Systemic lupus erythematous is a chronic multifactorial autoimmune disease that affects many organs including kidney. Lupus nephritis is a common manifestation characterized by heterogeneous clinical and histopathological finding and often associate with poor progression and despite potent anti-inflammatory and immunosuppressive therapies still end in CKD or ESRD for too many patient. lupus nephritis is an immune complex GN that develop as a frequent complication of SLE. The pathogenesis of lupus nephritis involve a variety of pathogenic mechanisms, intra renal pathomechanisn of SLE related nephritis immune complex formation and classical complement pathway activation. Lupus nephritis doesn't develop in the absence of antinuclear antibodies. Circulating polyclonal autoantibodies bind to intrarenal nucleosomes and other autoantigen, which lead to local complement activation , cell injury and subsequent cytokine and chemokine secretion . The current management of lupus nephritis remain based on steroids, cyclophosphamide, azathioprine ,mycophenolate mefetile which are all unselective immunosuppressive drugs, these drugs have proven to be efficient in reducing lupus nephritis disease activity but the long term outcomes of lupus nephritis have not further improved during the last 30 years . Identification of renal survival is mandatory for certain purposes i.e, evaluation of efficacy of different treatment strategies among our patients and factors associated with the survival data as compared with other specialized centers.

Systemic lupus erythematous is a chronic multifactorial autoimmune disease that affects many organs including kidney. Lupus nephritis is a common manifestation characterized by heterogeneous clinical and histopathological finding and often associate with poor progression and despite potent anti-inflammatory and immunosuppressive therapies still end in CKD or ESRD for too many patient. lupus nephritis is an immune complex GN that develop as a frequent complication of SLE. The pathogenesis of lupus nephritis involve a variety of pathogenic mechanisms, intra renal pathomechanisn of SLE related nephritis immune complex formation and classical complement pathway activation. Lupus nephritis doesn't develop in the absence of antinuclear antibodies. Circulating polyclonal autoantibodies bind to intrarenal nucleosomes and other autoantigen, which lead to local complement activation , cell injury and subsequent cytokine and chemokine secretion . The current management of lupus nephritis remain based on steroids, cyclophosphamide, azathioprine ,mycophenolate mefetile which are all unselective immunosuppressive drugs, these drugs have proven to be efficient in reducing lupus nephritis disease activity but the long term outcomes of lupus nephritis have not further improved during the last 30 years . Identification of renal survival is mandatory for certain purposes i.e, evaluation of efficacy of different treatment strategies among our patients and factors associated with the survival data as compared with other specialized centers.

Inclusion Criteria:

1. Age>18years old
2. Patients with SLE as defined by EULAR/ACR criteria and lupus nephritis classification according to ISN/RPS classification.
3. Available medical records for 2 and 5 years of follow up after diagnosis of lupus nephritis

Exclusion Criteria:

1. Transplant recipients
2. Pregnant females
3. Patients with combined renal pathology other than LN.
4. Those who had no baseline information in hospital medical records and had a follow up duration < 24 months will be excluded

nephrology department, Assiut University Hospital inpatient and outpatient clinics