Discussion on latest management of lupus nephritis (Part 3)
We now continue our discussion of lupus nephritis treatment (LN).
The patients with systemic lupus erythematosus (SLE) with any signs of kidney involvement such as glomerular haematuria and/or cellular casts, proteinuria >0.5g/24 hours (or spot urine protein-to-creatine ratio (UPCR) > 500 mg/g), unexplained decrease in glomerular filtration rate (GFR)) may need to undergo kidney biopsy.
There are mild presentations that can be linked with active histological lesions.
In a review of biopsies that were done from 1970-2016, earlier use of biopsy based on urinary abnormalities, which were done from 2001 to 2016, was linked with improved results despite similar rates of severe histology.
There should be a balance in the benefits of histological evaluation versus advanced bleeding risk in some patients such as those taking anticoagulants.
Patients with SLE, with special focus with suspected kidney involvement, needs to be tested for antiphospholipid antibodies (aPL), since renal manifestations of antiphospholipid syndrome, such as thrombotic microangiopathy (TMA), may carry prognostic implications.
Testing for anti-dsDNA and anti-Clg autoantibodies should be considered in patients with suspected LN, together with all complement levels (C3 and C4).
The 2003 International Society of Nephrology/Renal Pathology Society‘s (ISN/RPS) classification remains as the gold standard for assessment kidney biopsy in LN TMA lesions.
While the LN TMA lesions are not pathognomonic, nonetheless should raise suspicion of antiphospholipid syndrome nephropathy and thus, should carry out aPL (re-)testing immediately.
As such, TMA has been reported in up to 25% of LN biopsies.
As a result, prognostic implications remain undetermined. For this reason, Tubulointerstitiał lesions, such as interstitial fibrosis and tubular atrophy, are associated with poor kidney health.
In a revision of the 2003 ISN/RPS classification has been proposed recently and the endorsement is still pending as of this writing.
Moreover, the treatment using immunosuppresive therapy is the preferred in treating of active class LN regardless of coexisting histological chronicity.
For class V LN it is preferred that immunosuppression pertaining to patients with nephroti-range proteinuria usually linked with a grim prognosis, likewise addition to cases with proteinuria >1g/24 hours despite optimal use of renin-angio- tensin-aldosterone system blockers for a time period (eg, at least 3 months). Class II LN may not need specific immunosuppressive therapy, but this people may be prone to histological transformation to more aggressive disease on the repeat biopsy.
The presence of significant proteinura should prompt histological reassessment for detection of proliferative changes that may have been overlooked in the course of the examination of the patient.