The level of urinary α1 microglobulin excretion is a useful marker of peritubular capillaritis in antineutrophil cytoplasmic antibody associated vasculitis

Ohashi, Naro; Ishigaki, Sayaka; Kitajima, K.; Tsuji, Naoko; Isobe, Shinsuke; Iwakura, Takamasa; Ono, Masafumi; Fujikura, Tomoyuki; Tsuji, Takayuki; Sakao, Yukitoshi; Kato, Akihiko; Yasuda, Hideo

doi:10.1007/s10157-014-1073-z

Cited by 7 publications

(6 citation statements)

References 18 publications

(22 reference statements)

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“…Interestingly, tubulointerstitial nephritis with normal glomeruli in AAV have been described in the first renal biopsy with necrotizing and crescentic ANCA GN in the second renal biopsy thereafter [ 46 , 47 ]. These observations suggest that AAV is a small vessel vasculitis manifesting to glomerular (necrotizing and crescentic ANCA GN) and tubulointerstitial compartments (intimal arteritis), and that the characteristics of each manifestation are independent [ 48 ]. Based on our findings that complement components C3 and C4 indicate vasculitis manifestations to distinct renal compartments in ANCA GN, it is attractive to speculated that innate immunity facilitates kidney injury by pathomechanisms attributed to specific complement system components.…”

Section: Discussionmentioning

confidence: 99%

Complement Components C3 and C4 Indicate Vasculitis Manifestations to Distinct Renal Compartments in ANCA-Associated Glomerulonephritis

Hakroush

Tampe

Korsten

et al. 2021

IJMS

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Background: Acute kidney injury (AKI) is a common and severe complication of antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV) causing progressive chronic kidney disease (CKD), end-stage renal disease (ESRD) or death. Pathogenic ANCAs, in particular proteinase 3 (PR3) and myeloperoxidase (MPO), trigger a deleterious immune response resulting in pauci-immune necrotizing and crescentic glomerulonephritis (GN), a common manifestation of glomerular injury in AAV. However, there is growing evidence that activation of the complement pathway contributes to the pathogenesis and progression of AAV. We here aimed to compare glomerular and tubulointerstitial lesions in ANCA GN and extrarenal manifestation of AAV in association with levels of circulating complement components C3c and C4. Methods: Plasma levels of C3c and C4 in a total number of 53 kidney biopsies with ANCA GN were retrospectively included between 2015 and 2020. Glomerular and tubulointerstitial lesions were evaluated according to established scoring systems for ANCA GN and analogous to the Banff classification. Results: We here show that circulating levels of C3c and C4 in ANCA GN were comparable to the majority of other renal pathologies. Furthermore, hypocomplementemia was only detectable in a minor subset of ANCA GN and not correlated with renal or extrarenal AAV manifestations. However, low levels of circulating C3c correlated with AKI severity in ANCA GN independent of systemic disease activity or extrarenal AAV manifestation. By systematic scoring of glomerular and tubulointerstitial lesions, we provide evidence that low levels of circulating C3c and C4 correlated with vasculitis manifestations to distinct renal compartments in ANCA GN. Conclusions: We here expand our current knowledge about distinct complement components in association with vasculitis manifestations to different renal compartments in ANCA GN. While low levels of C4 correlated with glomerulitis, our observation that low levels of circulating complement component C3c is associated with interstitial vasculitis manifestation reflected by intimal arteritis implicates that C3c contributes to tubulointerstitial injury in ANCA GN.

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Section: Discussionmentioning

confidence: 99%

Complement Components C3 and C4 Indicate Vasculitis Manifestations to Distinct Renal Compartments in ANCA-Associated Glomerulonephritis

Hakroush

Tampe

Korsten

et al. 2021

IJMS

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“…1,2 Under normal conditions, approximately 99.9% of the free α1-MG filtered freely through the renal glomerular basement membrane is reabsorbed by the proximal tubular cells. Any proximal tubular cell dysfunction could result in increased quantities of α1-MG in the urine, hence urinary α1-MG has been recognized as a sensitive marker for the early detection of tubular injury in many diseases, 3,4 especially in diabetic kidney disease in recent years. 5,6 Urinary α1-MG has been recommended by expert consensus on clinical diagnosis of diabetic nephropathy as an indicator to screen early tubular involvement in Chinese adults.…”

Section: Introductionmentioning

confidence: 99%

A study on the biological reference interval of urinary alpha 1‐microglobulin in a group of Chinese people

Zhang

Cui³

et al. 2017

Clinical Laboratory Analysis

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“…We sampled arterioles with inflammation and destructed internal elastic lamina and found large fibrotic foci, which could represent scarring originating from arteritis in the kidney biopsy. Ohashi et al 13 suggested that not only PTC, but also arteriolitis could play an important role in the pathogenesis of tubulointerstitial nephritis due to AAV. In our case, arteriolitis but not PTC was observed.…”

Section: Discussionmentioning

confidence: 99%

Antineutrophil cytoplasmic antibody-associated vasculitis predominantly manifesting tubulointerstitial nephritis: A case report

Nishioka,

Yamaguchi,

Hashiguchi

et al. 2023

SAGE Open Medical Case Reports

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The common histopathology of antineutrophil cytoplasmic antibody-associated vasculitis comprises pauci-immune crescentic glomerulonephritis with concomitant tubulointerstitial nephritis. Tubulointerstitial nephritis in the absence of glomerular involvement in patients with antineutrophil cytoplasmic antibody-associated vasculitis is uncommon. We report a case of antineutrophil cytoplasmic antibody-associated vasculitis-associated acute kidney injury manifesting as tubulointerstitial nephritis without glomerulonephritis. A 75-year-old woman with fever, cough, and myalgia developed kidney dysfunction with inflammatory reactions and tubular-type proteinuria, without glomerular hematuria. A kidney biopsy revealed tubulointerstitial nephritis with arteritis. We ruled out important underlying etiologies of tubulointerstitial nephritis, including infection, drug reactions, and autoimmune diseases. Since chest high-resolution computed tomography demonstrated mild interstitial pneumonia in bilateral lower lung fields, myeloperoxidase antineutrophil cytoplasmic antibody was measured and found to be positive. Therefore, we diagnosed the patient with antineutrophil cytoplasmic antibody-associated vasculitis-associated tubulointerstitial nephritis but not glomerulonephritis, and interstitial pneumonia. The patient’s kidney function and symptoms markedly improved with prednisolone treatment. Clinicians should maintain high-level vigilance for antineutrophil cytoplasmic antibody-associated vasculitis as a possible underlying component of tubulointerstitial nephritis, particularly when kidney function deteriorates with tubulointerstitial injuries without glomerular features.

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The level of urinary α1 microglobulin excretion is a useful marker of peritubular capillaritis in antineutrophil cytoplasmic antibody associated vasculitis

Cited by 7 publications

References 18 publications

Complement Components C3 and C4 Indicate Vasculitis Manifestations to Distinct Renal Compartments in ANCA-Associated Glomerulonephritis

Complement Components C3 and C4 Indicate Vasculitis Manifestations to Distinct Renal Compartments in ANCA-Associated Glomerulonephritis

A study on the biological reference interval of urinary alpha 1‐microglobulin in a group of Chinese people

Antineutrophil cytoplasmic antibody-associated vasculitis predominantly manifesting tubulointerstitial nephritis: A case report

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