Diagnosis and treatment of kidney disease

Lupus nephritis remains a strong predictor for death and the development of end-stage renal disease (ESRD) in patients with SLE. Definition of renal involvement varies but overt renal disease is found in at least one-third of SLE patients, with up to 60% of adults and 80% of children developing lupus nephritis. Clinical presentation has been found to bear little relationship to renal biopsy findings. Renal biopsy is therefore informative for all patients with SLE with abnormal urinalysis or reduced renal function, even with serum creatinine in the normal range, to guide treatment decisions. Current treatment regimens combine corticosteroids with cyclophosphamide, azathioprine or ciclosporin, although mycophenolate mofetil has received much recent attention as a potentially superior immune suppressive. The toxicity of current drug regimens contributes significantly to existing morbidity and mortality. A new era of biological therapies holds the potential for safer, more effective therapies in the future.     

Simultaneous presentation of systemic lupus erythematosus and lupus nephritis in mother and son

The pathogenesis of systemic lupus erythematosus (SLE) has been attributed to complex interactions between genetic, hormonal and environmental factors. The influence of a genetic predisposition to SLE is supported by family aggregation and a high concordance rate in monozygotic twins. Here we present a rare case of simultaneous presentation of SLE and lupus nephritis in a mother and son. Both patients had nephrotic-range proteinuria, and the renal pathological classifications of the son and his mother were Class IV-G (A) and Class III (A/C), respectively, according to the International Society of Nephrology/Renal Pathology Society (ISN/RPS) 2003 classification of lupus nephritis. Apart from the renal involvement, both patients had leucopenia and anemia, and the mother also had typical cutaneous lesions and secondary Sj?gren's syndrome. This case supports the genetic role in the etiology of SLE, and displayed different clinical presentations and disease severity in familial SLE patients of different gender and age.     

Histological appraisal of lupus nephritis

The importance of renal biopsy in systemic lupus erythematosus (SLE) patients with nephritis resides not only in the diagnosis, but mostly in its role in guiding and assessing therapy. The potential benefits of treatment in lupus nephritis include a dramatic clinical improvement and a direct impact on renal survival. However, these benefits can be achieved only if they are carefully weighed against the complex, prolonged, and potentially toxic treatment regimens. This review on lupus nephritis emphasizes on the histological appraisal of lupus nephritis, which may demonstrate some variations among institutions, but should be clearly defined if one expects to have more useful information for the routine management of patients, as well as in clinical trials.     

How to manage patients with cardiopulmonary disease?

Systemic lupus erythematosus (SLE) is a connective tissue disease characterized by the formation of autoantibodies and immune complexes. The heart and lungs are among the organ systems commonly affected in SLE. Pericarditis, premature coronary atherosclerosis, pleuritis and pulmonary infections are the most prevalent cardiopulmonary manifestations. Other rare associations include myocarditis, coronary arteritis, acute lupus pneumonitis/pulmonary haemorrhage, acute reversible hypoxaemia and 'shrinking lung' syndrome. Current imaging modalities may provide earlier detection of subclinical disease, which may aid in preventing these potentially fatal complications. The response to treatment varies, depending on the presentation of disease. In this chapter we address the frequency, diagnosis and monitoring, and treatment regimens of cardiac and pulmonary involvement in patients with SLE.     

Do current arterial hypertension treatment guidelines apply to systemic lupus erythematosus patients? A critical appraisal

Objective

Arterial hypertension (HTN) is reported to burden up to 74% of systemic lupus erythematosus (SLE) patients and contributes significantly to accelerated atherosclerosis and increased cardiovascular (CV) risk. Current HTN treatment guidelines have not incorporated lupus patients in their recommendations; whether these guidelines can be fully implemented in SLE is doubtful.

Methods

A critical appraisal of the existing HTN guidelines in regard to SLE is presented in this review, based upon clinical and experimental data. Particular issues addressed are the time of antihypertensive therapy initiation, the optimal blood pressure level, the antihypertensive agent of first-choice and the need for reduction of the total cardiovascular risk in SLE.

