E.S.

Conflict of Interest: No conflict of interest was declared by the authors.

Financial Disclosure: The authors declared that this study received no financial support.


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