“Protenuria in SLE: Is it always lupus?”

Lupus ◽  
2021 ◽  
pp. 096120332098345
Author(s):  
Alessandra Ida Celia ◽  
Roberta Priori ◽  
Bruna Cerbelli ◽  
Francesca Diomedi-Camassei ◽  
Vincenzo Leuzzi ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Nephritis ◽  
Fabry Disease ◽  
Histological Examination ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Kidney Involvement ◽  
History Of ◽  
Genetic Assay

Proteinuria is one of the most typical manifestations of kidney involvement in Systemic Lupus Erythematosus (SLE). We report the case of a 23-year-old woman with a 6-year-long history of SLE presenting with proteinuria after a three-year remission on hydroxychloroquine. Kidney histological examination showed alterations inconsistent with lupus nephritis and suggestive of hydroxychloroquine toxicity or Fabry disease. The latter was confirmed by genetic assay.

scholarly journals Trichophyton erinacei Onychomycosis: The First to Evidence a Proximal Subungual Onychomycosis Pattern

2019 ◽  
Vol 11 (2) ◽  
pp. 198-203 ◽  
Author(s):  
Sutasinee Phaitoonwattanakij ◽  
Charussri Leeyaphan ◽  
Sumanus Bunyaratavej ◽  
Kittipoom Chinhiran
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Decision Making ◽  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Drug Susceptibility ◽  
Mycological Cure ◽  
Drug Susceptibility Test ◽  
Systemic Lupus ◽  
Trichophyton Erinacei ◽  
History Of

Trichophyton erinacei is an emerging cause of dermatophyte infections, which are frequently isolated from hedgehogs. Nail infections from T. erinacei are rarely reported. We describe the case of a 23-year-old Thai female who had a history of systemic lupus erythematosus with lupus nephritis type III and who developed widespread skin and nail infections caused by T. erinacei that were most likely transmitted from a hedgehog. Although the patient did not demonstrate a clinical improvement or mycological cure following systemic itraconazole and fluconazole treatment, she achieved clinical and mycological cures after terbinafine therapy. A drug susceptibility test should be performed in patients with T. erinacei infections to facilitate decision-making about antifungal therapy. Here, we are the first to report a case of proximal subungual onychomycosis from a T. erinacei infection.

Albumin-to-globulin ratio (AGR) as a potential marker of predicting lupus nephritis in Chinese patients with systemic lupus erythematosus

Lupus ◽  
2021 ◽  
pp. 096120332098113
Author(s):  
Xin-Ran Liu ◽  
Yuan-Yuan Qi ◽  
Ya-Fei Zhao ◽  
Yan Cui ◽  
Xiao-Yang Wang ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Nephritis ◽  
Renal Impairment ◽  
Lupus Erythematosus ◽  
Newly Diagnosed ◽  
Systemic Lupus ◽  
Increased Risk ◽  
History Of ◽  
Albumin To Globulin Ratio

Objectives To evaluate a potential role of albumin-to-globulin ratio (AGR) in the development of lupus nephritis (LN) and determine the potential to use AGR as a marker for future LN in systemic lupus erythematosus (SLE) patients. Methods 194 newly diagnosed SLE patients without renal impairment were followed. The clinical data were collected and analyzed at the time of initial diagnosis of SLE and the end of follow-up. We compared baseline characteristics between those who did or did not develop LN on follow-up. Univariate and multivariate Cox hazard analysis were used to identify predictors of lupus nephritis. Results Among the 194 newly diagnosed SLE patients without renal impairment, 26 (13.40%) patients were diagnosed with LN during a median follow-up of 53.87 months. On univariate Cox analysis, patients with the history of alopecia, higher SBP, lower AGR, lower CRP, lower C3, lower C4, higher anti-dsDNA Ab, presence of ANA homogeneous patterns or higher SLEDAI had an increased probability of developing LN. In a multivariate model, the history of alopecia (adjust hazard ratio, aHR = 3.614, 95%CI 1.365-9.571 P = 0.010), lower AGR (aHR = 6.968, 95%CI 1.873-25.919, P = 0.004), lower CRP (aHR = 4.230, 95%CI 1.591-11.247, P = 0.004) and higher level of anti-dsDNA (aHR = 2.675, 95%CI 1.008-7.093, P = 0.048) were independently associated with an increased risk of developing LN after adjusting for covariates. Conclusion Our findings indicated that SLE patients with low AGR, low CRP, high anti-dsDNA and the history of alopecia were more likely to develop LN in the course of SLE. AGR shown the greatest hazard for developing LN among them, it may be a strong predictor.