Results

Antihypertensive therapy should be recommended at levels of 140/90 mmHg (systolic and diastolic BP, respectively) in newly diagnosed lupus patients without overt target organ involvement. In the case of lupus nephritis (LN) or diabetes mellitus (DM), therapy should be implemented at lower levels, such as 130/80 mmHg. Hypertensive lupus patients should be considered at high or very high CV risk and, consequently, the optimal BP level should be less than 130/80 mmHg. Angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) seem to be a safe and efficacious first-choice antihypertensive treatment in lupus patients. Total CV risk should be considered and co-morbidities (dyslipidemia, antiphospholipid syndrome, etc.) should be managed promptly.

Conclusions

Current HTN therapeutic guidelines, lacking data from large-scale clinical trials, may not adequately apply to SLE patients. The assessment of the aforementioned recommendations in randomized clinical trials is expected to confirm their value in reducing CV risk in SLE.     

Methotrexate therapy in systemic lupus erythematosus

There are 12 non-controlled and only two controlled studies using methotrexate (MTX) in a total of 207 SLE patients in the literature. The majority of these studies evaluated mainly cutaneous and/or articular involvement and attained good results. Two studies evaluated a small number of patients with lupus nephritis, achieving discordant results. Two other studies in pediatric onset systemic lupus erythematosus (SLE) also presented conflicting results, it being relevant that the one with poor response had the majority of patients with nephritis. One of the controlled trials was retrospective and concluded that MTX was effective in the treatment of antimalarial-resistant lupus arthritis and that toxicity leading to discontinuation of MTX was infrequent. The other controlled study was a double-blind, randomized, placebo-controlled clinical trial that evaluated SLE patients with mild activity. The authors concluded that MTX was effective in controlling cutaneous and articular activity and permitted prednisone dose reduction. The side effects were frequent but only 10% of patients needed to discontinue the medication. The accumulative evidence suggests that MTX in a low weekly dose may be effective in SLE patients with articular and/or cutaneous involvement with no response to antimalarials and low-dose prednisone and in patients in whom we can not reduce prednisone dose due to articular or cutaneous activity. Caution is required concerning the side effects.     

IgA nephropathy in systemic lupus erythematosus

Renal involvement in systemic lupus erythematosus (SLE) is a typical manifestation of the disease. The occurrence of non-lupus nephritis in SLE patients has rarely been reported; we describe the case of a woman suffering from SLE and IgA nephropathy (IgAN). Although IgAN and lupus nephritis share some common physiopathological characteristics, their laboratory and histopathologic findings and the extra-renal clinical manifestations are different and support a different pathogenesis. Our case highlights the importance of renal biopsy in lupus patients with urinary alterations since a correct diagnosis would permit the most appropriate treatment to be started, thus avoiding unnecessary immunosuppressive treatments.     

Lupus Nephritis: Review of the Literature

Physicians in practice should be knowledgeable regarding several aspects of autoimmune disorders, especially systemic lupus erythematosus (SLE) and lupus nephritis. These disorders can present to the clinician’s clinic and private office regardless of their speciality. This review will discuss various aspects of SLE, its mechanisms of disease, role of accelerated atherosclerosis, proinflammatory cytokines, and therapeutic approaches. The role of vascular endothelial growth factor in which and plasma levels have been associated with disease activity, classification of severity, and diagnosis of lupus nephritis is addressed. Current treatment options, prognosis, and future therapeutic approaches and common side effects are also discussed.     

FcgammaRIIa/IIIa polymorphism and its association with clinical manifestations in Korean lupus patients

