ABSTRACT
Background: Systemic inflammation has been associated with severe coronavirus disease 2019 (COVID-19) disease and mortality. Hyponatremia can result from inflammation due to non-osmotic stimuli for vasopressin production. Methods: We prospectively studied 799 patients hospitalized with COVID-19 between March 7 and November 7, 2020, at Hospital Posadas in Buenos Aires, Argentina in order to evaluate the association between hyponatremia, inflammation, and its impact on clinical outcomes. Admission biochemistries, high-sensitivity C-reactive protein (hsCRP), ferritin, patient demographics, and outcome data were recorded. Outcomes (within 30 days after symptoms) evaluated included ICU admission, mechanical ventilation, dialysis-requiring acute kidney injury (AKI), and in-hospital mortality. Length of hospital stay (in days) were evaluated using comprehensive data from the EHR. Results: Hyponatremia (median Na = 133 mmol/L) was present on admission in 366 (45.8%). Hyponatremic patients had higher hsCRP (median 10.3 [IR 4.8-18.4] mg/dl vs. 6.6 [IR 1.6-14.0] mg/dl, p < 0.01) and ferritin levels (median 649 [IQR 492-1,168] ng/dl vs. 393 [IQR 156-1,440] ng/dl, p = 0.02) than normonatremic patients. Hyponatremia was associated with higher odds of an abnormal hsCRP (unadjusted OR 5.03, 95%CI: 2.52-10.03), and remained significant after adjustment for potential confounders (adjusted OR 4.70 [95%CI: 2.33-9.49], p < 0.01). Hyponatremic patients had increased mortality on unadjusted (HR 3.05, 95%CI: 2.14-4.34) and adjusted (HR 2.76, 95%CI:1.88-4.06) in Cox proportional hazard models. Crude 30-day survival was lower for patients with hyponatremia at admission (mean [SD] survival 22.1 [0.70] days) compared with patients who were normonatremic (mean [SD] survival 27.2 [0.40] days, p < 0.01). Conclusion: Mild hyponatremia on admission is common, is associated with systemic inflammation and is an independent risk factor for hospital mortality. Clinical Trial Registration: www.ClinicalTrials.gov, identifier NCT04493268.
ABSTRACT
BACKGROUND: 3% sodium chloride solution is the accepted treatment for hyponatremic encephalopathy, but evidence-based guidelines for its use are lacking. STUDY DESIGN: A case series. SETTING & PARTICIPANTS: Adult patients presenting to the emergency department of a university hospital with hyponatremic encephalopathy, defined as serum sodium level < 130 mEq/L with neurologic symptoms of increased intracranial pressure without other apparent cause, and treated with a continuous infusion of 500mL of 3% sodium chloride solution over 6 hours through a peripheral vein. PREDICTORS: Hyponatremic encephalopathy defined as serum sodium level < 130 mEq/L with neurologic symptoms of increased intracranial pressure without other apparent cause. OUTCOMES: Change in serum sodium level within 48 hours, improvement in neurologic symptoms, and clinical evidence of cerebral demyelination, permanent neurologic injury, or death within 6 months' posttreatment follow-up. RESULTS: There were 71 episodes of hyponatremic encephalopathy in 64 individuals. Comorbid conditions were present in 86% of individuals. Baseline mean serum sodium level was 114.1±0.8 (SEM) mEq/L and increased to 117.9±1.3, 121.2±1.2, 123.9±1.0, and 128.3±0.8 mEq/L at 3, 12, 24, and 48 hours following the initiation of 3% sodium chloride solution treatment, respectively. There was a marked improvement in central nervous system symptoms within hours of therapy in 69 of 71 (97%) episodes. There were 12 deaths, all of which occurred following the resolution of hyponatremic encephalopathy and were related to comorbid conditions, with 75% of deaths related to sepsis. No patient developed neurologic symptoms consistent with cerebral demyelination at any point during the 6-month follow-up period. LIMITATIONS: Lack of a comparison group and follow-up neuroimaging studies. Number of cases is too small to provide definitive assessment of the safety of this protocol. CONCLUSIONS: 3% sodium chloride solution was effective in reversing the symptoms of hyponatremic encephalopathy in the emergency department without producing neurologic injury related to cerebral demyelination on long-term follow-up in this case series.
