| Abstract|| |
Transformation of the urothelium to the intestinal type of epithelium is rare in the pelvis with very few cases reported in the literature. The present study reports extensive intestinal metaplasia of the pelvi-calyceal system without residual urothelium in a 35-years-old woman with a 2 years history of renal calculi. Right - sided Nephrectomy was undertaken. Immunohistochemistry of the metaplastic epithelium revealed positive expression of CK20, low Ki-67 index and negative expression of p53. In this patient long standing metaplastic changes did not progress to adenocarcinoma which indicates that extensive intestinal metaplasia is not always associated with malignancy.
Keywords: Intestinal metaplasia, nephrolithiasis, pelvi-calyceal system
|How to cite this article:|
Shukla P, Gulwani HV. Extensive intestinal metaplasia of renal pelvis: Report of a case and literature review. Indian J Pathol Microbiol 2015;58:483-6
|How to cite this URL:|
Shukla P, Gulwani HV. Extensive intestinal metaplasia of renal pelvis: Report of a case and literature review. Indian J Pathol Microbiol [serial online] 2015 [cited 2021 Jul 25];58:483-6. Available from: https://www.ijpmonline.org/text.asp?2015/58/4/483/168890
| Introduction|| |
The pelvi-calyceal system in human kidneys is normally lined by transitional epithelium. Chronic irritation may lead to metaplastic changes in the epithelium which is usually of squamous type. Although intestinal metaplasia is frequently encountered in the urinary bladder, it is very rare to find such metaplasia in upper urinary tract including renal pelvis and ureter. Only a few cases have been described in the medical literature wherein extensive intestinal metaplasia has replaced the entire transitional epithelium of pelvi-calyceal system with no evidence of any dysplasia or malignancy.,, A rare such case is being described here in a middle-aged female patient.
| Case Report|| |
A 35-year-old woman presented with complaints of pain in the right flank for last 1 month that was radiating to the inguinal region. She underwent ultrasound 2 years back and was diagnosed to have nephrolithiasis subsequent to which pyelolithotripsy was attempted which was unsuccessful.
Routine laboratory investigations at the time of present admission were chiefly within normal limits except for mild anemia (Hb-9.8 g/dl). Total leukocyte count was raised (TLC-14,400/cumm), and differential count showed increased polymorphs (Neutrophils 88%, lymphocytes 10%, and eosinophils 2%). Urine analysis revealed the values of 2-4 white blood cells/hpf, occasional red blood cells/hpf, proteinuria 50 mg/l, and no bacteriuria. An Isotope renogram was performed which was suggestive of the right nonfunctioning kidney. Computed tomography abdomen showed features suggestive of multiple renal calculi and pyonephrosis [Figure 1].
|Figure 1: Axial postcontrast computed tomography image showing heterogeneous right renal mass with high attenuation and foci of calcification suggesting pyelonephritis|
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With a clinical diagnosis of emphysematous pyelonephritis, right nephrectomy was performed. Intraoperatively dense adhesions were present in the right retroperitoneum. The kidney was densely adhered to Gerota's fascia, ascending colon, duodenum, inferior vena cava, liver, and psoas muscle.
On gross examination, the kidney was normal in size. The renal capsule was adherent to perinephric fat. Cut surface showed marked destruction of the renal parenchyma and was almost largely replaced by dilated pelvi-calyceal system with fatty infiltration [Figure 2]. An impacted stone was seen in the pelvis that measured 1.2 cm in diameter. Mucinous secretions were noted in the focal area.
|Figure 2: Gross photograph of right kidney showing destruction of renal parenchyma and replacement by dilated pelvi-calyceal system and fatty infiltration|
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On microscopic examination, features of chronic pyelonephritis were evident. There was marked glomerular and tubular atrophy with thyroidization of tubules, dense interstitial fibrosis, and lymphoplasmacytic cell infiltrate. There was the striking replacement of entire transitional epithelium of pelvi-calyceal system by a large intestinal type of epithelium. In one area, the intestinal mucosa was hyperplastic and forming a small polyp with the presence of several dilated glands. The intestinal glands were lined by tall columnar epithelium with numerous goblet cells [Figure 3]a. No residual transitional epithelium was noted in the entire kidney, and there was no squamous metaplasia evident. In two foci, small, atrophic renal tubules surrounded by fibromuscular collars were noted [Figure 3]b. Several small calcific deposits were seen in the renal parenchyma. There was no evidence of dysplasia or invasive malignancy in any of the sections examined.