The aim of this study was to determine the distribution of the FcgammaRlla and FcgammaRIIIa polymorphisms and their association with clinical manifestations in Korean lupus patients. Three hundred SLE (systemic lupus erythematosus) patients (48 male, 252 female) meeting 1982 ACR criteria and 197 Korean disease-free controls were enrolled. Genotyping for FcgammaRlla 131 R/H and FcgammaRIIIa 176 F/V was performed by PCR of genomic DNA using allele-specific primers and the FcgammaRIIIa genotype was confirmed by direct sequencing of PCR product in some cases. There was significant skewing in the distribution of the three FcgammaRIIa genotypes between the SLE and the controls (P=0.002 for R/R131 vs R/H131 and H/H131, OR 2.5 (95% Cl 1.4-4.5), but not in FcgammaRIIIa genotypes. FcgammaRIIa-R allele was a significant predictor of lupus nephritis, as compared with SLE patients without nephritis (P=0.034 for R131 vs H131, OR 1.4 (95% Cl 1.03-1.9)), but proliferative nephritis (WHO class III and IV) was less common in patients with FcgammaRlla-R/R131 and in FcgammaRIIa-R allele. In 300 SLE patients, high binding allele combination H131/V176 was less common in SLE with nephritis than in SLE without nephritis. Hemolytic anemia was less common in R131/F176 allele combination among four FcgammaRIIa/FcgammaRIIIa allelic combinations. Male SLE patients showed a higher frequency of renal involvement, serositis, thrombocytopenia, malar rash and discoid rash than female SLE, and male SLE had a higher frequency of FcgammaRIIa-R/R131 or R131-allele than male controls, but FcgammaRIIa or FcgammaRIIIa genotypes had no association with renal involvement in male SLE patients. FcgammaRIIa-H/H131 showed a higher frequency of hemolytic anemia and less pulmonary complications in male SLE. Female SLE patients showed higher frequency of any hematologic abnormality, lymphopenia, anticardiolipin antibody (+) and anti-Ro antibody (+) than male SLE, and had earlier onset of first symptoms. There was no skewing in FcgammaRIIa or FcgammaRIIIa genotypes between female SLE and female controls, but FcgammaRIIa-R131 allele showed skewing between female SLE with nephritis and female SLE without nephritis. The age at onset of thrombocytopenia was earlier in FcgammaRIIa R/R131 among three FcgammaRIIa genotypes, and serositis in FcgammaRIIIa-F/F176 among three FcgammaRIIIa genotypes. FcgammaRIIa-R131 homozygote was a major predisposing factor to the development of SLE and FcgammaRIIa-RI31 homozygote and R131 allele were a predisposing factor, and H131/V176 was a protective allele combination in lupus nephritis. In contrast to other ethnic patients, in our study cohort, clinical manifestation was different between male and female, and FcgammaRIIa and FcgammaRIIIa showed somewhat different clinical associations between the genders.     

Adrenomedullin--a potential disease activity marker and suppressor of nephritis activity in systemic lupus erythematosus

OBJECTIVES: To investigate whether plasma adrenomedullin (AM) level is elevated in lupus nephritis and to examine if plasma AM level is correlated with systemic lupus erythematosus (SLE) disease activity and severity of lupus nephritis after multivariate adjustment. METHODS: Consecutive SLE patients and healthy volunteers of age >/=16 were recruited from the rheumatology clinics of two hospitals in Hong Kong. SLE patients with nephritis fulfilled the American College of Rheumatology criteria for renal involvement and had percutaneous renal biopsy performed. Subjects were divided into three groups: (i) SLE patients with nephritis, (ii) SLE patients without nephritis and (iii) normal controls. The demographic and clinical variables were compared between these groups of patients and plasma AM level was determined by radioimmunoassay. Factors associated with plasma AM level were explored by regression analysis with adjustment of confounding factors. RESULTS: Sixty SLE patients (39 with nephritis and 21 without) and 23 normal subjects were studied. The plasma AM level of SLE patients was significantly higher than that of normal controls. SLE patients with nephritis had significantly higher plasma AM level than those without nephritis and normal controls (P<0.001). In regression analysis, proteinuria was negatively associated with plasma AM level (P=0.006) whereas SLE disease activity index was positively associated with plasma AM level after multivariate adjustment (P=0.002). CONCLUSIONS: Plasma AM is elevated in lupus nephritis, which correlates with lupus disease activity. It is negatively associated with urine protein excretion although it is unrelated to the type of renal pathology per se. Plasma AM may play a role to suppress the activity of lupus nephritis.     

Angiotensin-converting enzyme gene polymorphism and vascular manifestations in Korean patients with SLE

