Collapsing glomerulopathy after hepatitis C pegylated interferon treatment. Recovery of renal function with high-dose steroid treatment

Berdichevski, Roberto Herz; Carvalho, Eduardo M. De; Edelweiss, Maria Isabel Albano; Gonçalves, Luiz Felipe Santos; Manfro, Roberto Ceratti

doi:10.1093/ndtplus/sfq155

Cited by 4 publications

(3 citation statements)

References 8 publications

(8 reference statements)

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“…118 Other renal lesions associated with hepatitis C virus in native kidneys include membranous nephropathy, 119 fibrillary glomerulonephritis, 120 thrombotic microangiopathy, 121 and collapsing glomerulopathy following therapy with interferon 122 or pegylated interferon. 123 Kidney allografts may be similarly affected, including reports of thrombotic microangiopathy, 111 fibrillary glomerulonephritis, 124 and collapsing glomerulopathy. 125 Gallay et al 126 first noted the association of hepatitis C virus with transplant glomerulopathy in a report of two cases that concurrently had features of membranoproliferative glomerulonephritis.…”

Section: Hepatitis C Virus Infectionmentioning

confidence: 99%

Transplant glomerulopathy

Filippone¹,

McCue

Farber

2018

Modern Pathology

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In the renal allograft, transplant glomerulopathy represents a morphologic lesion and not a specific diagnosis. The hallmark pathologic feature is glomerular basement membrane reduplication by light microscopy or electron microscopy in the absence of immune complex deposits. Transplant glomerulopathy results from chronic, recurring endothelial cell injury that can be mediated by HLA alloantibodies (donor-specific antibodies), various autoantibodies, cell-mediated immune injury, thrombotic microangiopathy, or chronic hepatitis C. Clinically, transplant glomerulopathy may be silent, detectable on protocol biopsy, or present with overt manifestations, including up to nephrotic range proteinuria, hypertension, and declining glomerular filtration rate. In either case, transplant glomerulopathy is associated with reduced graft survival. This review details the morphologic features of transplant glomerulopathy found on light microscopy, immunofluorescence microscopy, and electron microscopy. The pathophysiology of the causes and risk factors are discussed. Clinical manifestations are emphasized and potential therapeutic modalities are examined.

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Section: Hepatitis C Virus Infectionmentioning

confidence: 99%

Transplant glomerulopathy

Filippone¹,

McCue

Farber

2018

Modern Pathology

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“…For severely ill patients, the physiologic disturbances caused by the illness and the therapies employed to address viral acute respiratory distress syndrome are potential causes for ATI. Collapsing glomerulopathy is strongly associated with elevated levels of type I and type II interferons that can result from iatrogenic [66][67][68], genetic [69], hematologic [70,71], autoimmune [72,73] and infectious causes [74][75][76][77] ]. High-interferon states can synergize with APOL1 risk genotypes to induce collapsing glomerulopathy [68,69].…”

Section: Discussionmentioning

confidence: 99%

Pathogenesis of coronavirus disease 2019-associated kidney injury

Smith

Akilesh

2021

Current Opinion in Nephrology &Amp; Hypertension

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Purpose of review The current review summarizes the pathologic findings in kidneys from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected patients who have had autopsies or undergone biopsy, and the pathogenic mechanisms implicated in coronavirus disease 2019 (COVID-19)-associated kidney diseases. Recent findings Direct infection of the kidney by SARS-CoV-2 is not common, and convincing morphologic evidence of substantive kidney infection by SARS-CoV-2 is lacking. Severe COVID-19-associated acute kidney injury is likely multifactorial and results from the physiologic disturbances and therapies used to treat this illness. COVID-19-associated collapsing glomerulopathy (COVAN) is seen almost exclusively in patients with apolipoprotein L1 high-risk genotypes with no evidence of direct infection of the kidney by SARS-CoV-2. Summary The prevailing evidence does not support substantive or persistent infection of kidneys in COVID-19 and indirect means of tissue injury are favored, although a ‘hit and run’ model cannot be excluded. COVAN frequently occurs in patients with mild respiratory systems, suggesting that innate and adaptive immune responses to SARS-CoV-2 infection may provide the second hit needed for the development of collapsing glomerulopathy in susceptible individuals.

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“…2). A causal role for interferon is supported by cases of iatrogenic collapsing glomerulopathy developing in patients with hepatitis C infection undergoing treatment with recombinant interferon [13,14]. Collapsing glomerulopathy has also been seen in the rare genetic disorder, Stimulator of Interferon Genes (STING)-Associated Vasculopathy with Onset in Infancy (SAVI), in which patients have high circulating interferon levels [15].…”

Section: Apol1-associated Collapsing Glomerulopathymentioning

confidence: 99%