Fate of full‐house immunofluorescence staining in renal allograft: A case report

Sawada, Anri; Unagami, Kohei; Horita, Shigeru; Kawanishi, Kunio; Okumi, Masayoshi; Taneda, Sekiko; Ishida, Hideyuki; Hattori, Motoshi; Tanabe, Kazunari; Honda, Kazuho; Uchida, Keiko; Shimizu, Akira; Koike, Junki; Nitta, Kosaku; Nagashima, Yoji

doi:10.1111/pin.12847

Cited by 3 publications

(1 citation statement)

References 17 publications

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“…Previous reports have shown that transmitted IgA nephropathy and membranous glomerulonephritis resolved after renal transplantation 22,23 . We also reported the full‐house immunofluorescence staining in renal allograft that resolved gradually on follow‐up biopsies 24 . These findings indicate that monoclonal TBMID can be interpreted as a donor‐derived non‐pathognomonic deposition.…”

Section: Discussionsupporting

confidence: 70%

Monoclonal and polyclonal immunoglobulin G deposits on tubular basement membranes of native and pretransplant kidneys: A retrospective study

Sawada

Okumi

Horita

et al. 2021

Pathology International

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Monoclonal tubular basement membrane immune deposits (TBMID) are associated with progression of interstitial injury in renal allograft. However, the significance of monoclonal and polyclonal TBMID in the native kidney remains unclear. We retrospectively analyzed 1894 native kidney biopsies and 1724 zero‐hour biopsies performed between 2008 and 2018 in our institution. The rate of immunoglobulin G (IgG) TBMID was found to be 8.4% among native kidney biopsies and 0.4% among zero‐hour biopsies. Polyclonal TBMID is common in IgG4‐related tubulointerstitial nephritis (37.5%), diabetic nephropathy (31.3%) and lupus nephritis (25.5%). Monoclonal IgG TBMID was identified in seven cases, including three zero‐hour biopsies. The combination of IgG1κ was observed in two cases, IgG1λ in three, and IgG2κ in two. Electron microscopy revealed powdery electron‐dense deposits in all cases. Monoclonal gammopathy of undetermined significance was diagnosed in one case. Although one patient with focal segmental glomerulosclerosis developed renal failure, all others exhibited stable renal function. Monoclonal IgG TBMID in the native kidney is not associated with renal prognosis. However, this may be an interesting immunopathological finding that would help clarify the pathogenesis of TBM immune deposits. Further study for both monoclonal and polyclonal TBMID is required in the future.

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Section: Discussionsupporting

confidence: 70%

Monoclonal and polyclonal immunoglobulin G deposits on tubular basement membranes of native and pretransplant kidneys: A retrospective study

Sawada

Okumi

Horita

et al. 2021

Pathology International

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Bartonella endocarditis and diffuse crescentic proliferative glomerulonephritis with a full-house pattern of immune complex deposition

et al. 2022

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Background Bartonella endocarditis is often a diagnostic challenge due to its variable clinical manifestations, especially when it is first presented with involvement of organs other than skin and lymph nodes, such as the kidney. Case presentation This was a 13-year-old girl presenting with fever, chest and abdominal pain, acute kidney injury, nephrotic-range proteinuria and low complement levels. Her kidney biopsy showed diffuse crescentic proliferative glomerulonephritis with a full-house pattern of immune complex deposition shown by immunofluorescence, which was initially considered consistent with systemic lupus erythematous-associated glomerulonephritis (lupus nephritis). After extensive workup, Bartonella endocarditis was diagnosed. Antibiotic treatment and valvular replacement surgery were undertaken with subsequent return of kidney function to normal range. Conclusion This case demonstrates the importance of considering the full clinical picture when interpreting clinical, laboratory and biopsy findings, because the treatment strategy for infective endocarditis versus lupus nephritis is drastically different.

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Nonlupus Full House Nephropathy

Uzzo,

Kronbichler,

Alberici

et al. 2024

CJASN

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Background: The presence of a full house pattern at immunofluorescence on kidney biopsy in a patient without clinical and laboratory features of systemic lupus erythematosus (SLE) has led to the descriptive term non-lupus full house nephropathy. This systematic review and meta-analysis focus on non-lupus full house nephropathy nomenclature, clinical findings and outcomes. Methods: In a reiterative process, all identified terms for non-lupus full house nephropathy and other MeSH terms were searched in PubMed. Out of 344 results, 57 records published between 1982 and 2022 were included in the analysis. Clinical data of single patients from different reports were collected. Patients were classified into three pathogenetic categories, which were compared according to baseline characteristics, treatments and outcomes. Results: Out of the 57 records, 61% were case reports. Non-lupus full house nephropathy was addressed with 17 different names. We identified 148 patients: 75(51%) were males; median age 35(23-58) years. Serum creatinine and proteinuria at onset were 1.4(0.8-2.5)mg/dL and 5.7(2.7-8.8)g/day. About half of patients achieved complete response. A causative agent was identified in 51(44%) patients, mainly infectious (41%). Secondary non-lupus full house nephropathy was mostly non-relapsing with worse kidney function at onset compared to idiopathic disease (P=0.001). Among the 57(50%) patients with idiopathic non-lupus full house nephropathy, complete response was comparable between patients treated with immunosuppression and supportive therapy; however, proteinuria and creatinine at onset were higher in patients treated with immunosuppression (P=0.09 and P=0.07). The remaining 7(6%) patients developed SLE after a median follow-up of 5.0(1.9-9.0) years. Conclusions: Our data support that SLE and non-lupus full house nephropathy are distinct clinical entities, with comparable outcomes. A small subset of patients develops SLE during follow-up. Non-lupus full house nephropathy is addressed by many different names in the literature. The identification of three pathogenetic categories provides further clues for the management of the disease.

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Fate of full‐house immunofluorescence staining in renal allograft: A case report

Cited by 3 publications

References 17 publications

Monoclonal and polyclonal immunoglobulin G deposits on tubular basement membranes of native and pretransplant kidneys: A retrospective study

Monoclonal and polyclonal immunoglobulin G deposits on tubular basement membranes of native and pretransplant kidneys: A retrospective study

Bartonella endocarditis and diffuse crescentic proliferative glomerulonephritis with a full-house pattern of immune complex deposition

Nonlupus Full House Nephropathy

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