Granulomatous Tubulointerstitial Nephritis in a Kidney Transplant Recipient: Case Report and Review of the Literature.


Journal

Transplantation proceedings
ISSN: 1873-2623
Titre abrégé: Transplant Proc
Pays: United States
ID NLM: 0243532

Informations de publication

Date de publication:
Oct 2021
Historique:
received: 22 05 2021
accepted: 03 08 2021
pubmed: 8 9 2021
medline: 26 11 2021
entrez: 7 9 2021
Statut: ppublish

Résumé

Granulomatous tubulointerstitial nephritis (GTIN) is a rare pathologic finding on kidney biopsy. GTIN can be associated with drugs, infection, systemic granulomatous disease, and tubulointerstitial nephritis with uveitis syndrome. We present a case of GTIN in a kidney transplant recipient (KTR) and a literature review of published cases of GTIN in KTRs. A 65-year-old man with a history of pulmonary and ocular tuberculosis (TB), who had undergone deceased donor kidney transplant 8 years prior, was admitted for acute kidney injury, hypercalcemia, and uveitis. His medications included rifabutin, isoniazid, and tacrolimus. Serum laboratory tests revealed creatinine of 2.65 mg/dL (baseline 1.1-1.5 mg/dL) and corrected calcium of 13.2 mg/dL. Hypercalcemia workup showed parathyroid hormone 7 pg/mL, 1,25(OH) vitamin D 54 pg/mL, parathyroid hormone-related peptide <2.0 pmol/L, and angiotensin-converting enzyme 47 U/L. Kidney biopsy showed GTIN with noncaseating granulomas. Universal polymerase chain reaction testing for acid-fast bacilli, fungus, and bacteria was negative. He was treated with prednisone, and his kidney function returned to baseline, and his hypercalcemia resolved. GTIN is a rare entity seen in less than 1% of transplanted kidney biopsies. The exactly etiology of this GTIN case remains unknown. TB could not be entirely ruled out, because the patient was receiving active anti-TB therapy. Our literature review showed infection to be the leading cause of GTIN in KTRs and that GTIN with concomitant uveitis remains exceedingly rare. Steroids may be useful in certain cases.

Sections du résumé

BACKGROUND BACKGROUND
Granulomatous tubulointerstitial nephritis (GTIN) is a rare pathologic finding on kidney biopsy. GTIN can be associated with drugs, infection, systemic granulomatous disease, and tubulointerstitial nephritis with uveitis syndrome. We present a case of GTIN in a kidney transplant recipient (KTR) and a literature review of published cases of GTIN in KTRs.
CASE PRESENTATION METHODS
A 65-year-old man with a history of pulmonary and ocular tuberculosis (TB), who had undergone deceased donor kidney transplant 8 years prior, was admitted for acute kidney injury, hypercalcemia, and uveitis. His medications included rifabutin, isoniazid, and tacrolimus. Serum laboratory tests revealed creatinine of 2.65 mg/dL (baseline 1.1-1.5 mg/dL) and corrected calcium of 13.2 mg/dL. Hypercalcemia workup showed parathyroid hormone 7 pg/mL, 1,25(OH) vitamin D 54 pg/mL, parathyroid hormone-related peptide <2.0 pmol/L, and angiotensin-converting enzyme 47 U/L. Kidney biopsy showed GTIN with noncaseating granulomas. Universal polymerase chain reaction testing for acid-fast bacilli, fungus, and bacteria was negative. He was treated with prednisone, and his kidney function returned to baseline, and his hypercalcemia resolved.
DISCUSSION CONCLUSIONS
GTIN is a rare entity seen in less than 1% of transplanted kidney biopsies. The exactly etiology of this GTIN case remains unknown. TB could not be entirely ruled out, because the patient was receiving active anti-TB therapy. Our literature review showed infection to be the leading cause of GTIN in KTRs and that GTIN with concomitant uveitis remains exceedingly rare. Steroids may be useful in certain cases.

Identifiants

pubmed: 34489112
pii: S0041-1345(21)00535-2
doi: 10.1016/j.transproceed.2021.08.004
pii:
doi:

Substances chimiques

Prednisone VB0R961HZT

Types de publication

Case Reports Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

2546-2551

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

Auteurs

Jordana Yahr (J)

Department of Internal Medicine, Cleveland Clinic Foundation, Cleveland, Ohio.

Mohamed Hassanein (M)

Department of Nephrology, Cleveland Clinic Foundation, Cleveland, Ohio.

Leal Herlitz (L)

Department of Pathology, Cleveland Clinic Foundation, Cleveland, Ohio; Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, Ohio.

Richard Fatica (R)

Department of Nephrology, Cleveland Clinic Foundation, Cleveland, Ohio; Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, Ohio. Electronic address: faticar@ccf.org.

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Classifications MeSH