Systemic lupus erythematosus (SLE) is an inflammatory multisystem disease of unknown etiology with immunologic aberrations. Many studies have shown that genetic and environmental factors are implicated in the development of SLE. Angiotensin-converting enzyme (ACE) affects various immune phenomena through the renin-angiotensin and kallikrein-kininogen systems by creating angiotensin II and inactivating bradykinin. We investigated the correlation between insertion/ deletion polymorphism of the ACE gene and the clinical manifestations of SLE, especially vascular involvement and lupus nephritis. Two-hundred and eleven Korean patients fulfilling the ACR criteria and 114 healthy subjects were enrolled. The ACE genotype was determined by polymerase chain reaction using genomic DNA from peripheral blood. The nephritis patients were classified by the WHO classification. In addition, the activity and chronicity index were used to assess the severity of renal involvement. We evaluated vascular involvement by the presence or absence of hypertension, Raynaud's phenomenon, livedo reticularis, antineutrophil cytoplasmic antibody and the SLICC/ACR Damage Index. The gene frequency of ACE gene polymorphism was as follows: II 39 vs 34%, ID 41 vs 50%, DD 20 vs 16% in SLE patients and controls, respectively. There was no difference in genotype frequency between both groups. There were no significant differences between the distribution of ACE gene genotypes and lupus nephritis and its related parameters, including WHO classification, activity index, chronicity index, renal dysfunction and amount of 24 h urinary protein. The ACE genotypes and alleles did not affect the presence of vascular manifestations evaluated, but the frequency of DD genotype was significantly low in SLE patients with Raynaud's phenomenon compared to those without Raynaud's phenomenon (P = 0.002 for ACE ID vs DD and II, OR 2.7, 95% CI 1.43-5.09; P=0.023 for ACE DD vs ID and II, OR 0.33, 95% CI 0.12-0.89). Also skewing from DD to II genotype was noted in patients with anti-Sm antibody compared to those without anti-Sm antibody (P = 0.025 for ACE DD vs ID and II, OR 0.21, 95% CI 0.05-0.93). The onset age of serositis was older in patients with the ID genotype than the others (ID= 34.5+/-10.8, II + DD = 25.6+/-10.2, P= 0.002). Also the onset age of malar rash was older in patients with II genotype than the others (II=26.7+/-8.4, ID+DD=21.3+/-9.0; P=0.021). The patients with I allele showed a significantly higher frequency of serositis (P = 0.022). Taken together, the I/D polymorphisms of ACE gene did not affect susceptibility of SLE, lupus nephritis and the vascular manifestations, including Raynaud's phenomenon, in Korean SLE patients, although the DD genotype was negatively associated with Raynaud's phenomenon among SLE patients. However, it would be valuable to evaluate the role of other genes potentially related to vascular events, such as endothelin, nitric oxide or angiotensin II receptor as well as ACE gene.     

Clinical significance of anti-dsDNA antibody isotypes: IgG/IgM ratio of anti-dsDNA antibodies as a prognostic marker for lupus nephritis

The objective of this paper is to investigate the association between patterns of anti-dsDNA antibody isotypes and specific clinical manifestations (categorized in renal, musculoskeletal, cutaneous, hematological, pulmonary, neurological and cardiac). Sera of 202 systemic lupus erythematosus (SLE) patients, 33 patients suffering from other autoimmune diseases and 115 healthy blood donors were analysed for anti-dsDNA antibodies by IgG-, IgA- and IgM-specific ELISA, Farr-assay and CLIF. A subset of 24 SLE patients was investigated in a longitudinal study over a period of one to six years. Disease activity of 105 SLE patients was measured according to the ECLAM score. In the cohort of SLE patients 63% were positive for the IgG class, 40% for the IgA and 57% for the IgM class specific anti-dsDNA ELISA. Sensitivity (79%) and specificity (99%) for the diagnosis of SLE appeared to be highest for the ELISA measuring all isotypes of anti-dsDNA antibodies. The concentrations of anti-dsDNA isotypes showed a strong correlation with disease activity. Analysing the relationship between IgG, IgA and IgM anti-dsDNA antibody isotypes and clinical manifestation, we found a significant association of the IgM isotype with cutaneous involvement and of the IgG isotype with lupus nephritis. The IgG/IgM ratio of anti-dsDNA antibodies represented a significant parameter to distinguish patients with lupus nephritis from those without renal involvement. In the longitudinal study, a continuous ratio under 0.8 was associated with absence of renal involvement throughout the investigated period. In conclusion, the evaluation of anti-dsDNA isotypes provides a diagnostic tool to define subsets within SLE patients with different clinical manifestations. In particular, the IgG/IgM ratio of anti-dsDNA antibodies could be used as a prognostic marker for lupus nephritis during the course of the disease.     