scholarly journals EP16 Challenges in treating new onset systemic lupus erythematosus with lupus nephritis and COVID-19 infection overlap

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Selma Dahou ◽  
Tim Leach ◽  
Kathryn Bostock ◽  
Jonathan Louden ◽  
Jonathan Raj ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Case Report ◽  
Lupus Nephritis ◽  
Immunosuppressive Therapy ◽  
Lupus Erythematosus ◽  
Childbearing Age ◽  
Systemic Lupus ◽  
Suitable Alternative ◽  
Increased Risk ◽  
History Of

Abstract Case report - Introduction COVID-19 infection caused by a novel coronavirus SARS-coV-2 has made the diagnosis and the treatment of inflammatory diseases incredibly challenging. On the one hand, because of its pro-inflammatory state, that may aggravate or trigger flares in autoimmune diseases such as systemic lupus erythematosus (SLE). On the other hand, the risk of an immunosuppressive therapy during the active phase SARS-coV-2 infection that may lead to catastrophic outcomes. We report a case of a 24-year-old female newly diagnosed with SLE during COVID-19 pandemic who developed COVID-19 infection during her induction treatment for lupus nephritis. Case report - Case description A 24-year-old Nepali female, with no past medical history of note, presented to her regional hospital with a history of flu-like symptoms few days ago, peripheral oedema, acute kidney injury with proteinuria and hypertension. Further investigations showed a high titre of double-stranded DNA antibodies, anti-cardiolipin IgM and B2 microglobulin positive and low C3. She also developed a haemolytic anaemia and thrombocytopenia during her admission. She received pulsed steroid therapy and was started on mycophenolate mofetil (MMF) for a probable lupus nephritis awaiting the results of biopsy, which showed later a lupus nephritis Class IV-G with active lesions. She then developed symptoms of COVID-19 infection and had a positive PCR leading to an interruption of her induction therapy. She was recruited to the RECOVERY trial on the lopinavir-ritonavir arm and made a good recovery. Case report - Discussion It is well known that viruses can trigger or aggravate auto-immune response in patients predisposed genetically. However, the role of SARS-coV-2 is not elucidated yet. The EULAR COVID-19 registry showed that rheumatoid arthritis and SLE were the most prevalent rheumatic diseases, and there was an increased risk in those who are on moderate to high dose corticosteroids. In patients with SLE and COVID-19 infection, it is agreed by all the national and international rheumatology societies to interrupt their immunosuppressive therapy until the symptoms resolve, especially those with renal involvement or an active disease. Which is the case in our patient. Luckily, she resumed her MMF a month later after a negative PCR and her renal function has continued to improve. Case report - Key learning points Lupus nephritis is a major risk factor for overall morbidity and mortality in SLE. It requires an early immunosuppressive treatment to induce remission. Randomized clinical trials showed that MMF is at least equally effective as cyclophosphamide in inducing remission and that it has been associated with a reduced risk of infection and amenorrhea. It seems to be a suitable alternative in women of childbearing age. In patients with concomitant COVID-19 disease, immunosuppressive therapy should be paused until the symptoms improve.

scholarly journals Effect of Add-on Hydroxychloroquine Therapy on Serum Proinflammatory Factor Levels in Patients with Systemic Lupus Erythematosus With or Without Lupus Nephritis

