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Year : 2021  |  Volume : 15  |  Issue : 4  |  Page : 378-380

Acute kidney injury due to obstructive nephropathy caused by fecal impaction in a renal transplant patient - A case report

Okinawa Prefectural Nanbu Medical Center, Children's Medical Center, Haebaru, Okinawa

Date of Submission20-Nov-2020
Date of Decision13-May-2021
Date of Acceptance18-May-2021
Date of Web Publication30-Dec-2021

Correspondence Address:
Dr. Tomoo Kise
Arakawa 118-1, Haebaru, Okinawa 901-1193
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijot.ijot_144_20

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Acute kidney injury (AKI) remains a major complication after transplantation; its common causes include acute rejection and urinary tract obstruction. Here, we report an unusual case of a 16-year-old renal transplant patient with congenital anomalies of the kidney and urinary tract (CAKUT) and anorectal malformation. She developed AKI owing to obstructive nephropathy caused by impacted stool in the colon. Our patient presented with complaints of hypertension and facial edema. She had a neurogenic bladder and a history of surgery for anal atresia. Abdominal computed tomography revealed renal hydronephrosis in the transplanted kidney and a mass of impacted stool in the sigmoid colon and rectum that compressed the neck of the bladder. Despite maintenance of daily defecation, the impacted stool had accumulated over several years; however, softening and removing the stool improved kidney function. Defecation management is therefore important in patients with CAKUT and anorectal malformation.

Keywords: Acute kidney injury, congenital anomalies of the kidney and urinary tract, obstructive nephropathy, renal transplantation, stool mass

How to cite this article:
Kise T, Fukuyama S, Uehara M. Acute kidney injury due to obstructive nephropathy caused by fecal impaction in a renal transplant patient - A case report. Indian J Transplant 2021;15:378-80

How to cite this URL:
Kise T, Fukuyama S, Uehara M. Acute kidney injury due to obstructive nephropathy caused by fecal impaction in a renal transplant patient - A case report. Indian J Transplant [serial online] 2021 [cited 2022 Aug 10];15:378-80. Available from: https://www.ijtonline.in/text.asp?2021/15/4/378/334422

  Introduction Top

In patients who undergo renal transplantation, acute kidney injury (AKI) is an important cause of allograft loss. Patients hospitalized for AKI after renal transplantation have a death or allograft loss rate of 12%.[1] Obstructive nephropathy is a cause of AKI after renal transplantation; however, there are few reports on obstructive nephropathy, resulting from bladder outlet compression by impacted stool. Here, we report an unusual case of a renal transplant patient with congenital anomalies of the kidney and urinary tract (CAKUT) and anorectal malformation, who developed AKI due to obstructive nephropathy caused by stool impaction, despite observing strict daily defecation management.

  Case Report Top

A 16-year-old girl presented at the emergency department with chief complaints of hypertension and facial edema. The patient's blood pressure was 140/90 mmHg, and she had undergone renal transplantation 4 years previously for end-stage renal failure due to bilateral hypoplastic kidneys. The patient had a deletion of the long arm of chromosome 10 and a neurogenic bladder and had undergone anal reconstruction surgery for anal atresia 15 months after birth. Enterostomy was performed in the ascending colon due to constipation 2 years after renal transplantation; as the urodynamic study conducted before renal transplantation indicated low bladder compliance and high bladder pressure, the patient's mother performed urethral catheterization for the patient every 6 h. She also managed the patient's defecation by injecting 200 ml of water into the enterostomy and administering the patient an enema. A week before admission, the patient drank 800–1000 ml of water daily, passed 500 ml of urine, and had a normal defecation volume each day.

On admission, the patient weighed 13.7 kg (11.0 kg was considered healthy) and was 109 cm tall, which at her age was considered failure to thrive. The patient's body temperature was 36.7°C and her blood pressure was 110/76 mmHg (90–100/40–50 mmHg was considered healthy). She had a regular heart rate of 90 beats/min without any murmurs, and her oxygen saturation was 99%; the breath sounds were vesicular. Her abdomen was distended, and a large hard mass was noticed in the lower part of her abdomen on palpation. The patient had facial edema, with no edema of the extremities.

Laboratory data were consistent with those of renal dysfunction and mild anemia [Table 1]. Chest radiography revealed cardiomegaly, with a cardiothoracic ratio of 0.64. There was no pleural effusion, abdominal ultrasound revealed Grade 3 hydronephrosis of the transplanted kidney, and abdominal computed tomography (CT) confirmed hydronephrosis of the transplanted kidney with hydroureters and multiple layers of large fecal masses in the sigmoid colon and rectum; the impacted stool compressed the neck of the bladder [Figure 1] and [Figure 2].
Table 1: Laboratory data of the patient at admission, discharge, and 2 months after discharge

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Figure 1: Abdominal computed tomography (coronal plane). K: Transplanted kidney, B: Bladder, S: Stool. Transplanted kidney has Grade 3 of hydronephrosis