New onset of lupus nephritis in two patients with SLE shortly after initiation of treatment with belimumab

PurposeBelimumab is currently approved for the treatment of patients with active SLE despite standard treatment. However, it has not been formally tested for patients with lupus nephritis because such patients had been excluded from the clinical trials. In this report, we present two patients with SLE who developed lupus nephritis de novo shortly after belimumab treatment initiation; both patients improved rapidly upon belimumab discontinuation.ResultsThe first patient (a 30-year-old female, with a 15-year disease duration, receiving prednisolone, hydroxychloroquine, and azathioprine, with no previous history of nephritis that was repeatedly anti-dsDNA negative) had exacerbation of a facial butterfly-like rash developed after 3 months of belimumab treatment initiation. Concomitantly, her urinalysis became abnormal for the first time during her long follow-up (15–20 red blood cells per hpf, and a 24-h urine protein of 1600 mg), and a renal biopsy documented the diagnosis of a Class III (WHO classification). Her anti-dsDNA titers became highly positive for the first time. Belimumab was discontinued and her proteinuria and abnormal urinalysis reverted to normal rapidly, and before MMF administration was approved by local regulatory authorities. Our second patient (a 38-year-old female with a 19-year disease duration) was being treated with prednisone and azathioprine. Two months following belimumab treatment initiation, she became edematous and had an active urine sediment (50–60 rbc per hpf, dysmorphic, and a 24-h urine protein levelabove 6000 mg) for the first time during her disease course. Her renal biopsy was compatible with a Class V membranous nephritis. Belimumab was discontinued and MMF (2 g/d) was substituted for azathioprine with her urinary protein declining to 2.7 g/d just 10 days afterwards.ConclusionsIn this report, apart from our two patients, we discuss the relevant literature consisting of a handful of studies and case reports. The studies analyze patients with renal involvement treated with belimumab and are inconclusive. There are only a few case reports in which belimumab along with other agents had a potential benefit, although not straightforward. There is only one case report with striking similarities to the two patients with SLE we report herein. It could be claimed that belimumab was unable to prevent the appearance of lupus nephritis during a potentially serious disease exacerbation. Certainly, a causative association between belimumab treatment and the de novo appearance of lupus nephritis cannot be claimed because of our report. However, a potential association between belimumab treatment and the development of such a serious manifestation cannot be entirely excluded. In support of the latter hypothesis is the quick resolution/significant reduction of proteinuria shortly after belimumab discontinuation and before other treatment measures had any reasonable effect. Studies evaluating the potential usefulness of belimumab in patients with lupus nephritis are currently ongoing; until then, one should keep in mind unanswered questions as far as renal safety is concerned.     

Systemic lupus erythematosus. III. Observations on clinical renal involvement and follow up of renal function: Dutch experience with 110 patients studied prospectively.

A prospective study of 110 patients with systemic lupus erythematosus (SLE) was undertaken to evaluate the reliability of clinical signs of lupus nephritis, which developed in 39 (35%) patients. Those patients with SLE who showed no clinical signs of lupus nephritis had an excellent survival rate (10 year survival 93%) and retained normal renal function (serum creatinine less than 130 mumols/l); clinical lupus nephritis developed mainly in the first three years after diagnosis of SLE and was associated with a decreased survival rate (10 year survival 62%). Increased mortality was found in male patients with lupus nephritis over 25 years of age and in female patients with lupus nephritis under 25 years of age, while renal failure rates did not differ between these groups. Treatment of lupus nephritis with high dose prednisone alone or in combination with immunosuppressants did not result in differences in patient survival or renal function preservation. It was concluded that clinical variables are a reliable guide in the management of patients with SLE, and routine use of renal biopsy in these patients is rejected.     

New treatment strategies for proliferative lupus nephritis: keep children in mind!

Renal involvement is frequent in children with systemic lupus erythematosus (SLE) and carries significant short and long-term morbidity. Treatment strategy in proliferative glomerulonephritis relies mainly on studies in adult patients where conventional treatment regimens including high doses of cyclophosphamide (CYC) and steroids may cause severe side effects. New strategies including sequential therapies of various combinations of low dose CYC, calcineurine inhibitors (cyclosporine or tacrolimus), mycophenolate mofetil, azathioprine, rituximab are now under investigation in adult patients with very few data in children. Organization of international registries and controlled trials in children with lupus nephritis is mandatory to determine long term prognosis and to validate less toxic therapy regimens in childhood.     

