Abstract. The currently used classification reflects our understanding of the pathogenesis of the various forms of lupus nephritis, but clinicopathologic studies have revealed the need for improved categorization and terminology. Based on the 1982 classification published under the auspices of the World Health Organization (WHO) and subsequent clinicopathologic data, we propose that class I and II be used for purely mesangial involvement (I, mesangial immune deposits without mesangial hypercellularity; II, mesangial immune deposits with mesangial hypercellularity); class III for focal glomerulonephritis (involving Ͻ50% of total number of glomeruli) with subdivisions for active and sclerotic lesions; class IV for diffuse glomerulonephritis (involving Ն50% of total number of glomeruli) either with segmental (class IV-S) or global (class IV-G) involvement, and also with subdivisions for active and sclerotic lesions; class V for membranous lupus nephritis; and class VI for advanced sclerosing lesions]. Combinations of membranous and proliferative glomerulonephritis (i.e., class III and V or class IV and V) should be reported individually in the diagnostic line. The diagnosis should also include entries for any concomitant vascular or tubulointerstitial lesions. One of the main advantages of the current revised classification is that it provides a clear and unequivocal description of the various lesions and classes of lupus nephritis, allowing a better standardization and lending a basis for further clinicopathologic studies. We hope that this revision, which evolved under the auspices of the International Society of Nephrology and the Renal Pathology Society, will contribute to further advancement of the WHO classification.The morphologic changes in a renal biopsy from a patient with systemic lupus erythematosus (SLE) comprise a spectrum of vascular, glomerular, and tubulointerstitial lesions. The classification of SLE nephritis has evolved over the past 40 years as more lesions were identified and defined. It has been an increasing challenge to apply new pathogenetic insights to the interpretation of the renal biopsy in SLE and to correlate pathologic findings with clinical symptoms, choice of treatment, and prognosis. The current classification, which was advanced in 1982 (1) and revised in 1995 (2), reflects our understanding of the pathogenesis of the various forms of renal injury in SLE nephritis. However, subsequent clinicopathologic studies have revealed the need for clarification of the different categories and the diagnostic terminology. The clas-

The currently used classification reflects our understanding of the pathogenesis of the various forms of lupus nephritis, but clinicopathologic studies have revealed the need for improved categorization and terminology. Based on the 1982 classification published under the auspices of the World Health Organization (WHO) and subsequent clinicopathologic data, we propose that class I and II be used for purely mesangial involvement (I, mesangial immune deposits without mesangial hypercellularity; II, mesangial immune deposits with mesangial hypercellularity); class III for focal glomerulonephritis (involving <50% of total number of glomeruli) with subdivisions for active and sclerotic lesions; class IV for diffuse glomerulonephritis (involving > or =50% of total number of glomeruli) either with segmental (class IV-S) or global (class IV-G) involvement, and also with subdivisions for active and sclerotic lesions; class V for membranous lupus nephritis; and class VI for advanced sclerosing lesions. Combinations of membranous and proliferative glomerulonephritis (i.e., class III and V or class IV and V) should be reported individually in the diagnostic line. The diagnosis should also include entries for any concomitant vascular or tubulointerstitial lesions. One of the main advantages of the current revised classification is that it provides a clear and unequivocal description of the various lesions and classes of lupus nephritis, allowing a better standardization and lending a basis for further clinicopathologic studies. We hope that this revision, which evolved under the auspices of the International Society of Nephrology and the Renal Pathology Society, will contribute to further advancement of the WHO classification.

Prehemodialysis and hemodialysis patients are at an increased risk of hepatitis B infection and have an impaired immune response to hepatitis B vaccines. We evaluated the immune response to the new adjuvant of hepatitis B vaccine AS04 (HBV-AS04) in this population. We measured antibody persistence for up to 42 months, and the anamnestic response and safety of booster doses in patients who were no longer seroprotected. The primary vaccination study showed that HBV-AS04 elicited an earlier antibody response and higher antibody titers than four double doses of standard hepatitis B vaccine. Seroprotection rates were significantly higher in HBV-AS04 recipients throughout the study. The decline in seroprotection over time was significantly less in the HBV-AS04 group with significantly fewer primed patients requiring a booster dose over the follow-up period. Solicited/unsolicited adverse events were rare following booster administration. Fifty-seven patients experienced a serious adverse event during the follow-up; none of which was vaccine related. When HBV-AS04 was used as the priming immunogen, the need for a booster dose occurred at a longer time compared to double doses of standard hepatitis B vaccine. Hence, in this population, the HBV-AS04 was immunogenic, safe, and well-tolerated both as a booster dose after HBV-AS04 or standard hepatitis B vaccine priming.

We investigated whether serum neutrophil gelatinase-associated lipocalin (NGAL) was an early predictive biomarker of contrast-induced nephropathy (CIN) in patients with chronic kidney disease (n = 100) undergoing coronary catheterization. Serum creatinine (SCr) levels were measured at baseline, 24 hours, and 48 hours post procedure. Serum NGAL was measured preprocedure, 4 hours, and 24 hours post procedure. The frequency of CIN was 11%. In patients with CIN, SCr achieved significance only at 48 hours (P = .006), whereas serum NGAL increased ≥25% from baseline at 24 hours in 7 of 11 patients with CIN (P = .04) but did not change in the other 4. However, serum NGAL also rose ≥25% in 12 of 89 non-CIN patients. This subgroup could have had "incipient CIN." Serum NGAL delta value at baseline, 24 hours was superior to SCr for early diagnosis of CIN. In conclusion, serum NGAL is an early predictive biomarker for CIN.

The improved immunogenicity profile and clinically acceptable reactogenicity of HB-AS04 vaccine are of key importance to provide a more rapid, enhanced, and longer seroprotection to these immunocompromised patients at risk for HB infection.