scholarly journals A Case of MPO-ANCA Positive Systemic Lupus Erythematosus Developed into Acute Kidney Injury

2019 ◽  
Vol 03 (06) ◽  
Author(s):  
Satoshi Suzuki ◽  
Kei Ogiwara ◽  
Takuya Nishi ◽  
Shota Sakuma ◽  
Maiko Akira ◽  
...  
2019 ◽  
Vol 12 (12) ◽  
pp. e233446
Author(s):  
Kevin John ◽  
Krupa Varughese ◽  
Ranil Johann Boaz ◽  
Tarun George

A 42-year-old woman presented with chronic fever, abdominal pain, intermittent loose stools and dysuria for 3 months. She had recently developed acute dyspnoea with acute kidney injury. She was found to have a contracted, thick-walled bladder with bilateral hydroureteronephrosis. She underwent bilateral percutaneous nephrostomies, following which her renal function recovered. She satisfied the clinical and immunological features of the Systemic Lupus International Collaborating Clinics criteria for systemic lupus erythematosus (SLE). She was initiated on immunosuppression. Lupus cystitis with a contracted bladder is an uncommon presentation of SLE.


2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Amol M. Patel ◽  
Lily Anne Romero Karam ◽  
Stephanie C. Fuentes Rojas ◽  
Warren E. Redfearn ◽  
Luan D. Truong ◽  
...  

Lupus nephritis is a common manifestation of systemic lupus erythematosus (SLE). IgA nephropathy is a common type of primary glomerulonephritis. Renal manifestations in SLE patients are often due to lupus nephritis; however, renal diseases unrelated to lupus nephritis are rarely reported. While crescentic IgA nephropathy with rapid clinical progression is rare, its development in patients with SLE in the absence of lupus nephritis is even more unusual. A 74-year-old woman with a history of SLE without known renal involvement, chronic kidney disease stage IIIa, congestive heart failure, hypertension, and type 2 diabetes mellitus presented with acute kidney injury. Her creatinine continued to rise rapidly. Renal biopsy revealed mesangial proliferative glomerulonephritis with crescent formation. Immunofluorescent staining showed IgA and C3 mesangial deposition and absence of C4 and C1q, consistent with IgA nephropathy. She received a course of methylprednisolone and plasmapheresis. Unfortunately, her renal function continued to deteriorate, and she was started on hemodialysis which was continued after hospital discharge. This case illustrates crescentic IgA nephropathy without lupus nephritis as the cause of acute kidney injury in a patient with SLE. It highlights the observation that renal diseases other than lupus nephritis can develop in SLE patients.


2020 ◽  
Vol 8 ◽  
pp. 2050313X2091002 ◽  
Author(s):  
Umut Selamet ◽  
Ramy M Hanna ◽  
Anthony Sisk ◽  
Lama Abdelnour ◽  
Lena Ghobry ◽  
...  

Drug-induced lupus erythematosus has features distinct from primary systemic lupus erythematosus. It can occur with a wide variety of agents that result in the generation of anti-histone or other types of antibodies. Systemic manifestations of drug-induced systemic lupus erythematosus may include renal dysfunction due to circulating immune complexes or due to other immune reactions to the culprit medication(s). Acute interstitial nephritis occurs due to DNA–drug or protein–drug complexes that trigger an allergic immune response. We report a patient who developed acute kidney injury, rash, and drug-induced systemic lupus diagnosed by serologies after starting chlorthalidone and amiodarone. A renal biopsy showed acute interstitial nephritis and not lupus-induced glomerulonephritis. It is important to note that systemic lupus erythematosus and acute interstitial nephritis can occur together, and this report highlights the role of the kidney biopsy in ascertaining the pathological diagnosis and outlining therapy in drug-induced lupus erythematosus.


2015 ◽  
Vol 41 (3) ◽  
pp. 241-247 ◽  
Author(s):  
Alvaro Orjuela ◽  
Adisak Suwanichkul ◽  
Debra Canter ◽  
Charles G. Minard ◽  
Sridevi Devaraj ◽  
...  

Background/Aims: There is a critical need for more noninvasive biomarkers to identify nephritis in patients with systemic lupus erythematosus (SLE). Recent studies in a model mouse and an adult SLE patient cohort suggest that anti-basement membrane antibody levels correlate well with lupus activity and kidney injury. The purpose of this study was to assess the anti-basement membrane reactivity in pediatric SLE (pSLE) patients with or without nephritis. Methods: Auto-antibodies to basement membrane antigens were assessed using an anti-matrigel ELISA. Endpoint titers were measured in pSLE patients and healthy children, as well as in autoimmune and non-immune mice, with good reproducing capabilities. Findings were also analyzed with respect to the presence or absence of nephritis, dsDNA antibodies, and other manifestations of pSLE. Results: MRL/lpr mice developed high-titer anti-matrigel antibodies, whereas C57BL/6 mice did not. In a cohort of 21 pSLE patients and 22 pediatric controls, high-titer anti-matrigel IgG, IgM and IgA antibody levels were specific for pSLE. High-titer anti-matrigel IgG3 levels could distinguish with good sensitivity the 13 pSLE patients with a history of nephritis from the 8 non-renal pSLE patients. High-titer anti-matrigel IgG, IgA, IgM or IgG3 did not correlate with positive anti-double stranded DNA, but defined an overlapping subset of patients. Conclusion: The addition of anti-basement membrane antibody testing to serologic testing in pSLE may help to monitor disease activity or to define important subsets of patients with risks for specific disease manifestations.


2020 ◽  
Vol 3 (1) ◽  
pp. 34-43
Author(s):  
Jessy J Alexander ◽  
Alexander Jacob ◽  
Anthony Chang ◽  
Richard J Quigg ◽  
James N Jarvis

Abstract Systemic lupus erythematosus (SLE) is an autoimmune disease that is a challenge to diagnose and treat. There is an urgent need for biomarkers to help define organ involvement, and more effective therapies. A unique population of T cells, the CD3+CD4−CD8− (DNeg) cells, is significantly increased in lupus patients. Twenty-seven cases (53%) of pediatric SLE patients had elevated DNeg cells in their peripheral blood, which correlated with kidney function (R2 = 0.54). Significant infiltration of DNeg cells was observed in both adult and pediatric lupus kidneys by immunofluorescence. For the first time, this study provides direct evidence that DNeg cells facilitate kidney injury in preclinical 8-week-old MRL/lpr lupus mice. In lupus mice, the increase in DNeg cells tracked with worsening disease and correlated with kidney function (R2 = 0.85). Our results show that DNeg cells per se can cause kidney dysfunction, increase in number with increase in disease pathology, and could serve as a potential biomarker.


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