Karyomegalic-like nephropathy, Ewing’s sarcoma and ifosfamide therapy

McCulloch, Tom; Prayle, Andrew; Lunn, Andy; Watson, Alan R.

doi:10.1007/s00467-011-1815-z

Cited by 23 publications

(24 citation statements)

References 14 publications

(13 reference statements)

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“…Most of reports show the chronic tubulointerstitial damage, although segmental glomerular sclerosis was also reported [8], which were also found in the present case. We also found the lesion typical of karyomegalic interstitial nephritis, which was also recently reported in ifosfamideinduced late-onset nephrotoxicity [9]. The authors presented three cases that were treated with ifosfamide, but without cisplatin.…”

Section: Discussionsupporting

confidence: 79%

“…There are several reports of the finding of renal biopsy for ifosfamide-induced late nephropathy [3,[8][9][10][11][12]. Most of reports show the chronic tubulointerstitial damage, although segmental glomerular sclerosis was also reported [8], which were also found in the present case.…”

Section: Discussionsupporting

confidence: 73%

“…McCulloch et al [9] prescribed corticosteroids to ifosfamide-induced chronic tubulointerstitial nephrites, without noticeable effect. Morland et al [8] speculated on the possible effect of steroid in ifosfamide-induced nephrotoxicity.…”

Section: Discussionmentioning

confidence: 99%

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Improvement in karyomegalic interstitial nephritis three years after ifosfamide and cisplatin therapy by corticosteroid

et al. 2014

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Long-term nephrotoxicity of ifosfamide is occasionally progressive, and, in such case, there has been no specific treatment to prevent progression. It has been reported that the presence of karyomegalic interstitial nephritis, which is rare type of interstitial nephritis, may be related to ifosfamide-induced nephropathy with poor prognosis and resistant to the immunosuppressive therapy. A 15-year-old boy presented with progressive nephrotoxicity 3 years after systemic chemotherapy with ifosfamide and cisplatin for the treatment of osteosarcoma. Renal biopsy revealed the severe tubulointerstitial nephritis with tubular atrophy and focal global and segmental glomerular sclerosis. It also showed tubular epithelial cells with variably sized nuclei, some of which were massively enlarged, abnormal hyperchromatic, irregular shaped, and bizarreappearing. These morphological changes were suggestive of the histology of karyomegalic interstitial nephritis. Corticosteroid retarded the progression of nephrotoxicity. The present case is the first report, suggesting that corticosteroid was effective against the late-onset renal toxicity by ifosfamide therapy. Our case also suggests that karyomegalic interstitial nephritis may be the result of long-term nephrotoxicity of ifosfamide. Since concurrent treatment with cisplatin is one of the risk factors for ifosfamide nephrotoxicity, there is a possibility that cisplatin may have a synergetic effect with ifosfamide for producing karyomegalic interstitial nephritis.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionsupporting

confidence: 73%

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Improvement in karyomegalic interstitial nephritis three years after ifosfamide and cisplatin therapy by corticosteroid

et al. 2014

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“…In a report by Hassan et al [5], high concentration of ochratoxin was found in the blood of affected siblings. McCulloch et al [6], reported KIN in three adolescent patients treated with ifosfamide for Ewings sarcoma. Tomokazu Matsuura et al reported a case of a 15-year-old boy presented with progressive nephrotoxicity 3 years after systemic chemotherapy with ifosfamide and cisplatin for the treatment of osteosarcoma.…”

Section: Discussionmentioning

confidence: 99%

Karyomegalic interstitial nephritis

Guebessi¹,

Karkouri

2015

CEN Case Rep

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Karyomegalic interstitial nephritis is a singular type of progressive chronic interstitial nephritis. The pathogenesis of this disease is unknown. The present study reported the case of a 22-year-old man who presented with a long history of recurrent upper respiratory tract infection episodes secondary to bronchiectasis and with progressive renal failure. Renal biopsy revealed chronic tubulointerstitial nephritis and a surprisingly marked karyomegaly specifically of the tubular epithelium.

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“…[6] All patients progressed to renal failure. A familial clustering is known and frequency of human leukocyte antigen (HLA)-A9 and HLA-B35 haplotypes suggest the possibility of genetic susceptibility.…”

Section: Discussionmentioning

confidence: 99%