eMedicine Specialties > Rheumatology > Systemic Rheumatic Disease
Nephritis, Lupus: Differential Diagnoses & Workup
Updated: Jun 23, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Differential Diagnoses
Glomerulonephritis, Chronic
Glomerulonephritis, Diffuse
Proliferative
Glomerulonephritis, Membranous
Glomerulonephritis, Rapidly Progressive
Polyarteritis Nodosa
Wegener Granulomatosis
Other Problems to Be Considered
Mesangial glomerulonephritis
Glomerulosclerosis
Workup
Laboratory Studies
- General4
- Evaluating renal function in patients with systemic lupus erythematosus (SLE) to detect any renal involvement early is important because early detection and treatment can significantly improve renal outcome.
- Laboratory tests to evaluate renal function include the following:
- Blood urea nitrogen (BUN) testing
- Serum creatinine assessment
- Urinalysis (to check for protein, RBCs, and cellular casts)
- Spot urine test for creatinine and protein concentration (Normal creatinine excretion is 1000 mg/24 h/1.75 m2; normal protein excretion is 150-200 mg/24 h/1.75 m2; normal urinary protein-to-creatinine ratio is <0.2.)
- Twenty-four–hour urine test for creatinine clearance and protein excretion
- Tests of SLE disease activity4
- Disease activity can be evaluated with anti-dsDNA, complement determinations (C3, C4, and CH50 ), and erythrocyte sedimentation rate (ESR) or C-reactive protein. The C-reactive protein level is generally not elevated in patients with SLE, even with active disease, unless the patient has significant arthritis or infection.
- Generally, an elevated ESR and anti-dsDNA and low C3 and C4 levels are associated with active nephritis, especially focal proliferative and diffuse proliferative lupus nephritis.
- Clinically relevant lupus nephritis is associated with a 30% decrease in creatinine clearance, proteinuria of greater than 1000 mg/d, and renal biopsy findings indicating active lupus nephritis.
- Anti-nucleosome antibodies appear early in the course of the autoimmune response in SLE, they have high sensitivity and specificity for a diagnosis of SLE, and the titers correlate with disease activity.22,23,24 Anti-C1q antibodies are associated with lupus nephritis; higher titers correlate with active renal disease.25,26
Procedures
- Renal biopsy4,27
- Renal biopsy should be considered in any patient with SLE who has clinical or laboratory evidence of active nephritis, especially upon the first episode of nephritis.
- Renal biopsy may be useful in patients with recurrent episodes of nephritis, depending on the clinical circumstances. By revealing the histologic pattern and stage of disease (activity and chronicity), renal biopsy is useful in determining prognosis and treatment.
- Findings from a thorough clinical and laboratory evaluation can be used to predict the histologic type of lupus nephritis in approximately 70-80% of patients; however, this is not accurate enough considering the toxicity of some of the treatment protocols. A good rule is to perform a renal biopsy if the findings will potentially alter patient management. If a particular patient has other manifestations of SLE (eg, severe CNS or hematologic involvement) and will be treated with cyclophosphamide, biopsy may not be necessary but should still be considered because it may help predict renal outcome.
- Sampling error can occur during a renal biopsy. Thus, the results of the biopsy should always be evaluated for consistency with the clinical and laboratory presentation of the patient.
- The experience of pathologists in reading lupus nephritis biopsy specimens vary considerably. Studies have suggested that the most consistent readers are in larger medical centers with substantial populations of patients with SLE.
Staging
- Pathologic classification28
- The classification of lupus nephritis was revised by the International Society of Pathology/Renal Pathology Society (ISN/RPS) in 2003 and is based on light microscopy, immunofluorescence, and electron microscopy findings from renal biopsy specimens. This is based on earlier classifications by the World Health Organization (WHO) in 1974 and 1982. See Table 2.
- In addition to the pathologic classification, activity and chronicity indices are scored pathologically and predict the renal prognosis (progression of renal disease). See Table 3.
- The activity index reflects the state of active inflammation observed at biopsy, which may be reversible with medical therapy.
- The chronicity index reflects the amount of fibrosis and scarring, which are unlikely to respond to therapy. Renal lesions with a high activity index are more likely to respond to aggressive therapy, whereas renal lesions with high chronicity are not.
