Lupus nephritis is an inflammation of the kidneys caused by systemic lupus erythematosus (SLE), an autoimmune disease. Approximately 10-30% of SLE patients develop lupus nephritis, which can progress to end-stage renal disease requiring dialysis or transplantation if not properly treated. Lupus nephritis is classified into six classes based on pathological findings. Treatment involves medications to suppress the immune system such as corticosteroids, immunosuppressants, and biologic drugs depending on the class of lupus nephritis. Prognosis is generally good if treatment can control proteinuria, hypertension, and renal dysfunction.

1. Lupus Nephritis
Presented by
Bijay Shah Kanu
Juniour clerckship, 3rd year
MBBS sixth batch
PAHS-SOM
APRIL,2019

2. Introduction
•Lupus nephritis- one of the most serious manifestations
of systemic lupus erythematous (SLE)
•Systemic lupus erythematosus (SLE) is an autoimmune
disease in which organs, tissues, and cells undergo
damage mediated by tissue-binding autoantibodies and
immune complexes
•Approximately 10 to 30 % of patients with lupus
nephritis progress to end-stage renal disease (ESRD)
•May require hemodialysis or renal transplantation if
ESRD occurs

3. Epidemiology
•Around 90% of affected individuals are women (F:M=
9:1)
•Peak Age at onset is between 20-40 years, children
with SLE have higher risk
•Race: common in African American, and Asians
•Mortality within 5 years of diagnosis is usually due to
organ failure or overwhelming sepsis

4. Pathophysiology
•Deposition of circulating immune complexes against
cellular antigens particularly anti-dsDNA in glomeruli.
•Complement cascade activation leading to:
•complement-mediated damage
• leukocyte infiltration
• release of various cytokines

5. Pathophysiology
Other pathogenic mechanisms:
•Infarction of glomerular segments
•Thrombotic microangiopathy
•Vasculitis
•Glomerular sclerosis
•Humoral response are main effective mediators, IgE
autoantibodies, basophils and type 2 helper cells are involved
•IgE containing immune complex trigger circulating
basophils get into secondary lymphoid organs activated
basophils secret IL-4 TH2 cell differentiation B-cell
differentiation production of auto reactive antibodies.

6. Classification of Lupus Nephritis
(International Society of Nephrology and
Renal Pathology Society)
•Class I- Minimal mesangial lupus nephritis
•Class II- Mesangial proliferative lupus nephritis
•Class III- Focal lupus nephritis
•Class IV- Diffuse lupus nephritis
•Class V- Membranous lupus nephritis
•Class VI- Advanced sclerotic lupus nephritis

9. Classifications
1. Minimal mesangial lupus nephritis
• Normal glomeruli  on light microscopy
• Minimal mesangial immune deposits  immuno-
fluorescent or electron microscopy
• Asymptomatic
2. Mesangial proliferative lupus nephritis
• With Mesangial hyper-cellularity and matrix
expansion
• Clinically mild renal disease

10. Classifications
3. Focal lupus nephritis
• Involving <50% of all glomeruli
• Sub-epithelial immune deposits seen
• Clinically: haematuria, proteinuria
• 10-20% of all LN
4. Diffuse lupus nephritis
• Involving >50% of all glomeruli
• Segmental and global lesions
• Subendothelial immune deposits present
• Clinically progression to: Nephrotic syndrome, HTN,
Renal insufficiency
• Most common and severe form of LN

11. Classifications
5. Membranous lupus nephritis
• Affects 10-20% of patients
• Can occur in combination with class III or IV lesions
• Good prognosis
6. Advanced sclerotic lupus nephritis
• >90% of glomeruli globally sclerosed without
residual activity
• Represents advanced stages of the above
• Immunosuppressive therapy is unlikely to help as it is
inactive
• Progressive CKD

12. Clinical manifestations
• Symptoms of active SLE: including arthralgia, fatigue, fever, malar rash,
oral or nasal ulcers, arthritis, serositis, or central nervous system disease
• Hypertension (headache, dizziness, visual disturbances)
• Peripheral edema
• Pleural and pericardial effusions
• Ascites
• Proteinuria
• Hematuria

13. Clinical manifestations

14. Investigations
•Subclinical renal involvement, with low-level
haematuria and proteinuria but minimally impaired or
normal renal function, is common in SLE
•Evaluating renal function in patients with SLE is
important because early detection and treatment can
significantly improve renal outcome
•Renal biopsy should be considered in any patient with
SLE who has clinical or laboratory evidence of active
nephritis

15. Investigations
•Full blood count,
•Blood urea nitrogen (BUN) testing
•Serum creatinine assessment
•Urinalysis (to check for protein, red blood cells , and
cellular casts): proteinuria, dysmorphic RBCs and RBC
casts
•A 24-hour urine test for creatinine clearance and protein
excretion
•Autoantibodies and serum complement C3 and C4 levels:
ANA, Anti ds DNAAb & hypo complementemia
•Renal biopsy & Immunofluroscence +ve for IgG, IgA,
IgM,C1q,C3&C4

16. Management
Medications used to treat SLE manifestations include the
following:
•Biologic DMARDs (disease-modifying antirheumatic
drugs): Belimumab, rituximab, IV immune globulin
•Nonbiologic DMARDS: Cyclophosphamide,
methotrexate, azathioprine, mycophenolate, cyclosporine
•Nonsteroidal anti-inflammatory drugs (NSAIDS; eg,
ibuprofen, naproxen, diclofenac)
•Corticosteroids (eg, methylprednisolone, prednisone)
•Antimalarials (eg, hydroxychloroquine)

17. •Initial treatment depends on clinical presentation but
Hypertension and oedema should always be treated
•Definite histopathological diagnosis required (Renal biopsy)
•Type I requires no treatment
•Type II usually runs a benign course but some are treated
with steroids
•A number of clinical trials with immunosuppressive agents
have been trialed in types III, IV and V (most severe forms)
• Steroids and high dose IV cyclophosphamide or
mycophenolate mofetil (MMF) usually used for induction
•Mycophenolate mofetil and azathioprine for maintenance
therapy
•B cell depletion with rituximab (anti-CD20) shown to be
effective

18. •Class II lupus nephritis may require treatment if
proteinuria is greater than 1000 mg/day
• Predniosolone (20-40 mg/day) for 1-3 months with
subsequent tapering
•Class III and IV
• Prednisone 1 mg/kg/day for at least 4 weeks
• Taper it gradually to a daily maintenance dose of 5-
10 mg/day for approximately 2 years

19. Class V
•Prednisolone for 1-3 months, tapering for 1-2 years if
response occurs
ESRD
•Hemodialysis
•Renal transplantation

20. Prognosis
•Treatment leading to normalization of proteinuria, HTN
and renal dysfunction indicates good prognosis
•Prognosis better in patient with types I, II and V Lupus
nephritis
•Glomerulosclerosis (type VI) predicts end-stage renal
disease

21. References
•Harrison’s Principle of Internal Medicine, 20th edition
•Davidson’s principle and practice of medicine, 23rd
edition

22. Thank You!