|Figure 3: (a) Photomicrograph is showing extensive intestinal metaplasia of the lining urothelium and almost complete replacement by large intestinal metaplasia. (b) Photomicrograph showing the presence of intestinal glands near pelvic mucosa (thick arrow) and residual atrophic renal tubules (thin arrow)|
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Immunohistochemistry showed expression of CK20 in the intestinal epithelium and CK7 in the residual renal tubules. Smooth muscle actin was positive in fibromuscular collars around the atrophic renal tubules. Ki-67 index was very low (<1%) and p53 expression was not noted in the metaplastic epithelium [Figure 4]a,[Figure 4]b,[Figure 4]c,[Figure 4]d.
|Figure 4: Immunohistochemical stain. (a) CK20 positive intestinal glands. (b) CK7 is showing the presence of few residual positive atrophic renal tubules (inset) and negative intestinal glands. (c) Smooth muscle actin is showing fibromuscular hyperplasia in renal parenchyma, more prominent around atrophic renal tubules. (d) The p53 stain reveals that none of the cells stained positive for this marker|
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Based on above findings, the diagnosis of chronic pyelonephritis with extensive intestinal metaplasia of pelvi-calyceal system was made.
| Discussion|| |
To the best of our knowledge, only 12 cases of pure intestinal metaplasia of renal pelvis without associated malignancy have been reported previously in the literature [Table 1].
|Table 1: Intestinal metaplasia of the renal pelvis not associated with malignancy|
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The age ranged from 24 to 79 years with an average age of 47 years. Male to female ratio was 1:1. Of 12 cases reported, eight of the cases were associated with multiple renal calculi and the majority has concurrent chronic pyelonephritis and hydronephrosis. Smooth muscle hypertrophy around the atrophic tubules was noted in two cases. This is the 13th case of pure intestinal metaplasia of the pelvis with complete replacement of the urothelium which was not associated with the evidence of carcinoma.
The urothelium is an increasingly responsive structure which is capable of developing metaplastic changes as a result of chronic irritation. Squamous metaplasia is much more common than intestinal metaplasia in renal pelvis and calyces. It is presumed that protoplastic conversion of the transitional epithelium to the intestinal type of epithelium occurs in response to mechanical factors such as calculi, chronic infection, and hydronephrosis. However, the exact explanation for such predilection is not known.
The present case is unusual because of the following features. First, there was extensive intestinal metaplasia of the pelvi-calyceal system and hyperplastic polyp formation with no residual urothelium in the entire kidney. Second, there was no evidence of any dysplasia or malignancy despite such long standing metaplastic changes. In addition, hyperplastic muscle fibers were noted around the atrophic tubules. The sequence of events that could have led to a chronic destructive process in the kidney may be hypothesized as follows-predisposition to nephrolithiasis leading to chronic pyelonephritis and the resultant extensive intestinal metaplasia.
Intestinal metaplasia of the urothelium evolves from constant irritation. The gradual transformation from glandular metaplasia to the premalignant lesion and then to frank malignancy has been historically documented. Coexistence of metaplasia and adenocarcinoma suggests that glandular metaplasia is a high-risk factor. However, the significance of this association and its weightiness demands further exploration as in the present case, despite long-standing metaplasia in the kidney, she did not progress to dysplasia or invasive malignancy as has been reported by several other studies.,,, The epithelium undergoing metaplasia is potentially unstable and can develop malignant changes as a result of the loss of control by cell cycle regulators such as p16 and p53. According to Deniz et al., strong expression of p53 gene signifies the development of dysplasia even before dysplasia is appreciated by microscopic analysis. In the present case, p53 was negative, and the Ki-67 index was <1%. This finding emphasizes the fact that association of intestinal metaplasia with malignancy is controversial.
| Conclusion|| |
Renal stones may also lead to extensive intestinal metaplasia. Although, this finding is associated with neoplasia but rarely this may be only a benign process as was noted in the present case.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Bullock PS, Thoni DE, Murphy WM. The significance of colonic mucosa (intestinal metaplasia) involving the urinary tract. Cancer 1987;59:2086-90.
