How do lupus glomerulonephritis and its treatment affect the renal reserve?

Patients with mesangial proliferative lupus glomerulonephritis (World Health Organization class II) are generally believed to have only mild to moderate proteinuria and normal renal function. However, there have been several reports of patients with mesangial lupus with nephrotic-range proteinuria. In this report, we present two additional cases and review the literature. Of seven reported cases, persistent nephrotic syndrome was observed in four, morphologic transformation occurred in three, and all but one presented with varying degrees of azotemia. These cases reinforce the concept that in systemic lupus erythematosus, laboratory findings may not correlate well with the underlying glomerular lesion, and therefore, the renal biopsy is an essential clinical tool in the approach to lupus nephritis.

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Cgnz1 allele confers kidney resistance to damage preventing progression of immune complex–mediated acute lupus glomerulonephritis

Journal of Experimental Medicine ◽

10.1084/jem.20130731 ◽

2013 ◽

Vol 210 (11) ◽

pp. 2387-2401 ◽

Cited By ~ 32

Author(s):

Yan Ge ◽

Chao Jiang ◽

Sun-Sang J. Sung ◽

Harini Bagavant ◽

Chao Dai ◽

...

Keyword(s):

Immune Complex ◽

Organ Damage ◽

Distal Region ◽

Chromosome 1 ◽

Chronic Glomerulonephritis ◽

Female Mice ◽

Inflammatory Parameters ◽

Stage Renal Disease ◽

End Stage ◽

Lupus Glomerulonephritis

Cgnz1 and Agnz1 on the distal region of mouse chromosome 1 are associated with chronic glomerulonephritis (cGN) and acute GN (aGN). NZM2328.Lc1R27 (R27) was generated by introgressing a C57L/J region where Cgnz1 is located to NZM2328. R27 female mice developed aGN mediated by immune complex (IC) deposition and complement activation without progression to cGN with severe proteinuria. End stage renal disease (ESRD) was not seen in R27 mice as old as 15 mo. Thus, aGN and cGN are under separate genetic control, and IC-mediated proliferative GN need not progress to cGN and ESRD. NZM2328 and R27 female mice have comparable immune and inflammatory parameters. In contrast to NZM2328, R27 mice were resistant to sheep anti–mouse GBM serum-induced nephritis, supporting the hypothesis that aGN is mediated by autoimmunity and resistance to the development of cGN is mediated by end organ resistance to damage. Thus, autoimmunity should be considered distinct from end organ damage. The Cgnz1 region has been mapped to a 1.34 MB region with 45 genes. Nine candidate genes were identified. Clinical relevance of these observations is supported by case studies. Clinical implications and the significance to human lupus and other diseases are presented.

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Diffuse proliferative lupus glomerulonephritis. Recovery from prolonged renal failure

JAMA ◽

10.1001/jama.244.1.63 ◽

1980 ◽

Vol 244 (1) ◽

pp. 63-65

Author(s):

W. S. Moore

Keyword(s):

Renal Failure ◽

Lupus Glomerulonephritis

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Podocyte Injury in Lupus Nephritis

Journal of Clinical Medicine ◽

10.3390/jcm8091340 ◽

2019 ◽

Vol 8 (9) ◽

pp. 1340 ◽

Cited By ~ 3

Author(s):

Hamza Sakhi ◽

Anissa Moktefi ◽

Khedidja Bouachi ◽

Vincent Audard ◽

Carole Hénique ◽

...

Keyword(s):

Epithelial Cells ◽

Lupus Nephritis ◽

Lupus Erythematosus ◽

Glomerular Injury ◽

Crescent Formation ◽

Podocyte Injury ◽

Inflammatory Processes ◽

Lupus Podocytopathy ◽

Parietal Epithelial Cells ◽

Lupus Glomerulonephritis

Systemic lupus erythematosus (SLE) is characterized by a broad spectrum of renal lesions. In lupus glomerulonephritis, histological classifications are based on immune-complex (IC) deposits and hypercellularity lesions (mesangial and/or endocapillary) in the glomeruli. However, there is compelling evidence to suggest that glomerular epithelial cells, and podocytes in particular, are also involved in glomerular injury in patients with SLE. Podocytes now appear to be not only subject to collateral damage due to glomerular capillary lesions secondary to IC and inflammatory processes, but they are also a potential direct target in lupus nephritis. Improvements in our understanding of podocyte injury could improve the classification of lupus glomerulonephritis. Indeed, podocyte injury may be prominent in two major presentations: lupus podocytopathy and glomerular crescent formation, in which glomerular parietal epithelial cells play also a key role. We review here the contribution of podocyte impairment to different presentations of lupus nephritis, focusing on the podocyte signaling pathways involved in these lesions.

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