2020 ◽  
Author(s):  
Risa Wakiya ◽  
Kiyo Ueeda ◽  
Shusaku Nakashima ◽  
Hiromi Shimada ◽  
Tomohiro Kameda ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Nephritis ◽  
Disease Activity ◽  
Proinflammatory Cytokines ◽  
Lupus Erythematosus ◽  
Serum Levels ◽  
Systemic Lupus ◽  
Low Disease Activity ◽  
Tnf Α ◽  
History Of

Abstract Background: We investigated the effects of add-on hydroxychloroquine (HCQ) therapy on the expression of proinflammatory cytokines and other factors in systemic lupus erythematosus (SLE) patients with low disease activity.Methods: Patients who had low disease activity of at least 3 months duration were included. Patients with a history of lupus nephritis (LN+) must have been in remission for at least 3 months prior to enrollment. Serum levels of interferon interferon-α, S100A8, S100A9, tumor necrosis factor(TNF) -α, interleukin(IL)-2, IL-6, IL-8, vascular endothelial growth factor (VEGF)-A, Monocyte Chemotactic Protein-1, macrophage inflammatory protein-1α, IL-1β, Interleukin 1 receptor antagonist(IL-1ra), and Granulocyte Colony Stimulating Factor were measured immediately before and 3 months after treatment with oral HCQ treatment.Results: Of the 42 patients enrolled in the study (4 males, 38 females, mean age ± standard deviation age 41.4±13.3 years), 19 patients had a history of lupus nephritis but were currently in remission (LN+), and the remaining 23 patients had no history of LN (LN−). Serum levels of IL-1ra, S100A8, and S100A9 at baseline were significantly higher in the LN+ group compared with the LN− group (p=0.0092, p=0.012, and p=0.0043, respectively). In the full cohort, HCQ treatment led to significantly reduced serum levels of TNF-α, IL-6, VEGF-A, IL-1ra, IL-2, S100A8, and S100A9, and to decreased, albeit not significantly, levels of IL-8 and MIP-1α. The HCQ-induced changes in serum IL-8, IL-1ra, S100A8, and S100A9 levels were greater for patients in the LN+ group than those in the LN−group (p=0.0039, p=0.0011, p=0.0201, and p=0.0092, respectively). Conclusion: Add-on HCQ treatment decreased several proinflammatory cytokines levels in SLE patients with low disease activity, especially those with LN. The ability of HCQ to reduce IL-8 levels in patients with a history of LN suggests that HCQ treatment may improve the prognosis of LN.

THE CLINICAL, LABORATORY MANIFESTATIONS AND HISTOPATHOLOGY IN NEPHROTIC PATIENTS WITH LUPUS NEPHRITIS

2018 ◽  
pp. 52-58
Author(s):  
Le Thuan Nguyen ◽  
Bui Bao Hoang
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Clinical Laboratory ◽  
Activity Index ◽  
Clinical Manifestations ◽  
Systemic Lupus ◽  
Cross Sectional ◽  
Organ Systems ◽  
Tubulointerstitial Lesions

Introduction: Systemic lupus erythematosus (SLE) is an autoimmune disease involving multiple organ systems. The kidney appears to be the most commonly affected organ, especially nephrotic is a serious kidney injury. The clinical, laboratory manifestations and histopathology are very useful for diagnosis, provide the means of predicting prognosis and guiding therapy in nephrotic patients with lupus nephritis. Methods: Descriptive cross-sectional study of nephrotic patients with lupus treated in the Department of Nephrology Trung Vuong Hospital and Cho Ray Hospital between May/2014 and May/2017. Renal histopathological lesions were classified according to International Society of Nephrology/Renal Pathology Society - ISN/RPS ’s 2003. The clinical, laboratory manifestations and histopathological features were described. Results: Of 32 LN with nephritic range proteinuria cases studied, 93.7% were women. The 3 most common clinical manifestations were edema (93.8%), hypertension (96.8%) and pallor (68.9%), musculoskeletal manifestions (46.9%), malar rash (40.6%). There was significant rise in laboratory and immunological manifestions with hematuria (78.1%), Hb < 12g/dL (93.5%), increased Cholesterol (100%), and Triglycerid (87.5%), Creatinine > 1.4 mg/dL (87.5%), increased BUN 71.9%, ANA (+) 93.8%, Anti Ds DNA(+) 96.9%, low C3: 96.9%, low C4: 84.4%. The most various and severe features were noted in class IV with active tubulointerstitial lesions and high activity index. Conclusion: Lupus nephritis with nephrotic range proteinuria has the more severity of histopathological feature and the more severity of the more systemic organ involvements and laboratory disorders were noted. Key words: Systemic lupus, erythematosus (SLE) lupus nepphritis, clinical