Salm R. Combined intestinal and squamous metaplasia of the renal pelvis. J Clin Pathol 1969;22:187-91.
Ward AM. Glandular neoplasia within the urinary tract. The aetiology of adenocarcinoma of the urothelium with a review of the literature. I. Introduction: The origin of glandular epithelium in the renal pelvis, ureter and bladder. Virchows Arch A Pathol Pathol Anat 1971;352:296-311.
Mathur S, Singh MK, Rao SI, Seth A. Mucinous metaplasia of the renal pelvic epithelium in a case of recurrent urolithiasis and pyelonephritis. Urol Int 2004;72:355-7.
Brutt H. Uber Pyelitis Glandularis. Z Urol Chir 1923;14:157.
Plaut A. Diffuses deckharne bulisches Adenom des Nierenbeckens mit geschwulstartiger Wucherung von Gesfässmuskulatur. Z Urol Chir 1929;26:562.
Foot NC. Glandular metaplasia of the epithelium of the urinary tract. South Med J 1944;37:137-42.
Torassa GL Jr. Pyelitis glandularis. J Urol 1948;60:393-7.
Maclean JT, Fowler VB. Pathology of tumors of the renal pelvis and ureter. J Urol 1956;75:384-415.
Gordon A. Intestinal metaplasia of the urinary tract epithelium. J Pathol Bacteriol 1963;85:441-4.
Towers RP. Aspects of metaplasia in genito-urinary pathology. J Ir Med Assoc 1963;53:179-83.
Lam KY, Choi CH. Massive enlargement of the kidney in glandular metaplasia of the renal pelvis. Nephron 1995;69:91-2.
Deniz K, Kala M, Kaya R. Intestinal metaplasia of the renal pelvis. Urol J 2010;7:287-9.
Zhou W, Zhong K, Wang J, Gu Y, Huang L, Jiang Z, et al.
Intestinal metaplasia of the renal pelvis: A case report and literature review. Oncol Lett 2014;8:2664-8.
Spires SE, Banks ER, Cibull ML, Munch L, Delworth M, Alexander NJ. Adenocarcinoma of renal pelvis. Arch Pathol Lab Med 1993;117:1156-60.
Manunta A, Vincendeau S, Kiriakou G, Lobel B, Guillé F. Non-transitional cell bladder carcinomas. BJU Int 2005;95:497-502.
Mostofi FK. Potentialities of bladder epithelium. J Urol 1954;71:705-14.
Ranadive NU, Vaze AM, Abhyankar SC, Bapat SD, Deodhar KP. Primary carcinomas of renal pelvis. (A follow up study). Indian J Pathol Microbiol 1984;27:11-7.
Solanki RL, Ramdeo IN, Gupta DP, Mahawal BS. Primary tumours of renal pelvis. Indian J Cancer 1980;17:230-6.
Guha T, Datta BN, Aikat BK, Kataria PN. Neoplasms of the kidney, renal pelvis and ureter. A study of 92 primary and 44 metastic tumours. Indian J Cancer 1974;11:60-8.
Powari M, Singh SK, Radotra BD. Intestinal metaplasia with dysplasia in pelvis of a horse-shoe kidney. Indian J Pathol Microbiol 2001;44:457-8.
Dr. Hanni V Gulwani
Department of Pathology, B-19, Type II Doctor Quarters, Bhopal Memorial Hospital and Research Centre Campus, Raisen Bypass Road, Bhopal - 462 038, Madhya Pradesh
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2], [Figure 3], [Figure 4]