- Table 2. International Society of Nephrology/Renal Pathology Society 2003 Classification of Lupus Nephritis
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Class I
Minimal mesangial lupus nephritisLight microscopy findings Normal Immunofluorescence electron microscopy findings Mesangial immune deposits Clinical manifestations Mild proteinuria Class II Mesangial proliferative lupus nephritis Light microscopy findings Purely mesangial hypercellularity or mesangial matrix expansion with mesangial immune deposits Immunofluorescence electron microscopy findings Mesangial immune deposits; few immune deposits in subepithelial or subendothelial deposits possible Clinical manifestations Mild renal disease such as asymptomatic hematuria or proteinuria that usually does not warrant specific therapy Class III Focal lupus nephritis
Class III (A)
Active lesions - Focal proliferative lupus nephritis
Class III (A/C)
Active and chronic lesions - Focal proliferative and sclerosing lupus nephritisClass III (C)
Chronic inactive lesions - Focal sclerosing lupus nephritisLight microscopy findings Active or inactive focal, segmental, or global glomerulonephritis involving <50% of all glomeruli Immunofluorescence electron microscopy findings Subendothelial and mesangial immune deposits Clinical manifestations Active generalized SLE and mild-to-moderate renal disease with hematuria and moderate proteinuria in many patients; worsening renal function in significant minority, potentially progressing to class IV lupus nephritis Class IV Diffuse lupus nephritis
Class IV-S (A)
Active lesions - Diffuse segmental proliferative lupus nephritis
Class IV-G (A)
Active lesions - Diffuse global proliferative lupus nephritis
Class IV-S (A/C)
Active and chronic lesions - Diffuse segmental proliferative and sclerosing lupus nephritisClass IV-G (A/C)
Active and chronic lesions - Diffuse global proliferative and sclerosing lupus nephritis
Class IV-S (C)
Chronic inactive lesions with scars - Diffuse segmental sclerosing lupus nephritis
Class IV-G (C)
Chronic inactive lesions with scars - Diffuse global sclerosing lupus nephritisLight microscopy findings Active or inactive diffuse, segmental or global glomerulonephritis involving >50% of all glomeruli; subdivided into diffuse segmental (class IV-S) when >50% of involved glomeruli have segmental lesions (involving less than half of glomerular tuft) and diffuse global (class IV-G) when >50% of involved glomeruli have global lesions Immunofluorescence electron microscopy findings Subendothelial immune deposits Clinical manifestations Clinical evidence of renal disease including hypertension, edema, active urinary sediment, worsening renal function, and nephrotic range proteinuria in most cases; active extrarenal SLE in many patients Class V
Membranous lupus nephritisLight microscopy findings Diffuse thickening of glomerular basement membrane without inflammatory infiltrate; possibly, subepithelial deposits and surrounding basement membrane spikes on special stains, including silver and trichrome; may occur in combination with class II or IV; may show advanced sclerosis Immunofluorescence electron microscopy findings Subepithelial and intramembranous immune deposits; subendothelial deposits present only when associated proliferative component is present Clinical manifestations Clinical and laboratory features of nephrotic syndrome, usually without manifestations of active SLE Class VI
Advanced sclerosis lupus nephritisLight microscopy findings Advanced glomerular sclerosis involving >90% of glomeruli, interstitial fibrosis, and tubular atrophy, all morphological manifestations of irreversible renal injury Clinical manifestations Significant renal insufficiency or end-stage renal disease in most cases; unlikely to respond to medical therapy Class I
Minimal mesangial lupus nephritisLight microscopy findings Normal Immunofluorescence electron microscopy findings Mesangial immune deposits Clinical manifestations Mild proteinuria Class II Mesangial proliferative lupus nephritis Light microscopy findings Purely mesangial hypercellularity or mesangial matrix expansion with mesangial immune deposits Immunofluorescence electron microscopy findings Mesangial immune deposits; few immune deposits in subepithelial or subendothelial deposits possible Clinical manifestations Mild renal disease such as asymptomatic hematuria or proteinuria that usually does not warrant specific therapy Class III Focal lupus nephritis
Class III (A)
Active lesions - Focal proliferative lupus nephritis
Class III (A/C)
Active and chronic lesions - Focal proliferative and sclerosing lupus nephritisClass III (C)
Chronic inactive lesions - Focal sclerosing lupus nephritisLight microscopy findings Active or inactive focal, segmental, or global glomerulonephritis involving <50% of all glomeruli Immunofluorescence electron microscopy findings Subendothelial and mesangial immune deposits Clinical manifestations Active generalized SLE and mild-to-moderate renal disease with hematuria and moderate proteinuria in many patients; worsening renal function in significant minority, potentially progressing to class IV lupus nephritis Class IV Diffuse lupus nephritis
Class IV-S (A)
Active lesions - Diffuse segmental proliferative lupus nephritis
Class IV-G (A)
Active lesions - Diffuse global proliferative lupus nephritis
Class IV-S (A/C)
Active and chronic lesions - Diffuse segmental proliferative and sclerosing lupus nephritisClass IV-G (A/C)
Active and chronic lesions - Diffuse global proliferative and sclerosing lupus nephritis
Class IV-S (C)
Chronic inactive lesions with scars - Diffuse segmental sclerosing lupus nephritis
Class IV-G (C)