scholarly journals Assessment of serum macrophage migration inhibitory factor (MIF), adiponectin, and other adipokines as potential markers of proteinuria and renal dysfunction in lupus nephritis: a cross-sectional study

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Jorge Ivan Gamez-Nava ◽  
Valeria Diaz-Rizo ◽  
Edsaul Emilio Perez-Guerrero ◽  
Jose Francisco Muñoz-Valle ◽  
Ana Miriam Saldaña-Cruz ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Linear Regression ◽  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Macrophage Migration Inhibitory Factor ◽  
Cross Sectional Study ◽  
Macrophage Migration ◽  
Sectional Study ◽  
Systemic Lupus ◽  
Cross Sectional

Abstract Background To date, the association of serum macrophage migration inhibitory factor (MIF) and serum adipokines with lupus nephritis is controversial. Objective To assess the utility of serum MIF, leptin, adiponectin and resistin levels as markers of proteinuria and renal dysfunction in lupus nephritis. Methods Cross-sectional study including 196 systemic lupus erythematosus (SLE) patients and 52 healthy controls (HCs). Disease activity was assessed by Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Renal SLE involvement was investigated by renal-SLEDAI. MIF, adiponectin, leptin and resistin levels were quantified by ELISA. We assessed the correlations of quantitative variables by Spearman correlation (rs). Multivariable linear regression adjusted the variables associated with the severity of proteinuria. Results SLE patients had higher MIF (p = 0.02) and adiponectin (p < 0.001) than HCs. Patients with renal SLE involvement (n = 43) had higher adiponectin (19.0 vs 13.3 μg/mL, p = 0.002) and resistin (10.7 vs 8.9 ng/mL, p = 0.01) than patients with non-renal SLE (n = 153). Proteinuria correlated with high adiponectin (rs = 0.19, p < 0.009) and resistin (rs = 0.26, p < 0.001). MIF (rs = 0.27, p = 0.04). Resistin correlated with increased creatinine (rs = 0.18, p = 0.02). High renal-SLEDAI correlated with adiponectin (rs = 0.21, p = 0.004). Multiple linear regression showed that elevated adiponectin (p = 0.02), younger age (p = 0.04) and low MIF (p = 0.02) were associated with the severity of proteinuria. Low MIF and high adiponectin levels interacted to explain the association with the severity of proteinuria (R2 = 0.41). Conclusions High adiponectin combined with low MIF concentrations int+eract to explain the severity of proteinuria in renal SLE. These findings highlight the relevance of adiponectin, resistin and MIF as markers of LN.

scholarly journals SAT0211 RENAL INJURY IN SYSTEMIC LUPUS ERYTHEMATOSUS CHARACTERIZED BY THROMBOTIC MICROANGIOPATHY

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1048.1-1048
Author(s):  
W. Hu
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Nephritis ◽  
Renal Biopsy ◽  
Lupus Erythematosus ◽  
Thrombotic Microangiopathy ◽  
Renal Injury ◽  
Renal Outcome ◽  
Pathological Examination ◽  
Systemic Lupus ◽  
Tubulointerstitial Lesions

