Abstract
Background: An uncommon cause of recurrent renal colic is mucous tissue passage secondary to renal papillae necrosis. Because of its low prevalence, the correct management of recurrent obstructive uropathy produced by renal papillary necrosis (RPN) is not well defined.
Case Presentation: We present a case of recurrent renal colic associated with the expulsion of mucous tissue in a young woman's urine with a history of excessive consumption of nonsteroidal anti-inflammatory drugs (NSAIDs). The patient required multiple admissions to the emergency department because of recurrent episodes of renal colic. A retrograde pyelogram and histopathologic study of the expulsed tissue supported the diagnosis of RPN. The patient was managed with Double-J stents for 12 months, complete withdrawal of NSAIDs, and large volume intake of water. A satisfactory outcome was seen radiologically and endoscopically after treatment. The patient stopped experiencing new renal colic episodes because of the passive ureteral dilatation despite still presenting the mucous tissue expulsion in the urine.
Conclusions: Passive ureteral dilatation with Double-J stents could possibly be an effective treatment for patients with recurrent renal colic secondary to persistent renal papillae necrosis.
Keywords: ureteroscopy, ureteroscopy instrumentation, stents, obstruction, infection/inflammation
Introduction and Background
Acute renal colic is associated with urolithiasis in >80% of the cases. However, additional uncommon causes of acute renal colic should also be considered—particularly in negative CT scans. Among rare causes of renal pain is the sloughed tissue from a necrosed renal papilla.1 The sloughed papilla tissue presents as a mucous material that can obstruct the ureteral lumen, provoke recurrent renal colic, and produce persistent obstruction that could be associated with urinary tract infection. The detachment of papillary tissue is caused by a deterioration of the vascular flow in the renal pyramids. Renal papillary necrosis (RPN) has been associated primarily with diabetes, urinary tract infection, and nonsteroidal anti-inflammatory drugs (NSAIDs).2 The correct management of obstructive uropathy produced by this rare disease is not well defined. Thus, we present a case report to demonstrate the endourologic management of recurrent obstructive uropathy caused by renal papillae necrosis.
Case Presentation
Clinical history and physical examination
We present a 31-year-old young woman with a history of reactive arthritis and chronic NSAID consumption (ketorolac and ibuprofen for ∼15 years).
In the past 4 years, the patient experienced mild recurrent left back pain, with spontaneous remission after the expulsion of a mucous and membranous-like material in the urine (Fig. 1a).
FIG. 1.
(a) Mucous—membranous tissue expulsed in the urine. (b) Retrograde pyelography with arrows pointing irregularities and bulging of the superior calices with clefts that extend from the fornices to the pyramid tip (lobster claw sign).
After 2 years since the first episode of back pain and recurrent urinary expulsion of mucous tissue, the patient presented to the emergency department (ED) with severe left renal colic on several occasions. The patient underwent flexible ureteroscopy and retrograde pyelography at her local hospital, with no specific findings commented by her previous urologist.
Diagnosis
Blood tests showed hemoglobin 12.3 g/dL, leukocytes 5340 mm3, lymphocytes 33%, eosinophils 7.5%, neutrophils 54%, platelets 230,000 μL, glucose 83 mg/dL, and creatinine of 0.84 mg/dL. Urinalysis showed 40 leukocytes per field, 15–20 erythrocytes per field, and a positive urine culture for Enterococcus faecalis.
In the ultrasonography, left hydronephrosis was reported without evidence of lithiasis. After adequate antibiotic therapy, the patient underwent another bilateral retrograde pyelogram, which showed irregularity and bulging of the upper calices with fissures extended from the fornices to the tip of the pyramid compatible with the “lobster clamp sign” (Fig. 1b). The patient underwent diagnostic flexible ureteroscopy without specific findings on the renal papillae with a regular appearance at the time of the procedure. (Fig. 2). Histopathologic evaluation of mucosal tissue expelled in the urine was described as mixed inflammatory elements with lymphocytes, macrophages, and polymorphonuclear cells associated with bacterial groups. In addition, embedded fibroblasts were observed in a hemorrhagic background, compatible with an exacerbated chronic inflammatory process (Fig. 3). Radiographic, endoscopic, and pathologic findings taken together supported the diagnosis of RPN.
