Diagnosing Lupus

This site is intended for healthcare professionals as a useful source of information on the diagnosis, treatment and support of patients with lupus and related connective tissue diseases.
Early diagnosis is essential to reduce the risks of long term organ damage. Although as nurses we would never be expected to diagnose this complex condition, we do need to have a good working knowledge of how the diagnosis is reached.

As the British Society of Rheumatology states in the executive summary of its SLE guidelines, “SLE is a multisystem autoimmune disorder. The diagnosis requires a combination of clinical features and the presence of at least one relevant immunological abnormality. If there is a clinical suspicion of lupus, blood tests (including serological marker tests) should be checked”.

Active lupus is indicated by the presence of a variety of antibodies which react against some of the proteins in the cell. The condition can normally be diagnosed with a thorough history, patient examination and more SLE focused blood tests including ANA, anti-dsDNA test, and Complement proteins C3 & C4. Very often when lupus is becoming or is more active there is a rise in the anti-double stranded DNA (also referred to as anti-dsDNA or sometimes seen as DNAq) and
a fall in the complement (C3 & C4) blood test result over several visits. Blood tests are essential to the diagnosis of lupus, due to the multi-system nature of the disease. Monitoring of other aspects of disease activity and systemic review in clinic is essential to prevent major flares of lupus.

A patient needs to meet four out of the following eleven criteria to be classified as having lupus according to the American College of Rheumatology (ACR). Although this was developed as entry criteria to clinical trials, they provide a good objective framework:-
Malar rash

Discoid rash


Mucosal ulcers



Renal disorder

Neurological disorder


Immunological disorder

Antinuclear Antibody (ANA)
Fixed malar erythema, flat or raised, over malar eminences tending to spare nasolabial folds.

Red patches of skin associated with keratotic scaling and follicular plugging, some atrophy in older lesions.

Skin rash of unusual reaction after exposure to sunlight.

Oral or nasopharyngeal ulcers, may be painless.

Serosal surface inflammation – pleura, or pericardium.

Non-erosive arthritis involving 2 or more peripheral joints, characterised by tenderness, swelling or effusion.

Persistent proteinuria of >0.5 g/day (PCR >50mg/mmol or >+3 if quantitation not performed) OR red cell, haemoglobin, granular, tubular or mixed cell casts.

Seizures or psychosis in the absence of drug or known metabolic derangement e.g. uremia, ketoacidosis or electrolyte imbalance.

Haemolytic anaemia with reticulocytosis, leucopoenia <4000/mm3 on 2 or more occasions, lymphopenia <1500/mm3 on 2 or more occasions or thrombocytopenia <100000/mm3 in the absence of offending drug.

Anti-dsDNA antibodies at an abnormally high level, or presence of anti-Sm antibody, or presence of APLs antiphospholipid antibodies with abnormal IgM or IgG; or positive lupus anticoagulant; or false positive over >6months for syphilis serology.

Abnormally high ANA in the absence of drugs known to cause drug-induced lupus symptoms.
Other antibodies, quoted in variable frequencies in reported studies, that can be found in lupus include:

Anti-Smith (anti-Sm)
Anti-Ribosomal RNP
Anti-U1 snRNP
Anti-Ro (anti-SS-A) and Anti-La (anti-SS-B)

Frequency in lupus

Sensitivity poor, seen in overlap syndromes
Ro – up to 50%
La – 10-15%
Also associated with:

Specific for SLE
CNS lupus
Sjögren’s syndrome

Drug-induced lupus
Full blood count can reveal a normochromic and normocytic anaemia (known as anaemia of chronic disease), lymphopenia, and thrombocytopenia which if severe can lead to internal bleeding and purpura. In active lupus the erythrocyte sedimentation rate (ESR) and plasma viscosity (PV) are usually elevated. Interestingly, other tests for acute phase inflammation such as C-reactive protein (CRP) may remain normal or only slightly raised providing helpful diagnostic data for the clinician. If the CRP is elevated infection should be considered as a possible cause. This is discussed in more detail in the BSR SLE guidelines - READ GUIDELINES HERE

Urine analysis is very important as proteinuria can indicate kidney involvement. Clinic urinalysis dip testing can be the first indicator that there is a change that needs careful monitoring. We should be aiming to dip a SLE patient’s urine at every contact (i.e. every rheumatology hospital appointment whether that’s with us as nurses, with doctors or with other specialist AHP SLE appointments) and we should encourage patient autonomy to request testing at every GP or other outpatient clinic appointment. If significant protein change occurs due to renal involvement, a renal biopsy may be useful. This relatively straight forward diagnostic test can give a clear indicator of the type of kidney disease and will guide which treatment is most suitable. Understandably patients can be hesitant about having the procedure however knowing exactly what is happening in the kidney is essential and it is not suggested lightly as lupus is not the only cause of abnormalities.