Quick review of the autoantibodies that may be useful in the diagnosis and management of patients with lupus-related kidney disease:
anti-nuclear antibody (ANA): as well as know from our internal medicine days: very sensitive, but not very specific. In addition to being present in over 95% of patients with SLE, ANA is also frequently positive in scleroderma, dermato/polymyositis, and Sjogren’s syndrome among others.
anti-dsDNA (antibodies against DNA) and anti-Smith (antibodies against snRNPs): these antibodies are much less sensitive, but also fairly specific. I have also seen other nephrologists follow anti-dsDNA titers as a means of monitoring disease severity and/or response to therapy.
anti-Ro (SSA) and anti-La (SSB) antibodies: these antibodies, also frequently associated with Sjogren’s syndrome, are noted to be important in the pathogenesis of neonatal lupus.
anti-RNP antibody: this autoantibody, also associated with other mixed connective tissue disease, may be linked to flares of lupus cerebritis.
anti-histone antibody: this tends to be positive in drug-induced lupus.
anti-phospholipid antibody: the “antiphospholipid antibody” screen should include detection for both anti-cardiolipin antibodies and lupus anticoagulant. The distinction between anti-phospholipid antibody-mediated renal injury and lupus nephritis is an important one to make, as the former is a thrombotic microangiopathy which should be treated with anticoagulation therapy, whereas the latter is typically treated with immunosuppressants.
Finally, although these are not autoantibodies, two of the most useful serologic tests to send in the diagnosis of lupus nephritis are serum complements (C3 & C4): both of which should be low in the setting of an immune complex-mediated GN.
Healthy diet and good exercise is good, if not universal sound advice. However it isn't specific to SLE patients. It should be taken into consideration that the first-line therapy isn't laying off beer or walking more but effective immunosuppresants. This is a conditions with much more complex underlying mechanisms than environmental factors.
The immune complexes diposited by the autoreactive B cells and the hypothetical DNA from this self-damage can be found almost anywhere. They circulate in the blood supply. Conditions are so variable it is almost impossible to pinpoint a single common symptom to SLE. However, with continuing flare ups some if not all are likely to occur at some point.
The most common complication is Lupus Nephritis. It makes perfect sense, since a large quantity of blood is filtered through the kidney every day.
How SLE arises remains a mystery but hypotheses don't lack.
The only effective management right now are immunosuppressive regimes to maintain relatively complication free remission periods.
Lupus causes it to assault normally functioning, healthy tissues. Symptoms are: inflammation and harm to the joints, skin, blood, heart, lungs and kidneys etc. It has severe effects like: kidney damage, breathing distress. To prevent it, one should lead healthy lifestyle, have balanced diet, do regular low intensity exercise, one should always seek doctors consultation.