RESUMEN
BACKGROUND/AIMS: We assessed changes in hemodynamic and arterial stiffness parameters following reductions of dialysate calcium concentrations in patients undergoing hemodialysis. METHODS: In this prospective study, 20 patients on maintenance hemodialysis (10 females, 10 males) with dialysate calcium concentrations of 1.75 mmol/L were enrolled. At the start of the study, the dialysate calcium level was lowered to 1.50 mmol/L. Serial changes in biochemical, hemodynamic, and arterial stiffness parameters, including pulse wave velocity (PWV) and augmentation index (AIx), were assessed every 2 months for 6 months. We also examined changes in the calcification-inhibitory protein, serum fetuin-A. RESULTS: During the 6-month study period, serum total calcium and ionized calcium decreased consistently (9.5 +/- 1.0 to 9.0 +/- 0.7, p = 0.002 vs. 1.3 +/- 0.1 to 1.1 +/- 0.1, p = 0.035). Although no apparent changes in blood pressure were observed, heart-femoral PWW (hf-PWV) and AIx showed significant improvement (p = 0.012, 0.043, respectively). Repeated-measures ANOVA indicated a significant effect of lowering dialysate calcium on hf-PWV (F = 4.58, p = 0.004) and AIx (F = 2.55, p = 0.049). Accompanying the change in serum calcium, serum fetuin-A levels significantly increased (95.8 +/- 45.8 pmol/mL at baseline to 124.9 +/- 82.2 pmol/mL at 6 months, p = 0.043). CONCLUSIONS: Lowering dialysate calcium concentration significantly improved arterial stiffness parameters, which may have been associated with upregulation of serum fetuin-A.
Asunto(s)
Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Análisis de Varianza , Índice Tobillo Braquial , Arterias/efectos de los fármacos , Biomarcadores/sangre , Presión Sanguínea/efectos de los fármacos , Calcio/administración & dosificación , Adaptabilidad , Soluciones para Hemodiálisis/administración & dosificación , Estudios Prospectivos , Flujo Pulsátil/efectos de los fármacos , Diálisis Renal , República de Corea , Factores de Tiempo , Resultado del Tratamiento , alfa-2-Glicoproteína-HS/metabolismoRESUMEN
We have experienced two cases of bacteremia in liver cirrhosis patients caused by Vibrio parahemolyticus. One presented with acute gastroenteritidis symptoms such as vomiting, diarrhea. Vibrio parahemolyticus was cultured in the blood. In the other patients showed vesicular rash in lower extremities with a positive blood culture. Both patients had been treated with intravenous fluid and antibiotics.
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Humanos , Antibacterianos , Bacteriemia , Diarrea , Exantema , Cirrosis Hepática , Hígado , Extremidad Inferior , Vibrio , VómitosRESUMEN
We have experienced two cases of bacteremia in liver cirrhosis patients caused by Vibrio parahemolyticus. One presented with acute gastroenteritidis symptoms such as vomiting, diarrhea. Vibrio parahemolyticus was cultured in the blood. In the other patients showed vesicular rash in lower extremities with a positive blood culture. Both patients had been treated with intravenous fluid and antibiotics.
Asunto(s)
Humanos , Antibacterianos , Bacteriemia , Diarrea , Exantema , Cirrosis Hepática , Hígado , Extremidad Inferior , Vibrio , VómitosRESUMEN
Involvement of central nervous system is a well- known compication in uremic patients. However, development of acute extrapyramidal symptoms with bilateral basal ganglia involvement (acute basal ganglia syndrome), especially in non-diabetic hemodialysis patient is very rare. We report a case of acute basal ganglia syndrome in a non-diabetic hemodialysis patient. A 45-year-old man with autosomal dominant polycystic kidney disease (ADPKD) on chronic hemodialysis treatment for the last 4 years was admitted due to generalized myalgia. On admission, the patient was found to have rhabdomyolysis and intractable metabolic acidosis. Nine days after admission, he suddenly developed dysarthria, lateralizing ataxia, and bradykinesia. Brain MRI demonstrated low and high signals in bilateral basal ganglia and cerebellar vermis in T1-weighted and T2-weighted images, respectively. Intensified hemodialysis treatment combined with general supportive therapy resolved the severe metabolic acidosis and the neurologic manifestations gradually improved. Follow up brain CT scan taken 3 months later showed decreased size of initial low attenuation lesions in bilateral basal ganglia and cerebellar vermis. Although no definite pathophysiology is yet established, severe metabolic disorder is believed to play an important role in development of acute basal ganglia syndrome. Correction of metabolic acidosis and hypoglycemia in our patient lead to improvement in neurologic manifestations and organic brain lesions. Our case suggests that severe metabolic acidosis and hypoglycemia in uremic patient may act as risk factors for acute basal ganglia syndrome even in non-diabetic patient.