Renal Transplantation in Patients with Sarcoidosis

Aouizerate, Jessie; Matignon, Marie; Kamar, Nassim; Thervet, Éric; Randoux, Christine; Moulin, Anne‐Marie; Raffray, L.; Büchler, Matthias; Villar, Emmanuel; Mahévas, Mathieu; Desvaux, Dominique; Dahan, Karine; Diet, Carine; Audard, Vincent; Lang, Philippe; Grimbert, Philippe

doi:10.2215/cjn.03970510

Cited by 46 publications

(29 citation statements)

References 37 publications

(25 reference statements)

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“…Most commonly, sarcoidosis is discovered in donor solid organ allografts in recipients with a history of sarcoidosis [73][74][75][76][77][78][79][80], presumably inducing a granulomatous response by the recipient's immune system [81]. One report of sarcoidosis presenting following bone marrow transplantation suggests that this susceptibility may depend on donor MHC haplotypes [82].…”

Section: Models Of Sarcoidosis Pathobiologymentioning

confidence: 99%

Etiologies of Sarcoidosis

Chen

Möller

2015

Clinic Rev Allerg Immunol

117

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Since sarcoidosis was first described more than a century ago, the etiologic determinants causing this disease remain uncertain. Studies suggest that genetic, host immunologic, and environmental factors interact together to cause sarcoidosis. Immunologic characteristics of sarcoidosis include non-caseating granulomas, enhanced local expression of T helper-1 (and often Th17) cytokines and chemokines, dysfunctional regulatory T-cell responses, dysregulated Toll-like receptor signaling, and oligoclonal expansion of CD4+ T cells consistent with chronic antigenic stimulation. Multiple environmental agents have been suggested to cause sarcoidosis. Studies from several groups implicate mycobacterial or propionibacterial organisms in the etiology of sarcoidosis based on tissue analyses and immunologic responses in sarcoidosis patients. Despite these studies, there is no consensus on the nature of a microbial pathogenesis of sarcoidosis. Some groups postulate sarcoidosis is caused by an active viable replicating infection while other groups contend there is no clinical, pathologic, or microbiologic evidence for such a pathogenic mechanism. The authors posit a novel hypothesis that proposes that sarcoidosis is triggered by a hyperimmune Th1 response to pathogenic microbial and tissue antigens associated with the aberrant aggregation of serum amyloid A within granulomas, which promotes progressive chronic granulomatous inflammation in the absence of ongoing infection.

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Section: Models Of Sarcoidosis Pathobiologymentioning

confidence: 99%

Etiologies of Sarcoidosis

Chen

Möller

2015

Clinic Rev Allerg Immunol

117

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“…Granulomatous tubulointerstitial nephritis can recur in patients with kidney transplants, though this remains an extremely rare entity. A case series of renal transplant recipients found that only 3 out of 10 patients with sarcoidosis as their native renal disease (30%) had recurrence and reduced estimated glomerular filtration rate …”

Section: Discussionmentioning

confidence: 99%

“…A case series of renal transplant recipients found that only 3 out of 10 patients with sarcoidosis as their native renal disease (30%) had recurrence and reduced estimated glomerular filtration rate. 15 In summary, we describe a case series of patients who were referred for investigation of acute kidney injury, which was the presenting feature of underlying sarcoidosis. This is a rare phenomenon and is an important consideration in the patient with acute kidney injury and hypercalcaemia without an apparent alternative explanation.…”

Section: Discussionmentioning

confidence: 99%

Acute kidney injury as the presenting manifestation of sarcoidosis: A case series and review of literature

2018

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Acute kidney injury is rarely the presenting feature of sarcoidosis. We present a case series of patients whose diagnosis of sarcoidosis was only brought to light by the development of renal impairment. Concurrent hypercalcaemia was noted, prompting further investigation. The patients discussed experienced a significant and rapid improvement in both renal function and hypercalcaemia in response to therapy with prednisolone. This is out of keeping with previous reports of sarcoidosis-induced renal impairment. Our case series highlights the importance of testing for hypercalcaemia in the context of acute kidney injury. Sarcoidosis is primarily a disease of the lungs and reticuloendothelial system; however, the prevalence of renal involvement with sarcoidosis may be under-recognized. The renal manifestations of sarcoidosis are discussed in the context of the current literature. Furthermore, from our experience, we postulate that in the context of sarcoidosis-induced renal injury, concurrent hypercalcaemia may present prior to the development of chronic renal injury and therefore these patients may be more likely to recover renal function.

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“…Autopsy studies indicate that about 20% of sarcoidosis presents as GIN [4]. Recurrence of sarcoidosis on a transplanted kidney is relatively frequent (27%) and it often presents with GIN [5]. Hypercalcemia occurs in 10-20% of patients with sarcoidosis and it is thought to be a consequence of increased intestinal calcium absorption caused by accelerated 1,25(OH) 2 vitamin D production by activated macrophages [3].…”

Section: Discussionmentioning

confidence: 99%

Granulomatous interstitial nephritis in a renal allograft

et al. 2012

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We describe a middle-aged woman in whom granulomatous interstitial nephritis (GIN) developed in a renal allograft. She had undergone bowel resection due to an uncertain diagnosis of active granulomatous bowel disease 30 years earlier. Thereafter, frequent hyperoxaluria as well as calcium oxalate stone and recurrent urinary tract infections had resulted in a progressive deterioration in kidney function over a period of 20 years. She underwent living donor kidney transplantation; however, her kidney function progressively deteriorated, despite transplantation. A biopsy of the renal allograft revealed GIN with granulomatous vasculitis accompanied by calcium oxalate crystals. These as well as the laboratory findings indicated a diagnosis of sarcoidosis. We considered that the aggravated granulomatous inflammation on the allograft was caused by recurrent sarcoidosis accompanied by hyperoxaluria.

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Renal Transplantation in Patients with Sarcoidosis

Cited by 46 publications

References 37 publications

Etiologies of Sarcoidosis

Etiologies of Sarcoidosis

Acute kidney injury as the presenting manifestation of sarcoidosis: A case series and review of literature

Granulomatous interstitial nephritis in a renal allograft

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