Background:Classical lupus nephritis (LN) is characterized by glomerular immune complex(IC) deposition with glomerular proliferation, basement membrane destruction and cell infiltration. Non-IC mediated renal injury with thrombotic microangiopathy (TMA) was also reported in patients with systemic lupus erythematosus (SLE-renal TMA), but most studies were reported in patients with both LN and renal TMA.Objectives:In this study, clinical features and outcomes of SLE-renal TMA in absence of obvious IC in SLE patients were analyzed.Methods:Patients with glomerular TMA and/or vascular TMA in the absence of obvious subendothelial or epithelial immune deposits were screened out from 2332 biopsied in SLE patients who underwent first renal biopsy from January 2005 to August 2016. Their clinical, histological features and outcomes were retrospectively analyzed.Results:In 2332 renal biopsies obtained from SLE patients, 257 (11.0%) showed renal TMA, of which 237 showed both renal TMA and LN, and 20 biopsies had only renal TMA (SLE-renal TMA). There were 2 males and 18 females with an average age of (25 ± 10) years. The median course of SLE and LN were 3.0(1.0, 6.0) and 0.8(0.5, 1.9) months. All 20 patients deserved acute kidney injury, of which 11 (55%) needed renal replacement therapy (RRT) and 12 (60%) were nephrotic syndrome. Blood system involvement was found in all cases, including 13 cases (65.0%) with TMA triad (microvascular hemolytic anemia, thrombocytopenia and elevated lactate dehydrogenase).Pathological examination showed that 17 cases (85.0%) had both glomerular TMA and vascular TMA. Immunofluorescence and electron microscopy showed that 8 cases (40%) had no IC deposition in glomerulus and 12 cases (60%) had only IC deposition in mesangium. Acute tubulointerstitial lesions in patients requiring RRT were more serious than those no needing for RRT((43.6±24.9) %vs(21.7±20.1) %,P=0.047). The fusion range of foot process was positively correlated with proteinuria (r2= 0.347,P=0.006).All patients received high-dose methylprednisolone pulse therapy. Four patients received plasma exchange and three patients received gamma globulin, respectively. Eleven patients requiring RRT all stop RRT in a median time of 16.0 (9.0, 30.0) days. During a median follow-up of 58.0 (36.0, 92.3) months, complete remission (CR) was obtained in 15 cases, partial remission in 4 cases and no remission in 1 case. Six cases (30%) relapsed. No case died or progressed to end stage renal disease.Conclusion:Renal injury characterized by TMA is not uncommon in SLE renal biopsy cases. The clinical manifestation is special and the renal injury is serious. The renal outcome is good by intensive immunosuppressive therapy. It should be considered as a unique type of renal injury in SLE.References:[1]Moake JL. Thrombotic microangiopathies. N Engl J Med. 2002. 347(8): 589-600.[2]Anders HJ, Weening JJ. Kidney disease in lupus is not always ‘lupus nephritis’. Arthritis Res Ther. 2013. 15(2): 108.[3]Song D, Wu LH, Wang FM, et al. The spectrum of renal thrombotic microangiopathy in lupus nephritis. Arthritis Res Ther. 2013. 15(1): R12.[4]Hu WX, Liu ZZ, Chen HP, Zhang HT, Li LS, Liu ZH. Clinical characteristics and prognosis of diffuse proliferative lupus nephritis with thrombotic microangiopathy. Lupus. 2010. 19(14): 1591-8.[5]Tomov S, Lazarchick J, Self SE, Bruner ET, Budisavljevic MN. Kidney-limited thrombotic microangiopathy in patients with SLE treated with romiplostim. Lupus. 2013. 22(5): 504-9.[6]Li C, Yap D, Chan G, et al. Clinical Outcomes and Clinico-pathological Correlations in Lupus Nephritis with Kidney Biopsy Showing Thrombotic Microangiopathy. J Rheumatol. 2019 .[7]Chen MH, Chen MH, Chen WS, et al. Thrombotic microangiopathy in systemic lupus erythematosus: a cohort study in North Taiwan. Rheumatology (Oxford). 2011. 50(4): 768-75.[8]Park MH, AUID- Oho, Caselman N, Ulmer S, Weitz IC, AUID- Oho. Complement-mediated thrombotic microangiopathy associated with lupus nephritis. Blood Adv. 2018. 2(16): 2090-2094.Disclosure of Interests:None declared

Sign in / Sign up

Export Citation Format

Share Document