Liver function tests revealed a progressive rise in transaminases, with aspartate aminotransferase (AST) and alanine aminotransferase (ALT) peaking at 751 U/L and 325 U/L, respectively (Fig.2B). In contrast, coagulation and cholestatic markers showed only minor fluctuations with admission values of prothrombin time (PT) 15.0 sec, activated partial thromboplastin time (aPTT) 27.8 sec, INR 1.17, total bilirubin 5.12 µmol/L, direct bilirubin 3.38 µmol/L, and γ-glutamyl transferase (GGT) 20.37 IU/L.

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Blood count obtained at admission revealed leukocytosis with 11% band forms, suggestive of an ongoing systemic infectious process or systemic inflammatory response associated with rhabdomyolysis; therefore, empiric antibiotic therapy with ceftriaxone was started.

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Hyperkalemia was successfully managed, with serum potassium decreasing to 4.69 mmol/L; however, ionized calcium levels reached a low of 0.88 mmol/L on the fifth day of hospitalization. Concurrently, laboratory analysis showed a peak hyperphosphatemia of 2.2 mmol/L (Tab.2). These findings pointed towards the massive release of intracellular phosphate from necrotic myocytes, leading to subsequent calcium sequestration within damaged muscle tissue and the precipitation of calcium-phosphate complexes.

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Despite aggressive intravenous hydration and trial of loop diuretics, the patient remained oliguric, producing approximately 150 mL of urine over 24 hours. Laboratory studies revealed persistent metabolic acidosis with a blood pH of 7.1 (Tab.1). Rising serum creatinine levels to 405 μmol/L indicated significant deterioration in renal function. Urine output dropped to 50 mL/24 hours, indicating anuria. In the setting of progressive azotemia, refractory acidosis, and anuria, renal replacement therapy was initiated. The patient underwent 10 hemodialysis sessions.

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Following aggressive intravenous fluid resuscitation, serum creatine kinase levels began to decline within 24 hours. By the fifth day of hospitalization, the CK concentration had decreased by approximately 50%. Simultaneously, hemodialysis reduced phosphate levels, while calcium levels showed a reciprocal upward trend (Tab.2).

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The clinical course was further complicated by hypoalbuminemia, with serum albumin decreasing to 2.94 g/dL, prompting administration of intravenous albumin. Concurrently, liver enzymes demonstrated a progressive increase, with AST at 834 U/L and ALT at 540 U/L (Fig.2B). The patient received reduced glutathione to reduce oxidative stress. Prophylactic anticoagulation with Fraxiparine 0.4 mg/0.4 mL and stress ulcer prophylaxis with 40 mg pantoprazole were also provided.

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By hospital day 14, the patient developed severe anemia, with hemoglobin dropping to 5.1 g/dL. Laboratory studies showed an MCV of 87.40 fL and a platelet count of 174x109/L, both within normal limits. Coagulation studies, including aPTT (27.05 sec), PT (13.7), and INR (1.06), were unremarkable. No active or occult hemorrhage was identified. The presence of normocytic normochromic anemia, alongside elevated biochemical markers, specifically lactate dehydrogenase (LDH) of 1,243 U/L and indirect bilirubin of 2.1 mg/dL, pointed toward hemolytic anemia possibly caused by mechanical trauma (shear stress) from a kink in the dialysis circuit. Hemodialysis was temporarily halted, and the patient required a transfusion of three units of packed red blood cells to stabilize hemoglobin levels.

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The following day, laboratory findings were notable for elevated neutrophil counts and worsening renal function, with creatinine reaching 374 μmol/L. Urinalysis revealed proteinuria (100 mg/dL), marked hematuria, and moderate leukocyturia. Microscopic examination showed 25-30 white blood cells per high-power field and numerous intact red blood cells. Additionally, moderate uric acid crystals were present, along with a significant number of fungi and bacteria. Blood cultures were negative for bacteremia. These findings were suggestive of a complicated urinary tract infection. An infectious disease specialist was consulted, and antimicrobial therapy was changed from ceftriaxone to piperacillin-tazobactam to provide broader coverage against gram-negative rods.

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Following the correction of metabolic and infectious complications, a neurology consultation was requested to address the persistent numbness in the right lower extremity. Physical examination revealed swelling in the right hip and gluteal region. Functional assessment demonstrated impaired right hip flexion, reduced muscle strength, and diminished Achilles and patellar reflexes. Notably, there was a complete absence of active movement in ankle dorsiflexion and plantarflexion, resulting in a clinically significant foot drop. While these findings were highly suggestive of right sciatic nerve injury, no electrodiagnostic studies or advanced neuroimaging were performed during the hospitalization. A duplex scan of lower extremity vessels confirmed normal arterial and venous flow, ruling out primary vascular pathology. The deficit was managed as compression neuropathy. Therapeutic intervention was initiated with a combination of cytidine monophosphate, uridine monophosphate, and vitamin B complex to support nerve recovery.

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The patient was discharged in a stable condition on hospital day 23. Outpatient physical therapy and electrical stimulation were recommended for ongoing rehabilitation of right lower limb neuropathy.

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In a follow-up interview, the patient reported that her recent serum creatinine levels have returned to normal and she has achieved a full recovery from acute kidney injury without progression to chronic kidney disease. Outpatient nerve conduction studies confirmed sciatic axonal neuropathy. The patient is currently undergoing electrical stimulation with significant symptomatic improvement, though she has not yet reached a full neurologic recovery.