Abstract

Acute kidney injury (AKI) is the major complication of rhabdomyolysis. We aimed to identify the predictive factors for AKI and renal replacement therapy (RRT) requirement in poisoning-associated rhabdomyolysis. We conducted a cohort study including 273 successive poisoned patients (median age, 41 years) who developed rhabdomyolysis defined as creatine kinase (CK) >1000 IU/L. Factors associated with AKI and RRT requirement were identified using multivariate analyses. Poisonings mainly involved psychotropic drugs. AKI occurred in 88 patients (37%) including 43 patients (49%) who required RRT. Peak serum creatinine and CK were weakly correlated (R2 = 0.17, p < 0.001). Death (13%) was more frequent after AKI onset (32% vs. 2%, p < 0.001). On admission, lithium overdose (OR, 44.4 (5.3–371.5)), serum calcium ≤2.1 mmol/L (OR, 14.3 (2.04–112.4)), female gender (OR, 5.5 (1.8–16.9)), serum phosphate ≥1.5 mmol/L (OR, 2.0 (1.0–4.2)), lactate ≥ 3.3 mmol/L (OR, 1.2 (1.1–1.4)), serum creatinine ≥ 125 µmol/L (OR, 1.05 (1.03–1.06)) and age (OR, 1.04 (1.01–1.07)) independently predicted AKI onset. Calcium-channel blocker overdose (OR, 14.2 (3.8–53.6)), serum phosphate ≥ 2.3 mmol/L (OR, 1.6 (1.1–2.6)), Glasgow score ≤ 5 (OR, 1.12; (1.02–1.25)), prothrombin index ≤ 71% (OR, 1.03; (1.01–1.05)) and serum creatinine ≥ 125 µmol/L (OR, 1.01; (1.00–1.01)) independently predicted RRT requirement. We identified the predictive factors for AKI and RRT requirement on admission to improve management in poisoned patients presenting rhabdomyolysis.

Highlights

  • Rhabdomyolysis is commonly reported in the poisoned patient with variable consequences ranging from a simple increase in serum creatine kinase (CK) to life-threatening electrolyte disturbances and acute kidney injury (AKI) requiring renal replacement therapy (RRT) [1,2]

  • For rhabdomyolysis in poisonings admitted to the ICU

  • We found a weak correlation between peak CK and peak creatinine (Figure 2) as previously observed [3,16]

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Summary

Introduction

Rhabdomyolysis is commonly reported in the poisoned patient with variable consequences ranging from a simple increase in serum creatine kinase (CK) to life-threatening electrolyte disturbances and acute kidney injury (AKI) requiring renal replacement therapy (RRT) [1,2]. A 13-50% risk of AKI [1,2,3,4] and up to 83% risk of mortality [5] have been reported. Mechanisms by which toxicants cause rhabdomyolysis are variable including prolonged unconsciousness and immobility, agitation, seizures, fall, withdrawal and hyperthermia [1,2]. Nutritional deficiencies, hypophosphatemia and hypokalemia may represent coexistent risk factors for the development of rhabdomyolysis [2]

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