Disseminated histoplasmosis presenting as thrombotic microangiopathy

Dwyre, Denis M.; Bell, Adam M.; Siechen, Kathleen; Sethi, Sanjeev; Raife, Thomas J.

doi:10.1111/j.1537-2995.2006.00873.x

Cited by 27 publications

(19 citation statements)

References 36 publications

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“…Any organ can be involved with Histoplasma as cases of septic arthritis and prostatitis have been described in transplant recipients . Unusual presentations in more severely ill patients have also been reported as part of the clinical picture, such as thrombotic microangiopathy and hemophagocytic lymphohistiocytosis . Most infections occur within the first 1–2 years after transplantation, though patients can present over a broad time range from months to several years posttransplant .…”

Section: Histoplasmosismentioning

confidence: 99%

Endemic Fungal Infections in Solid Organ Transplantation

Miller

Assi

2013

American Journal of Transplantation

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Section: Histoplasmosismentioning

confidence: 99%

Endemic Fungal Infections in Solid Organ Transplantation

Miller

Assi

2013

American Journal of Transplantation

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“…Other causes: Several less common etiologies have been reported to be involved in TMA pathogenesis and include: Viral infection, e.g ., CMV infection[ 27 , 28 ], BK virus[ 29 ], parvovirus[ 30 , 31 ], chronic hepatitis C virus (with or without anti-cardiolipin seropositivity)[ 32 , 33 ], and antiviral medications, e.g ., ribavirin and interferon[ 34 ] and disseminated histoplasmosis[ 35 , 36 ]. Ischemia-reperfusion injury can augment complement-associated injury through complement activation[ 37 ].…”

Section: Introductionmentioning

confidence: 99%

Thrombotic microangiopathy after renal transplantation: Current insights inde novoand recurrent disease

Abbas¹,

Kossi

Kim

et al. 2018

WJT

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Thrombotic microangiopathy (TMA) is one of the most devastating sequalae of kidney transplantation. A number of published articles have covered either de novo or recurrent TMA in an isolated manner. We have, hereby, in this article endeavored to address both types of TMA in a comparative mode. We appreciate that de novo TMA is more common and its prognosis is poorer than recurrent TMA; the latter has a genetic background, with mutations that impact disease behavior and, consequently, allograft and patient survival. Post-transplant TMA can occur as a recurrence of the disease involving the native kidney or as de novo disease with no evidence of previous involvement before transplant. While atypical hemolytic uremic syndrome is a rare disease that results from complement dysregulation with alternative pathway overactivity, de novo TMA is a heterogenous set of various etiologies and constitutes the vast majority of post-transplant TMA cases. Management of both diseases varies from simple maneuvers, e.g., plasmapheresis, drug withdrawal or dose modification, to lifelong complement blockade, which is rather costly. Careful donor selection and proper recipient preparation, including complete genetic screening, would be a pragmatic approach. Novel therapies, e.g., purified products of the deficient genes, though promising in theory, are not yet of proven value.

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“…(8), orofacial disease including tongue and nares (9,10), ileal perforation (11,12), meningitis (13) and most commonly pulmonary with disseminated disease (14)(15)(16) (19,20). In the United States, H. capsulatum is endemic to the Ohio and Mississippi River valleys and anywhere from 5% to 25% of AIDS patients in these areas develop the disease (16,21).…”

Section: Opportunistic Infections With Viruses (Eg Ebv Cmv) and Fumentioning

confidence: 99%

Disseminated Histoplasmosis Associated with Hemophagocytic Lymphohistiocytosis in Kidney Transplant Recipients

Dixon

et al. 2010

American Journal of Transplantation

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Transplant patients are susceptible to infectious complications due to chronic immunosuppression. We present two cases of persistent fever, weight loss and pancytopenia in kidney transplant recipients (originally concerning for posttransplant lymphoproliferative disease) that were later diagnosed with disseminated histoplasmosis on bone marrow and lymph node biopsy. In both patients, pancytopenia was due to hemophagocytic lymphohistiocytosis (HLH) which has rarely been described in association with histoplasmosis and not previously reported in kidney transplant recipients with this fungal infection. The diagnosis of histoplasmosis can be complex due to nonspecific symptomatology, delays in isolating histoplasma by fungal culture and false-negative antibody titers in immunocompromised patients. A review of the literature including the clinical features of histoplasmosis in immunosuppressed patients (prevalence, current diagnostic testing and treatment options) as well as the association of HLH in immunocompromised states are discussed.

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Disseminated histoplasmosis presenting as thrombotic microangiopathy

Abstract: TMA occurs in transplant populations in association with infections, medications, and other factors. Appropriate management includes recognition and treatment of possible etiological factors. Disseminated histoplasmosis should be considered in transplant patients presenting with TMA.

Cited by 27 publications

References 36 publications

Endemic Fungal Infections in Solid Organ Transplantation

Endemic Fungal Infections in Solid Organ Transplantation

Thrombotic microangiopathy after renal transplantation: Current insights inde novoand recurrent disease

Disseminated Histoplasmosis Associated with Hemophagocytic Lymphohistiocytosis in Kidney Transplant Recipients

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