Saudi Journal of Kidney Diseases and Transplantation

: 2013  |  Volume : 24  |  Issue : 4  |  Page : 810--812

Bilateral pyonephrosis and end-stage renal disease secondary to pelvic organ prolapse

Naser Sabah Hussein1, Mohd Nor G Rahman2, Usama N Rifat3,  
1 Urology Department, Al-Karamah Teaching Hospital, Baghdad, Iraq
2 Surgical Department/Urology Unit, Hospital Universiti Sains Malaysia (HUSM), Kota Bahura, Malaysia
3 Urology Department, Medical City, Baghdad, Iraq

Correspondence Address:
Naser Sabah Hussein
Urology Department, Al-Karamah Teaching Hospital, Baghdad

How to cite this article:
Hussein NS, Rahman MG, Rifat UN. Bilateral pyonephrosis and end-stage renal disease secondary to pelvic organ prolapse.Saudi J Kidney Dis Transpl 2013;24:810-812

How to cite this URL:
Hussein NS, Rahman MG, Rifat UN. Bilateral pyonephrosis and end-stage renal disease secondary to pelvic organ prolapse. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2021 Jun 15 ];24:810-812
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Full Text

To the Editor,

The association between pelvic organ prolapse (POP) and hydronephrosis has been long recognized. However, severe hydronephrosis, POP and renal failure is rare. [1] Pyonephrosis and end-stage renal disease can be caused by complicated POP.

POP is the descent of the uterus, bladder or rectum protruding through the vagina, and occurs more frequently in old women. [2] There were few reported cases of end-stage renal disease caused by total uterine prolapse and cystocele. [3] We report a case of bilateral pyonephrosis and end-stage renal disease caused by complicated POP.

A 62-year-old woman with a history of diabetes mellitus type, hypertension and ischemic heart disease for the last ten years had grade three uterine prolapse for the last three years. The patient presented with high-grade fever associated with chills, nausea and vomiting. Pelvic examination revealed third degree uterine prolapse, cystocele and rectocele.

On admission, her serum creatinine was 812 μmol/L and her blood urea was 36.4 mmol/L. Her hemoglobin was 8.5 g/dL. The estimated glomerular filtration rate was 6 mL/min. Radiograph of the kidney, ureter and bladder (KUB) showed no evidence of radiopaque shadow. Abdominal ultrasonography showed bilateral moderate hydronephrosis and hydroureter with evidence of pyonephrosis and large post-voiding residual urine. The patient was treated urgently with bilateral double J stenting under local anesthesia and correction of her metabolic acidosis and dehydration status. The retrograde pyelogram (RPG) findings showed bilateral hydronephrosis and hydroureter without a clear cause for this dilation. The ureters were stented with difficulty due to uterine prolapse and displacement of both ureteric orifices. After seven days of intravenous antibiotic, fluid, ureteric stenting, continuous bladder drainage by Foley's catheter and control of blood sugar, her temperature normalized (37.1°C). After eight weeks, her blood urea and serum creatinine dropped to 25.5 mmol/L and 341 μmol/L, respectively.

Computerized tomography (CT) of the abdomen and pelvis without contrast enhancement was performed for etiological diagnosis. This showed extreme prolapse of the bladder, uterus and terminal ureters out of the pelvis [Figure 1]. The ureters were compressed between the cystocoele and the uterine prolapse [Figure 2]. Double J stents were in situ, extended out of pelvis. In view of medical co-morbidity, a vaginal ring was inserted to reduce the uterine prolapse. After 16 weeks of follow-up, degree of hydronephrosis, blood urea and serum creatinine did not improve. Hence, the patient was selected for renal replacement therapy.{Figure 1}{Figure 2}

POP can present with lower urinary tract, bowel, sexual and local symptoms that affect the quality of life and daily activities of women. Urinary tract symptoms can range from obstructive voiding symptoms, elevated post-void residual urine, unilateral or bilateral hydronephrosis, hydroureter and chronic renal failure. End-stage renal disease in severe cases of prolapse can occur, although it is a rare finding. Several hypotheses have been proposed to explain this association, including entrapment of ureters by genital hiatus against fundus of uterus, [4] kinking of ureters by cardinal ligaments of descened uterus, [5] compression of ureter by uterine blood vessels [6] and ureteral compression against the inferior pubic ramus. However, the exact mechanism of hydronephrosis has not been completely clarified, and may be multifactorial.

The cause of end-stage renal disease in our case was compression of the ureters between the uterus and the bladder [Figure 2], leading to bilateral hydronephrosis and hydroureter, with stasis of urine complicated by pyonephrosis and advanced chronic renal failure.


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