Lupus nephritis 46

Pyelonephritis, interstitial nephritis Glomerulonephritis, renal infard, lupus nephritis, vasculitis... 

Hogan, S. L. et al., Silica exposure in anti-neutrophil cytoplasmic autoantibody-associated glomerulonephritis and lupus nephritis, J. Am. Soc. Nephrol., 12, 134, 2001. 

Lupus nephritis, gastroesophageal reflux disease, peptic ulcer disease, visual disorders... 

Moore RA, Derry S. (2006) Systematic review and meta-analysis of randomised trials and cohort studies of mycophenolate mofetil in lupus nephritis. Arthritis Res Ther 8 R182. 

Walsh M, James M, Jayne D, Tonelli M, Manns BJ, Hemmelgam BR. (2007) Mycophenolate mofetil for induction therapy of lupus nephritis A systematic review and meta-analysis. Clin J Am Soc Nephrol 2 968-975. 

Contrast nephrotoxicity Lupus nephritis flare Lupus nephritis... 

Dooley MA, Falk RJ. Immunosuppressive therapy of lupus nephritis. Lupus 1998 7 630-4. 

Plane RS, Roberts MA, Strippoli GEM, Chadban SJ, Kerr PG, Atkins RC. Treatment for lupus nephritis. Cochrane Database Syst Rev 2004. 

Notwithstanding DMARDs therapy (NSAIDs and/or prednisolone and/or hydroxychloroquine and/or azathioprine) lupus nephritis still develops in 48% of patients with SLE. Of these 40% develop into End Stage Renal Disease and subsequent mortality mostly due to infections. 

Lupus nephritis is the most common manifestation of inadequately treated SLE. Its therapy serves as a module for treatment of other lupus manifestations. 

Single drug therapy is mostly adequate in lupus nephritis (LN) classified as renal biopsy WHO Class I and II. Single drug therapy in lupus nephritis Class III-V, and in particular Class VI is less or not effective. One immunosuppressant cannot suppress all aspects of autoimmune inflammation in the more serious forms of the disease. The SBC-5-IMNs is not required in Class I, IL and also not in Class VI. In Class VI nothing helps, except renal dialysis or renal transplantation. 

Lupus Nephritis is considered DMARD-Refractory if after 2 consecutive monthly evaluations of sin-gie DMARD or combination DMARDs therapy response is unsatisfactory with ESR > 40 mm and SLAM-R scores that are not reduced compared to... 

DMARD Refractory Lupus Nephritis is considered to be in remission when the SLAM-R Score is suppressed to zero, ESR is suppressed to 10 mm (male 5 mm) and 24 hours Micro-albuminuria is suppressed to <30 mg (normal <30 mg). Remission with oral drugs (RworalDs) is defined when Remission is maintained with MME and/or CyS for at least 2 years and remission without drug (RwD) when after 2 years therapy, oral drugs are tapered off with a sustained remission for at least 2 years. 

Darmawan J, Zhao DB, Soorosh GS, Chen S-L, Haq SY. Sustained remission in DMARD-refractory Lupus nephritis treated with step-down bridge comhination therapy of five immunosuppressants without corticosteroids a six years international study in Asia -WHO-ILAR COPCORD Stage 11 treatment. APLAR J Rheumatol 2007 10 in press. 

A 62-year old woman was admitted to hospital with lupus nephritis. A kidney biopsy showed a mesangio-proliferative glomerulonephritis (WHO class III). After 4 months of inadequate response to traditional... 

In a 15-year-old boy with previously quiescent lupus nephritis, laboratory markers of disease activity rose during somatropin treatment and returned to baseline concentrations within 3 months after withdrawal (88). 

Yap HK, Loke KY, Murugasu B, Lee BW. Subclinical activation of lupus nephritis by recombinant human growth hormone. Pediatr Nephrol 1998 12(2) 133-5. 

There is no cure for SLE. Guillermo el al. (G16) found only 10 randomized controlled trials during the past 5 years, 5 for lupus nephritis and 5 for all SLE patients. Compared to conventional therapies for lupus nephritis, a monthly bolus with intravenous cyclophosphamide is more effective than a monthly bolus with methyl prednisolone, but has significant side effects (including amenorrhea, cervical dysplasia, avascular necrosis, and herpes zoster) in both groups (G14). In order to avoid these side effects, more recent therapies have been developed. However, neither plasmapheresis (Wl), intravenous immunoglobulin (B21), recombinant human DNase (rhDNase) (D3), nor mycophenolate mofetil (C14) was shown to be more effective than conventional therapy. However, some of these... 

Anti-dsDNA antibodies are both specific and pathogenic to SLE. As mentioned previously, these autoantibodies are produced by an antigen-driven mechanism. They are organ-specific, especially kidney. We will discuss the close relationship between anti-dsDNA and lupus nephritis and the proposed mechanism by which anti-dsDNA leads to lupus nephritis. 

The close correlation between disease activity of SLE and level of anti-dsDNA has been documented repeatedly (D4, L24). Anti-dsDNA also represents a reliable marker for acute exacerbation of disease activity (S37, T3). Some report that high-avidity anti-dsDNA correlates with renal manifestations and active lupus nephritis (S37), whereas low-affinity antibodies are associated with cerebral complications (S21, S22). 

Evidence That Anti-dsDNA Antibodies Cause Lupus Nephritis... 

In spite of the strong evidence just cited, lupus nephritis is not invariably correlated with serum anti-dsDNA. (NZB x NZWjFi x NZW backcross mice may develop nephritis without anti-DNA antibodies (Y5). Patients with lupus nephritis also do not always have anti-dsDNA antibodies or have only low levels of antibodies (A23, H7, L21). Swaak et al. noted a sharp drop at the time of flareup of anti-dsDNA antibodies accompanied by low levels of Clq and C3 in patients with severe SLE flares (S36). 

Circulating Immune Complex. Anti-dsDNA/DNA immune complexes have long been considered responsible for the development of lupus nephritis. The level of immune complexes in SLE patients with active disease detected by monoclonal anti-DNA antibodies is higher (T7). About half of SLE patients had elevated amounts of DNA antigen in the immune complexes (N4, R2, S27). 

There are many other reports arguing against this mechanism as the major pathogenetic pathway of lupus nephritis. The presence of circulating DNA/anti-DNA immune complexes is difficult to detect (B25,13). Moreover, recent studies demonstrated that the levels of circulating DNA (nucleosome) immune complexes were low (B28, F8, L14). Data also suggest that DNA/anti-DNA complexes are rapidly cleared by the liver (E5) and bind poorly to glomerular basement membrane (GBM) (12). 

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