Chronic inactive lesions with scars - Diffuse global sclerosing lupus nephritisLight microscopy findings Active or inactive diffuse, segmental or global glomerulonephritis involving >50% of all glomeruli; subdivided into diffuse segmental (class IV-S) when >50% of involved glomeruli have segmental lesions (involving less than half of glomerular tuft) and diffuse global (class IV-G) when >50% of involved glomeruli have global lesions Immunofluorescence electron microscopy findings Subendothelial immune deposits Clinical manifestations Clinical evidence of renal disease including hypertension, edema, active urinary sediment, worsening renal function, and nephrotic range proteinuria in most cases; active extrarenal SLE in many patients Class V
Membranous lupus nephritisLight microscopy findings Diffuse thickening of glomerular basement membrane without inflammatory infiltrate; possibly, subepithelial deposits and surrounding basement membrane spikes on special stains, including silver and trichrome; may occur in combination with class II or IV; may show advanced sclerosis Immunofluorescence electron microscopy findings Subepithelial and intramembranous immune deposits; subendothelial deposits present only when associated proliferative component is present Clinical manifestations Clinical and laboratory features of nephrotic syndrome, usually without manifestations of active SLE Class VI
Advanced sclerosis lupus nephritisLight microscopy findings Advanced glomerular sclerosis involving >90% of glomeruli, interstitial fibrosis, and tubular atrophy, all morphological manifestations of irreversible renal injury Clinical manifestations Significant renal insufficiency or end-stage renal disease in most cases; unlikely to respond to medical therapy - Table 3. Active and Chronic Glomerular Lesions
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Activity Index Chronicity Index • Endocapillary hypercellularity with or without leukocyte infiltration; luminal reduction
• Karyorrhexis
• Fibrinoid necrosis
• Rupture of glomerular basement membrane
• Cellular or fibrocellular crescents
• Subendothelial deposits on light microscopy
• Intraluminal immune aggregates• Glomerular sclerosis; segmental, global
• Fibrous adhesion
• Fibrous crescentsActivity Index Chronicity Index • Endocapillary hypercellularity with or without leukocyte infiltration; luminal reduction
• Karyorrhexis
• Fibrinoid necrosis
• Rupture of glomerular basement membrane
• Cellular or fibrocellular crescents
• Subendothelial deposits on light microscopy
• Intraluminal immune aggregates• Glomerular sclerosis; segmental, global
• Fibrous adhesion
• Fibrous crescents - These indices serve as a prognostic tool and a general guide to therapy. Signs of activity justify aggressive medical therapy because such therapy may arrest or reverse the pathologic changes. Signs of chronicity suggest irreversibility, and aggressive therapy is less likely to affect the outcome. The activity and chronicity indices are evaluated at a single point in time, and renal lesions may transform from one class to another either spontaneously or as a result of treatment.
Mesangial proliferative lupus nephritis with moderate mesangial hypercellularity. International Society of Pathology/Renal Pathology Society (ISN/RPS) 2003 class II (hematoxylin and eosin stain; 200X magnification).
Focal lupus nephritis. International Society of Pathology/Renal Pathology Society (ISN/RPS) 2003 class III (hematoxylin and eosin stain; 100X magnification).
Focal lupus nephritis, immunofluorescence. International Society of Pathology/Renal Pathology Society (ISN/RPS) 2003 class III (200X magnification).
Diffuse lupus nephritis with hypertensive vascular changes. International Society of Pathology/Renal Pathology Society (ISN/RPS) 2003 class IV (hematoxylin and eosin stain; 200X magnification).
Diffuse lupus nephritis with early crescent formation. International Society of Pathology/Renal Pathology Society (ISN/RPS) 2003 class IV (hematoxylin and eosin stain; 200X magnification).
Diffuse lupus nephritis with extensive crescent formation (rapidly progressive glomerulonephritis). International Society of Pathology/Renal Pathology Society (ISN/RPS) 2003 class IV (hematoxylin and eosin stain; 200X magnification).
Membranous lupus nephritis. International Society of Pathology/Renal Pathology Society (ISN/RPS) 2003 class V (hematoxylin and eosin stain; 200X magnification).
Membranous lupus nephritis showing thickened glomerular basement membrane. International Society of Pathology/Renal Pathology Society (ISN/RPS) 2003 class V (silver stain; 200X magnification).
Advanced sclerosis lupus nephritis. International Society of Pathology/Renal Pathology Society (ISN/RPS) 2003 class VI (hematoxylin and eosin stain; 100X magnification).
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 Differential Diagnoses & Workup: Nephritis, Lupus |
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Further Reading
Keywords
lupus nephritis, systemic lupus erythematosus, SLE, end-stage renal disease, ESRD, end-stage kidney disease, chronic kidney disease, chronic renal disease, chronic renal failure, glomerulonephritis, hematuria, renal failure, kidney failure, mesangial nephritis, hypertension, proteinuria, active lupus nephritis, focal proliferative lupus nephritis, diffuse proliferative lupus nephritis, mesangial lupus nephritis, membranous lupus nephritis, active nephritis, sclerosing lupus nephritis, mesangial proliferative lupus nephritis, focal lupus nephritis, diffuse lupus nephritis, focal sclerosing lupus nephritis, diffuse segmental proliferative lupus nephritis, diffuse global proliferative lupus nephritis, diffuse segmental sclerosing lupus nephritis, diffuse global sclerosing lupus nephritis, advanced sclerosis lupus nephritis
