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Browsing Medicina by Subject "Acute kidney injury"

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  • Cystatin C as a marker of acute kidney injury in the emergency department
    Publication . Soto, K; Coelho, S; Rodrigues, B; Martins, H; Frade, F; Lopes, S; Cunha, L; Papoila, A; Devarajan, P
    BACKGROUND AND OBJECTIVES: The diagnosis of acute kidney injury (AKI) is usually based on changes in serum creatinine, which is a poor marker of early renal dysfunction. The discriminative and predictive abilities of serum and urinary cystatin C were examined for the prediction of AKI. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In this prospective cohort study, serum and urinary cystatin C were serially measured in a heterogeneous group of patients (n = 616) presenting to a tertiary care emergency department. The primary outcome was AKI, classified according to RIFLE and AKIN criteria. The secondary outcome was an adjudication based on clinical criteria to AKI, prerenal azotemia, chronic kidney disease (CKD), and normal kidney function. RESULTS: Patients were adjudicated to have AKI in 21.1%, prerenal azotemia in 25.8%, CKD in 2.4%, and normal kidney function in 50.7%. For the diagnosis of AKI, the discriminatory ability of urinary creatinine and cystatin C was marginal. Both serum cystatin C and serum creatinine (at presentation and 6 hours later) showed high discriminatory ability for the diagnosis of AKI. However, only serum cystatin C attained a significant early predictive power (Hosmer-Lemeshow P value > 0.05). Serum cystatin C could differentiate between AKI and prerenal azotemia, but not between AKI and CKD. CONCLUSIONS: Serum cystatin C is an early, predictive biomarker of AKI, which outperforms serum creatinine in the heterogeneous emergency department setting. However, neither biomarker discriminated between AKI and CKD. Additional biomarkers continue to be needed for improved specificity in the diagnosis of community-acquired AKI.
    2010Journal article Open access Show more
  • Reversible myocardial calcification following severe leptospirosis complicated with rhabdomyolysis-induced acute kidney injury and magnesium-wasting nephropathy
    Publication . Zakout, R; Perloiro, MC; Freitas, PT
    We present a patient with leptospirosis infection who presented septic shock with multiple-organ dysfunction syndrome, severe rhabdomyolysis and acute myocarditis. He developed biphasic blood calcium pattern with hypocalcemia in the oliguric phase followed by hypercalcemia during the recovery diuretic phase in the context of rhabdomyolysis and oliguric acute kidney injury. Meanwhile, he developed an extensive calcification of the myocardium. Severe renal magnesium wasting was observed during the convalescence phase. Follow-up showed progressive resorption and later almost total disappearance of the calcific deposits in the heart by the 18th month after discharge. Renal magnesium wasting decreased gradually, but yet persisted beyond the 18th and was normalized only by the 36th month after discharge. We discuss the pathophysiologic mechanisms involved in the myocardial calcification and renal magnesium wasting and suggest a possibility of a contributing role of magnesium renal wasting in mobilization of calcium deposits out of myocardium
    2013Journal article Open access Show more