Subject(s)
Brain Edema/diagnosis , Brain Edema/drug therapy , Hyponatremia/diagnosis , Hyponatremia/drug therapy , Saline Solution, Hypertonic/administration & dosage , Aged , Brain Edema/blood , Cohort Studies , Female , Humans , Hyponatremia/blood , Male , Middle Aged , Prospective Studies , Saline Solution, Hypertonic/chemistry , Treatment OutcomeABSTRACT
Toxic nephrophaties secondary to occupational exposure to metals have been widely studied, including membranous nephropathy by mercury, which is rare. Occupational poisoning by mercury is frequent, neurological symptoms are the main form of clinical presentation. Secondary renal involvement in chronic exposure to metallic mercury can cause glomerular disease by deposit of immune-complexes. Membranous glomerulopathy and minimal change disease are the most frequently reported forms. Here we describe the case of a patient with occupational exposure to metallic mercury, where nephrotic syndrome due to membranous glomerulonephritis responded favorably to both chelation and immunosuppressive therapy.
Subject(s)
Glomerulonephritis, Membranous/etiology , Mercury/toxicity , Occupational Exposure/adverse effects , Adult , Chelation Therapy , Glomerulonephritis, Membranous/therapy , Humans , Immunosuppressive Agents/therapeutic use , Male , Nephrotic Syndrome/etiology , Nephrotic Syndrome/therapyABSTRACT
Las nefropatías tóxicas secundarias a la exposición ocupacional a metales han sido ampliamente estudiadas. La nefropatía membranosa por mercurio es poco frecuente.La intoxicación ocupacional con mercurio sí es frecuente, siendo las principales formas de presentación las manifestaciones clínicas neurológicas. La afectación renal secundaria a la exposición crónica a mercurio metálico puede desarrollar enfermedad glomerular por depósito de inmunocomplejos. La glomerulopatía membranosa y a cambios mínimos son las más frecuentemente comunicadas.Se presenta el caso de un paciente con exposición ocupacional a mercurio metálico, con síndrome nefrótico y biopsia renal con glomerulopatía membranosa que presentó respuesta favorable luego del tratamiento quelante e inmunosupresor.
Toxic nephrophaties secondary to occupational exposure to metals have been widely studied, including membranous nephropathy by mercury, which is rare. Occupational poisoning by mercury is frequent, neurological symptoms are the main form of clinical presentation. Secondary renal involvement in chronic exposure to metallic mercury can cause glomerular disease by deposit of immune-complexes. Membranous glomerulopathy and minimal change disease are the most frequently reported forms. Here we describe the case of a patient with occupational exposure to metallic mercury, where nephrotic syndrome due to membranous glomerulonephritis responded favorably to both chelation and immunosuppressive therapy.
Subject(s)
Adult , Humans , Male , Glomerulonephritis, Membranous/etiology , Mercury/toxicity , Occupational Exposure/adverse effects , Chelation Therapy , Glomerulonephritis, Membranous/therapy , Immunosuppressive Agents/therapeutic use , Nephrotic Syndrome/etiology , Nephrotic Syndrome/therapyABSTRACT
Las nefropatías tóxicas secundarias a la exposición ocupacional a metales han sido ampliamente estudiadas. La nefropatía membranosa por mercurio es poco frecuente.La intoxicación ocupacional con mercurio sí es frecuente, siendo las principales formas de presentación las manifestaciones clínicas neurológicas. La afectación renal secundaria a la exposición crónica a mercurio metálico puede desarrollar enfermedad glomerular por depósito de inmunocomplejos. La glomerulopatía membranosa y a cambios mínimos son las más frecuentemente comunicadas.Se presenta el caso de un paciente con exposición ocupacional a mercurio metálico, con síndrome nefrótico y biopsia renal con glomerulopatía membranosa que presentó respuesta favorable luego del tratamiento quelante e inmunosupresor.(AU)
Toxic nephrophaties secondary to occupational exposure to metals have been widely studied, including membranous nephropathy by mercury, which is rare. Occupational poisoning by mercury is frequent, neurological symptoms are the main form of clinical presentation. Secondary renal involvement in chronic exposure to metallic mercury can cause glomerular disease by deposit of immune-complexes. Membranous glomerulopathy and minimal change disease are the most frequently reported forms. Here we describe the case of a patient with occupational exposure to metallic mercury, where nephrotic syndrome due to membranous glomerulonephritis responded favorably to both chelation and immunosuppressive therapy.(AU)
ABSTRACT
Toxic nephrophaties secondary to occupational exposure to metals have been widely studied, including membranous nephropathy by mercury, which is rare. Occupational poisoning by mercury is frequent, neurological symptoms are the main form of clinical presentation. Secondary renal involvement in chronic exposure to metallic mercury can cause glomerular disease by deposit of immune-complexes. Membranous glomerulopathy and minimal change disease are the most frequently reported forms. Here we describe the case of a patient with occupational exposure to metallic mercury, where nephrotic syndrome due to membranous glomerulonephritis responded favorably to both chelation and immunosuppressive therapy.