A case of systemic lupus erythematosus presenting with rectal ulcers as the initial clinical manifestation of disease

Gastrointestinal involvement is often seen in patients with systemic lupus erythematosus (SLE). All parts of the gastrointestinal tract may be affected. However, rectal involvement at onset is rare. We describe here a case of SLE in which rectal ulcers due to vasculitis occurred as the initial manifestation of the disease without involvement of any other organ. The ulcers worsened, along with the appearance of lupus nephritis 5 years later When steroid therapy was initiated, there was rapid clinical and radiographic improvement. Our case suggests that rectal ulcer is a rare but important complication of SLE and can represent the initial and sole clinical manifestation of the disease.     

Microangiopathic haemolytic anaemia secondary to lupus nephritis: an important differential diagnosis of thrombotic thrombocytopenic purpura

Systemic lupus erythematosus (SLE) has been described as a cause of microangiopathic haemolytic anaemia (MAHA), however there is little literature to support this assertion. We report on three patients presenting with SLE and MAHA with a clinical picture indistinguishable from thrombotic thrombocytopenic purpura (TTP), who had underlying lupus nephritis. They all had significant proteinuria and normal Von Willebrand Factor cleaving protease (vWF-CP) levels. Their MAHA fitted better for haemolytic syndrome (HUS) and their cerebral signs were explained either by malignant hypertension or cerebral lupus. Their MAHA only improved when the appropriate treatment for lupus nephritis was given.We propose that the previously described association between SLE and MAHA, in actuality relates to the underlying presence of lupus nephritis causing haemolytic uraemic syndrome, not TTP. Significant proteinuria was present in all cases of MAHA due to lupus nephritis, so may be a useful discriminatory sign. Furthermore the demonstration of a normal vWF-CP assay aided in the distinction between TTP and MAHA due to lupus nephritis. All our patients responded to mycophenolate mofetil suggesting this may be useful in other cases of lupus nephritis causing HUS.     

Preclinical and early systemic lupus erythematosus

The challenge of early diagnosis and treatment is a timely issue in the management of systemic lupus erythematosus (SLE), as autoimmunity starts earlier than its clinical manifestations. Hence, growing efforts for stratification of patients according to the individual risk of developing specific clinical manifestations and/or predicting a better response to a given treatment have led to the proposal of several biomarkers, which require validation for use in clinical practice. In this viewpoint, we aim at distinguishing and discussing the features and the approach to asymptomatic immunological abnormalities potentially heralding the development of SLE, defined as preclinical lupus, and clinical manifestations consistent with SLE not yet fulfilling classification criteria, defined as early lupus. In case of preclinical SLE, careful surveillance using available screening tools is paramount, while patients with early lupus deserve an appropriate and timely diagnosis and, consequently, a proper treatment including hydroxychloroquine as the anchor drug.     

C反应蛋白与系统性红斑狼疮的相关性

目的分析系统性红斑狼疮(systemic lupus erythemotosus,SLE)患者血清C反应蛋白(C-reactive protein,CRP)水平,了解SLE患者CRP与狼疮本身及合并感染的关系。方法对2009年1月至2011年5月北京大学第一医院住院SLE患者的病历进行回顾分析,研究SLE患者血清CRP水平与狼疮疾病活动度、器官受累的关系;并结合合并感染SLE患者血清CRP水平,探讨CRP对判定感染的敏感性及特异性。结果共入组283例SLE患者。在不合并感染的239例SLE患者中,血清CRP中位值为2.6 mgL,94.6%的患者CRP20.0 mgL。血液系统受累患者CRP水平高于无血液系统受累患者(3.2 mgL vs.2.0 mgL,P0.05),但合并浆膜炎、肾脏受累、关节炎的患者CRP水平与不合并上述表现的患者之间无显著性差异。在不同疾病活动度患者之间,CRP水平无显著差异(P0.05);但随着免疫抑制治疗患者疾病活动度降低,CRP、ESR水平均下降(P0.05)。合并感染SLE患者血清CRP水平明显高于不合并感染患者,差别具有统计学意义(13.6 mgL vs.2.6 mgL,P0.05),CRP21.3 mgL对于判断感染的特异性可达95.0%。结论不合并感染的SLE患者CRP水平多正常或轻度升高,免疫抑制治疗可以使患者CRP水平随病情改善而下降;血液系统受累患者CRP水平高于无血液系统受累患者。SLE患者合并感染时CRP水平可显著升高,故CRP可能作为临床上鉴别狼疮活动与感染的指标之一。