not-yet-known not-yet-known not-yet-known unknown Methods: Initial laboratory investigations revealed pancytopenia, impaired renal and liver function, and elevated pancreatic enzymes. (Table 1) Ultrasonography findings were consistent with acute pancreatitis. Given the clinical presentation, the provisional diagnosis was acute pancreatitis with septic shock and pre-renal acute kidney injury. The child was promptly admitted to the Pediatric Intensive Care Unit (PICU). In the PICU, management consisted of intravenous fluids, injectable ceftriaxone, proton pump inhibitors, anti-emetics, and analgesics. Further investigations were initiated to assess multisystem involvement and guide ongoing treatment. Subsequently, a peripheral blood smear and direct Coombs test (DCT) were conducted to investigate the cause of pancytopenia. Results indicated microcytic hypochromic anemia and mild leukopenia with adequate platelets. The DCT was negative. Given impaired renal function and multiorgan involvement, additional tests were performed, including urine protein creatinine ratio, ANA, ASO titer, C3, and C4. The ASO titer was elevated at 200 IU/ml. The urine protein creatinine ratio was 5.25:1, indicating significant proteinuria. Positive ANA, low C3, and C4 suggested a possible connective tissue disorder, probably SLE. Subsequent workup revealed positivity for anti-dsDNA, lupus anticoagulant antibody, and cardiolipin antibody. These findings prompted consideration of systemic lupus erythematosus (SLE). Due to suggestive laboratory findings of systemic lupus erythematosus (SLE) amidst multisystem involvement, including the kidney, a renal biopsy was planned; however, it could not be performed due to the patient’s hemodynamic instability. Consequently, treatment for SLE was initiated, starting with oral hydroxychloroquine at 4 mg per kg per day (200 mg once daily) following ophthalmological evaluation. Due to rapidly deteriorating renal function, hypertension, and anuria suggestive of rapidly progressive glomerulonephritis (RPGN) due to lupus nephritis, treatment was started. This included injectable methylprednisolone five doses followed by oral prednisolone 1mg/kg/day and injectable cyclophosphamide, adhering to KDIGO 2024 clinical practice guidelines for the management of lupus nephritis. (4) Hypertension was managed initially with injectable furosemide and subsequently with oral Amlodipine, Enalapril, Clonidine, Prazosin, and Labetalol. Hemodialysis was initiated due to anuria, rapid renal function decline, and hypertension refractory to multiple antihypertensives, as well as pulmonary edema. The patient underwent six cycles of hemodialysis, resulting in clinical improvement and normalization of laboratory parameters, as detailed in Table 1 . Moreover, bilateral Kaiser-Fleischer rings (KF rings) and chorioretinitis were seen during the ophthalmological evaluation. Due to the presence of KF rings and impaired liver function, serum ceruloplasmin and urinary copper levels were measured, and an autoimmune hepatitis panel was conducted to explore Wilson’s disease and autoimmune hepatitis as potential differentials. These tests indicated a low ceruloplasmin level and elevated urinary copper, strongly suggestive of Wilson’s Disease (WD). Treatment for WD was initiated with oral zinc sulfate. Consultation with a pediatric gastroenterologist was sought to manage WD further and consider the possibility of initiating penicillamine; however, penicillamine was avoided due to its potential to induce drug-induced lupus and may aggravate the symptoms of SLE. An autoimmune hepatitis panel returned negative, ruling out autoimmune hepatitis as a diagnosis. Once the patient achieved hemodynamic stability, plans were made to conduct a renal biopsy. Subsequent renal biopsy findings revealed diffuse lupus nephritis (Class IV), characterized by an activity index of 7/24 and a chronicity index of 0/12 (Figure 1). The biopsy also indicated patchy mild acute tubular injury and coarse pigmented/granular casts within the tubular lumina. Additionally, focal necrotizing vascular lesions and evidence of vascular immune deposits were identified in direct immunofluorescence (DIF) studies. Therefore, based on the constellation of clinical, laboratory, and histopathological findings, the patient was diagnosed with SLE with lupus nephritis and concomitant Wilson’s disease.