Renal Failure (Lupus Nephritis) is the Most Likely Explanation
The patient's presentation is classic for lupus nephritis with nephrotic syndrome, making renal failure (Option D) the correct answer. The combination of elevated creatinine (150 μmol/L), severe hypoalbuminemia (28 g/L), low complement levels (C3 0.5 g/L, C4 0.1 g/L), and fluid overload symptoms definitively points to active kidney disease as the primary driver of this clinical picture 1.
Key Diagnostic Features Supporting Lupus Nephritis
Laboratory Evidence of Active Renal Disease:
- Elevated creatinine (150 μmol/L) indicates impaired glomerular filtration, a hallmark of lupus nephritis 1
- Severe hypoalbuminemia (28 g/L) reflects nephrotic-range proteinuria, which is strongly associated with active lupus nephritis and provides information on both presence and prognosis of renal involvement 1, 2
- Low complement C3 (0.5 g/L) and C4 (0.1 g/L) are significantly associated with active renal disease in SLE and can predict flares 1, 3
- The combination of these three parameters (creatinine, albumin, complement) has established predictive value for kidney involvement and survival at 5 years 1
Clinical Manifestations Explained by Nephrotic Syndrome:
- Lower-extremity edema to the knees and shifting dullness (ascites) result from severe hypoalbuminemia causing decreased oncotic pressure 4
- Shortness of breath with low oxygen saturation (90%) likely reflects pulmonary edema from fluid overload secondary to nephrotic syndrome 4
- The 3-month progressive course is consistent with untreated or undertreated lupus nephritis 1
Why Other Options Are Less Likely
Constrictive Pericarditis (Option A) - Not the Primary Problem: While the physical examination findings (jugular venous distention with inspiration, distant heart sounds, prominent early diastolic sound) could suggest pericardial disease, these findings do not explain the laboratory abnormalities 1. Specifically:
- Constrictive pericarditis does not cause elevated creatinine, hypoalbuminemia, or low complement levels 1
- The hypoalbuminemia is too severe (28 g/L) to be explained by cardiac disease alone 2
- Pericarditis in SLE would not typically present with such profound complement consumption 1
Myocardial Infarction (Option B) - Inconsistent with Presentation:
- No chest pain or cardiac enzyme elevation mentioned 1
- The chronic 3-month course contradicts acute MI 1
- Does not explain the nephrotic syndrome laboratory pattern 1
Liver Failure (Option C) - Insufficient Evidence: While AST (100 IU/L) and ALT (94 IU/L) are elevated, these levels are modest and insufficient to cause:
- The degree of hypoalbuminemia observed (liver synthetic function would need to be far more impaired) 1
- The elevated creatinine and low complement levels 1
- Hepatorenal syndrome would require more severe liver dysfunction 4
Clinical Implications and Management
Immediate Diagnostic Steps:
- Quantify proteinuria with urine protein-to-creatinine ratio to confirm nephrotic-range proteinuria (>3.5 g/day) 1
- Perform urine sediment analysis looking for red blood cell casts, white blood cell casts, or acanthocytes (≥5%) 1
- Consider kidney biopsy to classify the lupus nephritis according to ISN/RPS criteria and guide immunosuppressive therapy 1
Treatment Approach:
- Initial therapy should combine corticosteroids with either cyclophosphamide or mycophenolate mofetil (MMF) for proliferative lupus nephritis 1
- Hydroxychloroquine should be initiated unless contraindicated, as it reduces disease flares and improves outcomes 1
- The risk of doubling serum creatinine is 7.4-8.5% at 5 years, emphasizing the need for aggressive early treatment 1, 3
Common Pitfall to Avoid: Do not delay immunosuppressive therapy while pursuing extensive cardiac workup based on physical examination findings alone. The laboratory pattern unequivocally indicates active lupus nephritis requiring urgent treatment 1. Renal disease relapses are common (up to 45% of patients) and early aggressive treatment improves long-term kidney survival 1, 5.