Renal Sarcoidosis Unmasked by Mycobacterium franklinii Infection

Introduction: Renal sarcoidosis, present in 0.7% of sarcoidosis cases, manifests as hypercalcemia, nephrocalcinosis, granulomatous interstitial nephritis (GIN). We report a rare case of GIN due to renal sarcoidosis diagnosed post-Mycobacterium franklinii infection, highlighting links between mycobacterial infections and sarcoidosis. Case Description: A 62-year-old female with hypertensiondeveloped fever and night sweats after a trip to Pakistan, and was found to have lymphadenopathy. A sputum culture revealed M. franklinii, and imaging showed liver lesions and lymphadenopathy. Fine-needle biopsy of a porta-hepatis lymph node revealed non-necrotizing granulomas, and a liver biopsy also revealed non-necrotizing granulomatous inflammation with negative acid fast and fungal stains. After six months of anti-tuberculous therapy, the patient’s lymphadenopathy and liver lesions improved, and sputum cultures were subsequently confirmed to be negative, but renal function began to decline, from a baseline of 0.8 mg/dL to 2.1 mg/dL. Renal biopsy (Figure 1) revealed non-necrotizing granulomatous interstitial nephritis and 25-30% interstitial fibrosis. Stains for microorganisms were negative. Diagnosed with renal sarcoidosis, she started prednisone 40 mg daily with tapering. Her creatinine improved from a peak of 2.3 to 1.26 mg/dL, and her proteinuria resolved. Discussion: This case underscores the exceptional rarity and diagnostic challenge of GIN secondary to renal sarcoidosis, especially with concurrent M. franklinii infection. GIN occurs in fewer than 1% of renal biopsies, and its association with M. franklinii is scarcely documented. The clinical course in this case suggests that M. franklinii may trigger or exacerbate sarcoid-like immunopathology despite resolution of the mycobacterial infection, highlighting the need to consider atypical infectious triggers and hypersensitivity responses in granulomatous diseases. Distinguishing infectious granulomas from sarcoid-related inflammation required careful exclusion of active mycobacterial involvement. The patient’s response to corticosteroids post-antimycobacterial therapy emphasizes the importance of sequential management. This case reinforces that renal biopsy is crucial in inadequately explained kidney injury, especially with systemic granulomatous disease, given the rarity and potential severity of renal sarcoidosis.

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Journal of the American Society of Nephrology
Published
2025-10-01
DOI
https://doi.org/10.1681/asn.20256p1z6xbn
Primary Topic
Sarcoidosis and Beryllium Toxicity Research
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article
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article

Renal Sarcoidosis Unmasked by Mycobacterium franklinii Infection

Xavier Vela Parada, Nawal Aamir, Vijay K. Vanguri, Gagan Aulakh et al.
Journal of the American Society of Nephrology
Sarcoidosis and Beryllium Toxicity Research
article

Renal Sarcoidosis Unmasked by Mycobacterium franklinii Infection

Xavier Vela Parada, Nawal Aamir, Vijay K. Vanguri, Gagan Aulakh, Hassan Abbas
article en

Abstract

Introduction: Renal sarcoidosis, present in 0.7% of sarcoidosis cases, manifests as hypercalcemia, nephrocalcinosis, granulomatous interstitial nephritis (GIN). We report a rare case of GIN due to renal sarcoidosis diagnosed post-Mycobacterium franklinii infection, highlighting links between mycobacterial infections and sarcoidosis. Case Description: A 62-year-old female with hypertensiondeveloped fever and night sweats after a trip to Pakistan, and was found to have lymphadenopathy. A sputum culture revealed M. franklinii, and imaging showed liver lesions and lymphadenopathy. Fine-needle biopsy of a porta-hepatis lymph node revealed non-necrotizing granulomas, and a liver biopsy also revealed non-necrotizing granulomatous inflammation with negative acid fast and fungal stains. After six months of anti-tuberculous therapy, the patient’s lymphadenopathy and liver lesions improved, and sputum cultures were subsequently confirmed to be negative, but renal function began to decline, from a baseline of 0.8 mg/dL to 2.1 mg/dL. Renal biopsy (Figure 1) revealed non-necrotizing granulomatous interstitial nephritis and 25-30% interstitial fibrosis. Stains for microorganisms were negative. Diagnosed with renal sarcoidosis, she started prednisone 40 mg daily with tapering. Her creatinine improved from a peak of 2.3 to 1.26 mg/dL, and her proteinuria resolved. Discussion: This case underscores the exceptional rarity and diagnostic challenge of GIN secondary to renal sarcoidosis, especially with concurrent M. franklinii infection. GIN occurs in fewer than 1% of renal biopsies, and its association with M. franklinii is scarcely documented. The clinical course in this case suggests that M. franklinii may trigger or exacerbate sarcoid-like immunopathology despite resolution of the mycobacterial infection, highlighting the need to consider atypical infectious triggers and hypersensitivity responses in granulomatous diseases. Distinguishing infectious granulomas from sarcoid-related inflammation required careful exclusion of active mycobacterial involvement. The patient’s response to corticosteroids post-antimycobacterial therapy emphasizes the importance of sequential management. This case reinforces that renal biopsy is crucial in inadequately explained kidney injury, especially with systemic granulomatous disease, given the rarity and potential severity of renal sarcoidosis.

Journal of the American Society of NephrologyVol. 36(10S)
University of Massachusetts Chan Medical School (US)
Openalex Percentile: Top 53%
Sarcoidosis and Beryllium Toxicity Research
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