FIG. 2.
Hematoxylin and eosin staining (100 × ) of the mucous expulsed material. Mixed inflammatory elements such as lymphocytes and macrophages, polymorphonuclear cells (white arrow) associated with bacterial groups (arrowhead) can be found. Also, some groups of fibroblasts embedded in a hemorrhagic background can be found that are compatible with an exacerbated chronic inflammatory process.
FIG. 3.
Endoscopic images of the last flexible ureteroscopy showing normal renal papillae. (a) Upper pole papillae and (b) interpolar papilla.
Intervention
A flexible ureteroscopy was performed, finding a normal endoscopic appearance of all renal papillae after the essential evaluation at our endourology department.
The ureteral stent was inserted and then changed every 60–90 days because renal colic persisted when the patient had the stent removed (with a total exchange number of 4). Finally, after 12 months, the last Double-J stent (4.7F/24 cm InLay Optima® from C.R. Bard, BD) was removed without reinsertion because of renal colic. All NSAIDs were suspended, and abundant hydration (>2.5 L/day) was prescribed.
Follow-up
The patient was followed up every 30 days. The ureteral stent was tolerated well, and the patient continued expelling mucous material in the urine without symptoms 12 months after removing the last Double-J stent (4.7F/24 cm InLay Optima® from C.R. Bard, BD) and suspension of NSAIDs. A retrograde control pyelogram (Fig. 4) and nonenhanced CT were performed as a follow-up protocol, both showing normal findings at this time.
FIG. 4.
Retrograde pyelography at 12 months of follow-up. With no irregularities and bulging of the superior calices (arrows) but retrograde contrast reflux.
Outcome
Currently, the patient has normal renal function and has not suffered from renal colic, even though she continues with the mucous tissue's expulsion from the sloughed papillae in the urine.
Discussion
Acute renal colic represents around 2% of all the admissions to the ED. This condition affects 5%–15% of the population, requiring urgent intervention.1 Endourologists are familiarized with the most common causes of renal colic, such as urinary stones. However, less frequent causes of acute renal colic could represent a real challenge for diagnosis and management. Therefore, urologists should consider all possible causes of renal colic, even the most uncommon etiologies.
Urinary bezoar and papillary necrosis are excellent examples of rare urinary tract obstruction causes and the consequent renal colic.3 The urinary bezoar has been described as a semisolid mucous material inside the urinary system formed secondary to fungal infections and necrotic tissue from renal papillae. Candida Albicans has been the fungi most commonly found in urinary bezoars. Patients with RPN and urinary bezoar could have a history of the recurrent passage of necrosed papilla tissue from the kidney through the ureter (Fig. 1a) with the consequent ureteral obstruction and hydronephrosis. Opposite to what is seen with urinary stones, this mucous tissue could provoke a transient renal obstruction and pain. Therefore, mucous material expulsion in urine and renal colic episodes could be recurrent if the etiologic agent is not eradicated.
A high index of suspicion is necessary to diagnose uncommon causes of renal colic correctly. Clinical history has a central place in the evaluation of the patient with RPN, and endourologists must investigate specifically the recurrent passage of mucous tissue in the urine. In addition, recurrence of the renal colic and its spontaneous resolution after the urinary expulsion of the mucous tissue in the urine could give to the endourologist a high index of suspicion for RPN as the etiologic agent of the acute renal colic. Most commonly, CT scans show hydronephrosis with no visible causes of obstruction.
The diagnosis of RPN is based on clinical history, imaging studies, and pathology report. Central papillary excavation (ball in tee), fornix excavation (lobster claw), and the signet ring sign have been RPN's characteristic imaging sings.2 These radiologic signs are explained by the entrance of contrast medium around to the damaged papillae. Our patient presented with the lobster claw sign, as evidenced in the retrograde pyelogram (Fig. 1b).