ABSTRACT
La cetoacidosis diabética (CAD) se acompaña de severa depleción hidroelectrolítica; aunque habitualmente se utiliza hidratación abundante, el ritmo de reposición de fluidos en esta patología continúa siendo controvertido. A fin de determinar la velocidad de infusión de líquidos adecuada en la CAD sin patología asociada, se realizó un estudio prospectivo, randomizado, en 27 pacientes sometidos a dos planes terapéuticos diferentes sólo en el ritmo del aporte de líquidos. Un grupo (14 pacientes) recibió solución salina al 0,9 por ciento a una velocidad de 1000 ml/h, y otro grupo (13 pacientes) a 500 ml/h; el flujo de reposición hidrosalina se redujo a la mitad después de 4 horas de tratamiento. Al ingreso y a las 2, 4, 8, 12 y 24 horas se realizaron determinaciones del estado ácido-base en sangre arterial, y de sodio, potasio y cloro en plasma. Ambos grupos fueron similares en las determinaciones bioquímicas al ingreso. Todos los pacientes corrigieron el cuadro de cetoacidosis y no se observó mortalidad ni complicaciones. No se hallaron diferencias significativas para ninguna de las variables metabólicas entre los grupos de tratamiento en ningún momento de la evolución. Se concluye que resulta igualmente efectivo utilizar una velocidad de reposición de líquidos de 500 ml/h que de 1000 ml/h, en cuanto a la morbimortalidad de los pacientes con CAD no asociada a severa depleción de volumen. El uso de cantidades modestas de fluidos para la hidratación en estos pacientes resultaría en menores costos.
Subject(s)
Adult , Humans , Male , Female , Diabetic Ketoacidosis/therapy , Fluid Therapy/methods , Diabetic Ketoacidosis/epidemiology , Dosage Forms , Fluid Therapy/economics , Prospective StudiesABSTRACT
La cetoacidosis diabética (CAD) se acompaña de severa depleción hidroelectrolítica; aunque habitualmente se utiliza hidratación abundante, el ritmo de reposición de fluidos en esta patología continúa siendo controvertido. A fin de determinar la velocidad de infusión de líquidos adecuada en la CAD sin patología asociada, se realizó un estudio prospectivo, randomizado, en 27 pacientes sometidos a dos planes terapéuticos diferentes sólo en el ritmo del aporte de líquidos. Un grupo (14 pacientes) recibió solución salina al 0,9 por ciento a una velocidad de 1000 ml/h, y otro grupo (13 pacientes) a 500 ml/h; el flujo de reposición hidrosalina se redujo a la mitad después de 4 horas de tratamiento. Al ingreso y a las 2, 4, 8, 12 y 24 horas se realizaron determinaciones del estado ácido-base en sangre arterial, y de sodio, potasio y cloro en plasma. Ambos grupos fueron similares en las determinaciones bioquímicas al ingreso. Todos los pacientes corrigieron el cuadro de cetoacidosis y no se observó mortalidad ni complicaciones. No se hallaron diferencias significativas para ninguna de las variables metabólicas entre los grupos de tratamiento en ningún momento de la evolución. Se concluye que resulta igualmente efectivo utilizar una velocidad de reposición de líquidos de 500 ml/h que de 1000 ml/h, en cuanto a la morbimortalidad de los pacientes con CAD no asociada a severa depleción de volumen. El uso de cantidades modestas de fluidos para la hidratación en estos pacientes resultaría en menores costos. (AU)
