Lupus nephritis

Lorenz, Georg; Desai, Jyaysi; Anders, Hans‐Joachim

doi:10.1097/01.mnh.0000444816.57378.21

Cited by 33 publications

(16 citation statements)

References 56 publications

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“…Renal pathology reveals that autoimmune reactions occur in both glomerular and tubulointerstitial tissues in LN 9. As shown in Table 2, immunofluorescence and electron microscopic studies have showed the deposition of immunoglobulins and complements on both sides of basement membrane of glomeruli.…”

Section: Immunopathological Mechanisms In Lnmentioning

confidence: 97%

“…As shown in Table 2, immunofluorescence and electron microscopic studies have showed the deposition of immunoglobulins and complements on both sides of basement membrane of glomeruli. These intrarenal IC depositions may derive from either circulating preformed or in situ-formed ICs in glomeruli 9. Further investigations have explored that two mechanisms of cytotoxic autoantibodies can cause glomerular damage via charge–charge interaction81–83 and direct binding to cross-reactive glomerular autoantigens to form in situ IC 84–86.…”

Section: Immunopathological Mechanisms In Lnmentioning

confidence: 99%

“…It is believed that urine is an ideal specimen for finding potential biomarkers of LN due to easy accessibility and can directly reflect the real-time status of the kidney inflammation and tissue damage. In addition, LN is considered an immune-mediated inflammation in both glomerular and tubulointerstitial tissues due to aberrant systemic and intrarenal immunity 5–9. Accordingly, a bunch of immune products including protein molecules, mRNAs, and microRNAs related to cytokines/chemokines/growth factors and their soluble receptors, adhesion molecules, enzymes, and activated endothelial/epithelial products have been successively discovered as surrogate urine biomarkers in LN 10–20.…”

Section: Introductionmentioning

confidence: 99%

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Potential serum and urine biomarkers in patients with lupus nephritis and the unsolved problems

Hsieh¹,

Tsai²,

Yu³

2016

OARRR

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Lupus nephritis (LN) is one of the most frequent and serious complications in the patients with systemic lupus erythematosus. Autoimmune-mediated inflammation in both renal glomerular and tubulointerstitial tissues is the major pathological finding of LN. In clinical practice, the elevated anti-dsDNA antibody titer concomitant with reduced complement C3 and C4 levels has become the predictive and disease-activity surrogate biomarkers in LN. However, more and more evidences suggest that autoantibodies other than anti-dsDNA antibodies, such as anti-nucleosome, anti-C1q, anti-C3b, anti-cardiolipin, anti-endothelial cell, anti-ribonuclear proteins, and anti-glomerular matrix (anti-actinin) antibodies, may also involve in LN. Researchers have demonstrated that the circulating preformed and in situ-formed immune complexes as well as the direct cytotoxic effects by those cross-reactive autoantibodies mediated kidney damage. On the other hand, many efforts had been made to find useful urine biomarkers for LN activity via measurement of immune-related mediators, surface-enhanced laser desorption/ionization time-of-flight mass spectrometry proteomic signature, and assessment of mRNA and exosomal-derived microRNA from urine sediment cell. Our group had also devoted to this field with some novel findings. In this review, we briefly discuss the possible mechanisms of LN and try to figure out the potential serum and urine biomarkers in LN. Finally, some of the unsolved problems in this field are discussed.

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Section: Immunopathological Mechanisms In Lnmentioning

confidence: 97%

Section: Immunopathological Mechanisms In Lnmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Potential serum and urine biomarkers in patients with lupus nephritis and the unsolved problems

Hsieh¹,

Tsai²,

Yu³

2016

OARRR

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Section: Introductionmentioning

confidence: 99%

“…Immune mediated renal injury can lead to local inflammation followed by progressive scarring from loss of intrinsic renal parenchymal cells [1, 2]. Renal injury in LN is known to affect glomerular, tubulointerstitial, and vascular compartments [2, 3]. In 2003, the International Society of Nephrology/Renal Pathology Society (ISN/RPS) classified LN into 6 classes according to the respective glomerular pathological characteristics [4, 5].…”

Section: Introductionmentioning

confidence: 99%

Relation of peritubular capillary features to class of lupus nephritis

et al. 2016

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BackgroundExperimental studies have linked peritubular capillary (PTC) loss with progression of chronic kidney disease. Minimal information on PTC in lupus nephritis (LN) has been reported. We therefore evaluated the PTC area in different classes of LN and determined if specific clinical characteristics correlated with PTC changes.MethodsRenal biopsies of 253 subjects with LN (categorized using the ISN/RPS 2003 classification) and 13 normal renal donors (the controls) were retrospectively evaluated for PTC morphology by staining for CD31 with immunohistochemistry method. The percent positive area of PTC (% PTC) was correlated with serum and urinary measures of renal function and renal pathology.ResultsSignificant PTC loss was observed in all classes of LN compared to controls. The % PTC area was highest in controls (7.64±1.48 %) with levels of 1.95±1.50, 4.16±3.85, 4.19±4.45, 5.02±1.79, and 4.45±3.75 in classes II, III, IV, IV combined with V and V, respectively (all p values < 0.05). The lowest PTC density was observed in class II LN, but this may be because some cases with worse classes of LN showed increased PTC density due to abnormally dilated capillaries associated with acute inflammation and angiogenesis. %PTC was increased in those with hematuria (5.8±5.2 vs. 3.6±3.4 %, red blood cells 3-10 vs. < 3 cells/high power field, p < 0.05) and was reduced in those with a moderately declined renal function (3.29±3.40 vs. 4.42±4.12, eGFR 15-59 vs. ≥ 60 ml/min/1.73 m2, p < 0.05). Nephrotic-range proteinuria also trended to be associated with lower PTC density although it did not reach statistical significance (3.1±2.6 vs. 4.9±4.5, p= 0.067).ConclusionsLN is associated with PTC loss and the severity correlates with reduced renal function. Further studies are needed to investigate whether a loss of PTC can predict long term renal outcomes in LN.Electronic supplementary materialThe online version of this article (doi:10.1186/s12882-016-0388-2) contains supplementary material, which is available to authorized users.

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Systemic Lupus Erythematosus

Durrani

2017

Uveitis

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Lupus nephritis

Abstract: Eventually, a better understanding of lupus nephritis pathogenesis will allow the identification of therapeutic targets that will prove effective not only in animal models but also in randomized clinical trials.

Cited by 33 publications

References 56 publications

Potential serum and urine biomarkers in patients with lupus nephritis and the unsolved problems

Potential serum and urine biomarkers in patients with lupus nephritis and the unsolved problems

Relation of peritubular capillary features to class of lupus nephritis

Systemic Lupus Erythematosus

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