It has been proposed that papillae detachment is caused by an ischemic process but has not been fully elucidated. Chronic use of NSAIDs, diabetes mellitus, chronic pyelonephritis, falciform anemia, obstructive uropathy, and tuberculosis have been described as possible causes of RPN. The chronic NSAID consumption caused by reactive arthritis was the stronger suspected etiology of papillary necrosis in our patient.2,4
Treatment of obstructive uropathy is essential to preserve renal function and prevent septic complications. The placement of a bilateral Double-J catheter to alleviate obstructive uropathy has already been described in one pediatric patient.4 In this previous report, the authors did not describe the patient's follow-up time, so there is significant uncertainty in this report.
Double-J stent insertion for 2 weeks has also been described as an effective treatment in adults.2
Our patient had had multiple severe episodes of recurrent renal colics, and we have treated her with a long-lasting Double-J ureteral catheter with replacements every 60–90 days. After 12 months of passive ureteral dilatation, the patient has never suffered from renal colic after the stent removal, even though she continued to expel mucous material in the urine despite the suppression of NSAIDs. We cannot be sure that a long-term Double-J ureteral catheter is the treatment of choice, but the ureteral dilatation provoked by the ureteral stent facilitated the constant mucous expulsion in the urine despite the patient's NSAIDs suppression. It is also unknown if we could have treated her for a longer or shorter period with the ureteral stents and the same result; it could be possible that the indwelling time would be different for each patient.
Flexible ureteroscopy has been described as a diagnostic and therapeutic method and could represent an excellent therapeutic option in those symptomatic patients with a high volume of mucous tissue in the collecting system.3 Nevertheless, in some patients similar to the patient we are describing, flexible ureteroscopy could not reveal any abnormalities inside the collecting system when asymptomatic, and its therapeutic utility in such cases is limited and plays just a diagnostic role (Fig. 2).
In this patient's case, she suffered from recurrent renal colic associated with membranous mucous material expulsion with multiple admission to the ED. Passive ureteral dilatation with long-term Double-J stents resolved her recurrent pain even though she continued to pass mucous material.
We do not recommend this treatment for different ureteral obstructive situations that could be resolved with surgery.
Conclusions
Passive ureteral dilatation, with Double-J stent, could possibly be an effective treatment method in patients with recurrent renal colic secondary to persistent renal papillae necrosis.
Acknowledgment
The authors thank Dr. Ayax Gilberto Salazar for the support given to this case.
Abbreviations Used
- CT
computed tomography
- ED
emergency department
- NSAIDs
nonsteroidal anti-inflammatory drugs
- RPN
renal papillary necrosis
Disclosure Statement
No competing financial interests exist.
Funding Information
No funding was received.
Cite this article as: Manzo BO, Tejeda E, Chew BH, Alarcon P, Flores E, Torres JE (2020) Long-term passive ureteral dilatation with Double-J stent: possibly an effective treatment for recurrent renal colic caused by papillary renal necrosis, Journal of Endourology Case Reports 6:4, 526–529, DOI: 10.1089/cren.2020.0141.
References
- 1. Gandhi A, Hashemzehi T, Batura D. The management of acute renal colic. Br J Hosp Med (Lond) 2019;80:C2–C6 [DOI] [PubMed] [Google Scholar]
- 2. Fadel MG, Carey M, Bolgeri M. Infected and obstructed kidney secondary to sloughed necrotic renal papilla. BMJ Case Rep 2018;2018:bcr2018227403. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3. Abuelnaga M, Khoshzaban S, Reda Badr M, Chaudry A. Successful endoscopic management of a renal fungal ball using flexible ureterorenoscopy. Case Rep Urol 2019;2019:9241928. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4. Broadis E, Barbour L, O'Toole S, et al. Bilateral ureteric obstruction secondary to renal papillary necrosis. Pediatr Surg Int 2010;26:867–869 [DOI] [PubMed] [Google Scholar]