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Figure 2: Abdominal computed tomography (axial plane). B: Bladder, S: Stool. The stool compressed the neck of the bladder

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A urethral catheter was inserted, and 300 ml of urine was drained. A Foley catheter was inserted into the bladder, and 1500 ml of urine was drained over 8 h. Serum creatinine levels did not improve; therefore, we ensured manual enterostomy care, injected 50 ml of gastrografin, and manually evacuated the rectum. The impacted stool became soft, decreased in size, and moved slightly toward the anus. Over the next 3 days, an intestinal lavage of 200 ml daily was infused through the enterostomy. If the urine volume was ≤500 ml within 8 h, furosemide (10 mg) was administered intravenously, and negative pressure was provided via the Foley catheter. Eight days later, the patient was discharged. Her body weight reduced to 10.58 kg, the blood pressure was 90/50 mmHg, and renal function parameters and hemoglobin levels were normal [Table 1].

Two months later, her renal function remained normal [Table 1], and abdominal ultrasound showed Grade 1 hydronephrosis. She passed firm stools daily, and her daily urine output was 1000–1500 ml. The lower abdominal mass was still palpable but was smaller than that at admission.

  Discussion Top

The cause of AKI after renal transplantation, in this case, was obstructive nephropathy due to bladder compression by impacted stool in the colon. Common causes of AKI after renal transplantation include acute rejection, ischemic–reperfusion injury, medication, infection, and urinary tract obstruction.[2] There are few reports on bladder compression caused by impacted stool that results in obstructive nephropathy after renal transplantation. The rate of CAKUT in patients with anorectal malformation is 15%,[3] and the incidence of constipation that requires laxatives and enemas after correction of an anorectal malformation is 77.4%.[4] In cases of deletion of the long arm of chromosome 10, although growth retardation has been reported that CAKUT and anorectal malformation are rare, uncharacteristic findings.[5],[6] These results indicate that CAKUT patients with anorectal malformation are more likely to require treatment for constipation; therefore, it is necessary to evaluate whether constipation is properly managed in such patients. Despite treatment, the stool was not completely evacuated, and this gradually accumulated in the sigmoid colon and rectum, compressing the bladder outlet, and resulting in obstructive nephropathy. The patient's family declined a colostomy; however, a colostomy was planned if the patient exhibited recurring features of obstructive uropathy.

In a study on 3066 renal transplant patients who were hospitalized due to AKI, Mehrotra et al. reported that the rate of allograft loss was 12.1% during hospitalization and 26.1% within 90 days after AKI onset.[1] Patients with good renal function before AKI onset were reported to be at a higher risk of transplant loss after the onset of AKI.[1] Early treatment of AKI is important to prevent derangement of renal function. Prompt diagnosis of AKI and removal of obstruction could improve and maintain renal function.[7] This case report indicates that abdominal ultrasound and CT are useful in determining the causes of obstructive nephropathy.

We reported the case of a patient with AKI secondary to obstructive nephropathy caused by impacted stool in the colon that compressed the bladder outlet. Prompt diagnosis and treatment led to improvement and maintenance of renal function. Daily defecation management is critical in patients with CAKUT and anorectal malformations.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient's parents have given their consent for her images and other clinical information to be reported in the journal. The patient's parents understand that her name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Mehrotra A, Rose C, Pannu N, Gill J, Tonelli M, Gill JS. Incidence and consequences of acute kidney injury in kidney transplant recipients. Am J Kidney Dis 2012;59:558-65.  Back to cited text no. 1
Mittal T, Kohli HS. Post renal transplant acute kidney injury. Indian J. Transplant 2014;8:S33-6.  Back to cited text no. 2
Bassam G, Jawdeh A, Govil A. Acute kidney injury in transplant setting: Differential diagnosis and impact on health case. Adv Chronic Kidney Dis 2017;24:228-32.  Back to cited text no. 3
Chang PC, Duh YC, Fu YW, Hsu YJ, Wei CH, Huang H. How much do we know about constipation after surgery for anorectal malformation? Pediatr Neonatol 2020;61:58-62.  Back to cited text no. 4
Irving M, Hanson H, Tumpenny P, Brewer C, Oglivie CM, Davies A, et al., Deletion of the distal long arm of Chromosome 10; Is there a characteristic phenotype? A report of 15 de novo and familial cases. Am J Med Genet 2003;123A: 153-63.  Back to cited text no. 5
Yatsenko SA, Kruer MC, Bader PI, Coizo D, Schutte J, Keegan CE, et al. Identification of critical regions for clinical features of distal 10q deletion syndrome. Clin Genet 2009;76:54-62.  Back to cited text no. 6
Kumar S, Ameli-Renani S, Hakim A, Jeon JH, Shrivastava S, Patel U. Ureteral obstruction following renal transplantation: causes, diagnosis and management. Br J Radiol 2014;87:20140169.  Back to cited text no. 7


  [Figure 1], [Figure 2]

  [Table 1]


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