I have recently had a kidney biopsy for a kidney inflammation which the doctors think is lupus nephritis, but all my blood tests for lupus have come back negative! (they did about 7)
They are still saying it is lupus nephritis as that is what the biopsy suggests. I'm completley confused!!!!!
Has anyone else encountered seronegative lupus?
Hi Bungle; Here is what I have been able to find out about seronegative Lupus nephritis:
Seronegative lupus nephritis’ describes patients with renal histology typical of lupus nephritis who have no clinical or serological evidence of systemic lupus erythematosus(SLE). There have been patients identified as having ‘seronegative lupus nephritis’ who met the diagnostic criteria for Lupus without the serological (C1q) nephropathy. The term ‘seronegative lupus nephritis’is unhelpful, and should be avoided when there is diagnostic uncertainty. The term C1q nephropathy should be preferred when these histological features are seen in the absence of overt lupus, when C1q deposition is dominant and when tubuloreticular bodies are absent. The clinical course in the cases reported here does not support the use of immunosuppressive therapy inC1q nephropathy.
I also found information regarding "incomplete Lupus". It may not be your case, but here is the information just in case it does fit you.
Many seronegative lupus patients are referred to rheumatologists to "rule out" systemic lupus erythematosus (SLE). There are usually several diagnostic possibilities for such cases. You may have what is called definite or incomplete SLE; You may have a connective tissue disease that has clinical overlap with SLE (i.e. Sjögren's syndrome); You may have an unspecified connective tissue disease.
Individuals with incomplete lupus erythematosus (ILE) are those who have some clinical features of SLE, but not all of the required diagnostic criteria based on the classification devised by the American College of Rheumatology. According to this classification, a person is said to have SLE if at least 4 of the 11 established criteria are met (see Table 1). Someone who meets only a few of these criteria might be considered to have ILE by their rheumatologist.
Common features of incomplete lupus
Common features of ILE are:
- low-grade fever
- joint pain
- hair loss
- the facial "butterfly rash"
- a positive test for antinuclear antibodies, or ANA.
This individual probably does have SLE, but shows only two ACR classification criteria: the butterfly rash and a positive ANA.
Only a few studies have been published on the clinical presentation and outcome of ILE cases, and the variation in selection criteria and methods used in these studies makes it difficult to reach conclusions.
Nevertheless, people with ILE appear to have a mild disease, frequently with arthritis, cutaneous involvement, and a positive ANA test. Organ-threatening disease such as kidney or brain involvement seems to be uncommon.
Can incomplete lupus develop into SLE?
The immediate question asked by people who are diagnosed with ILE is whether the disease will stay the same or will evolve into SLE.
Is there any way to predict who will develop SLE? A study that attempted to answer these questions was performed at the Universidad Central del Caribe School of Medicine, Bayamón, Puerto Rico. The results of this study were published in Lupus2000: 9, 110-115.
Because of the great clinical overlap that exists between SLE and other connective tissue diseases, the selection criteria were chosen very carefully (see Table 2). Excluded individuals were those who fulfilled the classification criteria for other rheumatic diseases, or who presented distinctive clinical features of other connective tissue diseases-for example, individuals with fibromyalgia syndrome, which shares many symptoms with SLE.
ILE study results
In this study, 87 Puerto Ricans (82 women, 5 men) met the study criteria for ILE, with an average disease duration of 4.4 years. These individuals were followed for an average of 2.2 years. The participants whose diagnosis remained ILE throughout the study were then compared to two different groups: those in the study whose disease evolved into SLE, and members of a well-established group of 94 SLE patients.
Of the total of 87 study subjects who were initially diagnosed with ILE, only eight cases (9 percent, all female) evolved into SLE. The average age at onset was lower in those who developed SLE (24 years) than in those who remained with ILE (34 years).
The average time interval between onset of ILE and development of SLE was 4.4 years. None of the individuals whose disease evolved into SLE had neurologic, cardiac, or pulmonary involvement. Only one person developed kidney disease, but never developed renal insufficiency or severe renal damage.
At baseline, individuals who remained with ILE were less likely than those whose disease evolved into SLE to have:
- elevated anti double-stranded DNA (anti-dsDNA) levels, or
- low C3 complement levels.
And when the initial symptoms of ILE were compared with all cases of SLE, those with ILE were less likely to have:
- butterfly rash
- oral ulcers
- Raynaud's phenomenon
- serologic abnormalities (such as low serum complements C3 and C4, elevated anti-dsDNA, positive anti-Sm, anti-RNP, anti-Ro and anti-La antibodies).
Statistical analysis showed that the most important factors to predict the evolution of ILE into SLE were:
elevated anti-dsDNA, and
The findings of our study are in agreement with other studies in three ways.
1) First, persons with ILE seem to have mild disease in which life-threatening complications are rare.
2) Second, only a small number of those with ILE develop further SLE manifestations.
3) Finally, those who develop SLE still continue with a mild disease.
On the other hand, marked differences are found in the predictors of disease evolution among ILE studies. Other studies have identified discoid (skin) lupus, homogeneous pattern of ANA, and positive anti-Sm antibodies as risk factors for SLE occurrence. In addition to different selection criteria, these variations could be attributed to ethnic or racial influence. It is known that clinical manifestations, immunologic features, and outcome of SLE may vary substantially among people from different ethnic origins.
Further studies are needed to determine the outcome of ILE and to identify the risk factors of disease progression. This information will help to provide better medical care to people with ILE, and to identify those who may develop disease progression.
To achieve these goals it will be necessary to:
1) establish more definitive and uniform criteria,
2) follow patients for longer periods of time, and
3) study patients of different ethnic backgrounds.
About the Author
Dr. Luis M. Vilá is Chief and Program Director, Division of Rheumatology, at the University of Puerto Rico School of Medicine in San Juan, PR. He was previously an Assistant Professor, Division of Rheumatology, at Universidad Central del Caribe School of Medicine in Bayamón, PR. Dr. Vilá is one of the Investigators for the LUMINA Study: "Lupus in minority populations: Nature vs Nurture."
I hope that this has been helpful...let me know if you need more information.
Peace and Blessings
Unlike my sister and I, my Sunt seems to have no bloodwork indicators of an autoimmune disease, but has typical Lupus and RA symptoms, like Raynaud's, fatigue, joint pain, sleeplessness, stomach problems, etc........
She hasnot had kidney problems like me, yet.
Thanks for the information.
I have been put on CellCept and got the first good news in months. My creatinine and urea levels have improved after 3 weeks of the treatment and I am now in the normal range.
I still don't have a definite diagnosis of lupus although the docs are pretty certain that was is the underlying cause. But as long as the meds are working I am happy
Are there any specific tests that will show lupus if i have it?
I am in much the same situation. I have no antibodies but a high ESR--inflammation marker. But Have been diagnosed with Lupus, Antiphospholipid Syndrome And Sjogrens on symptoms. I am lucky Dr Hughes in England recognises this. APS or Hughes syndrome was first recognised by him.
It is written that around 90% of Lupus sufferers are ANA positive, THat means around 1:10 are negative. It's time local Rheumatologists recognised this.