A woman presents to you with fever, arthralgia, ulcers, fatigue for the past six months, and new-onset hematuria. Urine examination reveals RBC casts and proteinuria. What is the likely diagnosis?

Correct Answer: A. Lupus nephritis

This is a classic presentation of systemic lupus erythematosus (SLE) with lupus nephritis. The discriminating features are the six-month chronic course with systemic manifestations (fever, arthralgia, fatigue) combined with active urinary findings (RBC casts and proteinuria). RBC casts specifically indicate glomerulonephritis, and their presence in the context of constitutional symptoms and hematuria is pathognomonic for lupus nephritis in an SLE patient. Lupus nephritis occurs in 40–50% of SLE patients and is a major cause of morbidity and mortality in Indian SLE cohorts. The presence of RBC casts (not just RBCs) indicates proliferative glomerulonephritis, most commonly WHO Class III or IV lupus nephritis. The six-month timeline rules out acute post-infectious causes and fits the indolent, relapsing-remitting course typical of SLE. The combination of systemic features (fever, arthralgia) with renal involvement is the hallmark of SLE-related glomerulonephritis. Diagnosis is confirmed by elevated anti-dsDNA antibodies, low complement levels (C3, C4), and kidney biopsy showing immune complex deposition on immunofluorescence.

Why the other options are wrong

B. IgA nephropathy — IgA nephropathy is the most common primary glomerulonephritis worldwide and in India, but it typically presents with episodic gross hematuria following upper respiratory tract infections, not with a six-month chronic course of systemic symptoms (fever, arthralgia, fatigue). IgA nephropathy lacks the extrarenal manifestations that define this case. While RBC casts can occur in IgA nephropathy, the combination of constitutional symptoms and proteinuria in a chronic setting strongly favors SLE. C. Poststreptococcal glomerulonephritis — PSGN is an acute post-infectious glomerulonephritis that typically presents 2–3 weeks after streptococcal pharyngitis or skin infection, with rapid onset of hematuria, hypertension, and edema. A six-month chronic course with systemic symptoms (fever, arthralgia, fatigue) is incompatible with PSGN, which is self-limited and resolves within weeks to months. The absence of a clear preceding infection and the presence of extrarenal manifestations exclude PSGN. D. Acute interstitial nephritis — AIN typically presents with acute kidney injury (days to weeks) triggered by drugs (NSAIDs, antibiotics, PPIs), infections, or autoimmune conditions. It does not produce RBC casts or hematuria as a primary feature; proteinuria is usually mild (<1 g/day). The six-month chronic course with systemic manifestations (fever, arthralgia) and active urinary sediment (RBC casts) is inconsistent with AIN, which is primarily a tubulointerstitial process, not a glomerulonephritis.

High-Yield Facts

Mnemonics

RASH in SLE (extrarenal features) Rash (malar), Arthralgia, Serositis, Hematologic abnormalities. When you see arthralgia + systemic symptoms + renal involvement, think SLE first. RBC Casts = Glomerulonephritis RBC casts (not just RBCs) always indicate active glomerulonephritis. In the context of systemic symptoms, lupus nephritis is the most likely diagnosis in India.

NBE Trap

NBE pairs "hematuria + proteinuria" with IgA nephropathy (the most common GN in India) to trap students who recognize urinary findings but miss the systemic features (fever, arthralgia, fatigue) and six-month chronic course that are diagnostic of SLE, not primary IgA disease.

Clinical Pearl

In Indian clinical practice, SLE predominantly affects young women (female:male = 9:1), and lupus nephritis is the most common cause of secondary glomerulonephritis in urban Indian hospitals. Early recognition of the triad of systemic symptoms + RBC casts + proteinuria allows timely immunosuppressive therapy (corticosteroids + cyclophosphamide or mycophenolate) to prevent progression to end-stage renal disease.

_Reference: Robbins Ch. 20 (Kidney); Harrison Ch. 378 (SLE); KD Tripathi Ch. 18 (Immunosuppressants in SLE)_