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Images in Nephrology
ARTICLE IN PRESS
doi:
10.25259/ijn_527_23

Osseous Metaplasia in Renal Allograft

Consultant Pathologist, Renopath, Center for Renal and Urological Pathology, Chennai, Tamil Nadu, India
Consultant Nephrologist, Apollo Hospitals, Chennai, Tamil Nadu, India

Corresponding author: Anila A. Kurien, Renopath, Center for Renal and Urological Pathology, No 27 and 28, VMT Nagar, Kolathur, Chennai, Tamil Nadu, India. E-mail: anila_abraham08@yahoo.com

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This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

How to cite this article: Malathi CV, Venkatesh Rajkumar S, Jansi Prema KS, Kurien AA. Osseous Metaplasia in Renal Allograft. Indian J Nephrol. doi: 10.25259/ijn_527_23

Osseous metaplasia (OM) is the presence of heterotopic bone tissue in the extraskeletal soft tissue. OM was described in many nontransplant organs like parotid, skin, lung, labyrinth, endometrium, and kidney.1 OM is a rare finding in the renal allograft biopsy.

A 35-year-old male developed end-stage renal disease as a result of chronic interstitial nephritis. The patient underwent live donor renal transplantation and was on triple drug regimen of tacrolimus, mycophenolate mofetil, and steroids. Three years posttransplant, the patient developed acute pyelonephritis, which was treated with appropriate antibiotics, following which the graft function stabilized. Five months later, he again developed graft dysfunction, with serum creatinine of 2 mg/dl. Serum calcium was 9.3 mg/dl. The kidney was normal on ultrasonogram; no calcification was seen. A renal biopsy was performed. Light microscopy showed eleven glomeruli, 2 were globally sclerotic. All the viable glomeruli were of normal cellularity. The capillary loops were patent and no fibrin thrombus was noted in the lumen. Glomerular basement membrane appeared normal. Interstitial fibrosis involved 50% of the sampled cortex. Lymphocytic infiltration was seen in the fibrosed cortex. There was a focus in the renal cortex where woven bone formation was noticed [Figure 1]. The osteocytes located in the lacunae were appreciated under higher magnification. Focal mineralization was also observed [Figure 2]. There were no hematopoietic cells or adipocytes in the region of bone formation. The biopsy showed no features of rejection, including tubulitis, peritubular capillaritis, or vasculitis. C4d immunostaining was negative. On follow-up, his graft function is stable, with serum creatinine maintained at 2 mg/dl.

(a) Woven bone is seen in the renal parenchyma. The surrounding tissue shows fibrosis of the interstitium (Masson trichrome stain, 100×). (b) There is a focus of mineralization within the woven bone (hematoxylin and eosin stain, 200×).
Figure 1:
(a) Woven bone is seen in the renal parenchyma. The surrounding tissue shows fibrosis of the interstitium (Masson trichrome stain, 100×). (b) There is a focus of mineralization within the woven bone (hematoxylin and eosin stain, 200×).
There are (a) osteocytes within lacunae and (b) a focus of mineralization (hematoxylin and eosin stain, 400×).
Figure 2:
There are (a) osteocytes within lacunae and (b) a focus of mineralization (hematoxylin and eosin stain, 400×).

OM results from the differentiation of mesenchymal pluripotent cells into bone tissue. The heterotopic bone matrix can be mineralized and be associated with adipocytes and hematopoietic cells. The osseous differentiation, considered aberrant tissue repair, requires a suitable environment and osteogenic signals. Various experimental studies have described the occurrence of OM in association with ischemia and inflammation. OM can be associated with the presence of hematopoietic elements (myeloid metaplasia) as reported by Azhir et al.2

There are limited cases of OM reported in the renal allograft [Table 1]. Majority of them were detected following allograft nephrectomy.1-4 The time taken for the appearance of OM varied between 6 months and 5 years. OM was observed during autopsy in one case.5 All except our case had concomitant features of rejection. Chronic inflammation or ischemic changes were present in all the cases.6 OM in our patient is likely to be the sequela of pyelonephritis. Similar to our patient, Bataille et al.1 observed OM in association with recurrent pyelonephritis.1 They hypothesized that OM resulted from chronic ischemia or inflammation following infection or as an immunologic process.

Table 1: Literature review of osseous metaplasia in the renal allografta
Author Age at Tx Specimen type Native kidney disease Rejection Type of donor Location of osseous metaplasia
Current case 35 Allograft biopsy Chronic interstitial nephritis No rejection Live Renal cortex
Bataille et al.1 21 Graft nephrectomy Interstitial nephritis Chronic Deceased Renal cortex
Azhir et al.2 28 Graft nephrectomy Diabetic Nephropathy Acute on chronic Live Renal cortex and medulla
Tousignant et al.3 15 Graft nephrectomy Renal dysplasia Acute on chronic Deceased Renal cortex
Chan et al.4 43 Graft nephrectomy IgA Nephropathy Chronic Deceased Renal parenchyma
Makhoba et al.5 11 Autopsy Unknown Chronic NA Renal parenchyma
Sanders et al.6 22 Allograft biopsy FSGS Collapsing variant Acute on chronic Deceased Renal cortex
Adapted from Sanders BP et al. Exp Clin Transplant. 2014;12(4):371-373. Tx = transplant, VUR = vesicoureteral reflux, FSGS = focal and segmental glomerulosclerosis, NA = Not Available

The calcification detected in the allograft by imaging studies could be due to nephrolithiasis, ectopic calcification, or OM.1 Nephrolithiasis is located in renal pelvis. Ectopic calcification is the inappropriate biomineralization in soft tissues with deposition of calcium salts and can occur in uremic patients due to mineral imbalance. OM is different from ectopic calcification. Unlike OM, bone formation, osteocytes, or hematopoietic elements are absent in ectopic calcification.

OM in the renal allograft is rare. Though not directly implicated in the graft dysfunction, its presence in the biopsy hints toward chronic injurious stimuli like inflammation, ischemia, or infection in the allograft.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent.

Conflicts of interest

There are no conflicts of interest.

References

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