American journal of nephrology
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Case Reports
Intradialytic hypercapnic respiratory failure managed by noninvasive assisted ventilation.
We report a hemodialysis patient with acute hypercapnic respiratory failure managed on noninvasive intermittent positive pressure ventilation and progressive metabolic acidosis. Dialysate bicarbonate concentration of 25 mEq/l was associated with exacerbation of metabolic acidosis, while higher dialysate bicarbonate concentration of 30 mEq/l induced a dangerous increase in PCO(2) level. Excessive bicarbonate buffering and CO(2) production induced by severe metabolic acidosis, malnourishment and tissue hypoxia, could explain inadequate correction of metabolic acidosis and worsening of hypercapnia in this patient. Our findings suggest the need for close monitoring of blood gases and cautious modulation of dialysate bicarbonate concentration in the presence of progressive metabolic acidosis in hypercapnic hemodialysis patients.
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The effect of hospitalization on an ESRD patient's hemoglobin (Hgb) level and erythropoietin (Epo) requirement has not been investigated. We postulated patients with end stage renal disease required an increased Epo dose to maintain stable Hgb during hospitalization and for a period following discharge. To evaluate this hypothesis, we conducted a retrospective chart review on 65 hemodialysis patients. All hemodialysis patients admitted for more than 2 days who did not have more than the index hospitalizations for 2 months prior to and following discharge were included. Multiple parameters including Hgb, Epo dose, intravenous iron dose, serum iron, TIBC, and ferritin during the 2 months before and the two months after hospitalization, Hgb at admission and discharge, Hgb trough, surgery, blood transfusions and co-morbid factors were evaluated. Statistical significance was evaluated using ANOVA or rank-sum testing, as appropriate. In 65 hemodialysis patients (24 M/41 F, age 58 +/- 2.2 years, mean +/- SEM), Hgb levels following discharge and for 2 subsequent months were significantly lower than 2 months prior to admission (11.4 +/- 0.25 vs. 10.7 +/- 0.22 g/dl, p < 0.01). This occurred in spite of an increase in Epo dose (128 +/- 14 vs. 185 +/- 21 U/kg/week, p < 0.0001) over this 2-month period. There was no difference in the iron saturation before and after hospitalization (22 vs. 23%,p > 0.05). There were also no apparent effects of comorbid factors, including surgery, or discharge diagnosis on the changes in Hgb or Epo requirements. However, patients who required a blood transfusion during the hospitalization had lower Hgb levels and higher Epo doses both prior to and after hospitalization, as well as lower Hgb trough levels. In addition, females had lower Hgb levels than males both prior to and after hospitalization, and were receiving a higher Epo dose 191 +/- 18 vs. 129 +/- 20 U/kg/week at 1 month and 215 +/- 18 U/kg/week vs. 134 +/- 22, p < 0.005 at 2 months after hospitalization. ⋯ This study points out that hemodialysis patients experience a significant and prolonged decrease in Hgb levels after hospitalization, even despite a moderate increase in Epo dosing.
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Cortical blindness as a complication of hemodialysis is not widely known, though visual disturbances related to uremia have been known for a long time. We recently observed cortical blindness caused by bilateral occipital infarcts in a patient after hemodialysis.
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We describe a case of lower gastrointestinal bleeding due to mixed infection of cytomegalovirus (CMV) and mucormycosis in a renal transplant recipient. A 33-year-old male received renal transplantation and his clinical course was uneventful. On the 18th postoperative day, acute rejection was developed and this was treated with high-dose methylprednisolone and OKT3. ⋯ The patient was successfully treated with amphotericin B (1.0-1.5 mg/kg) and ganciclovir (62.5-125 mg/day) for 5 weeks. To our knowledge, this is the first report showing coexistence of mucormycosis and CMV in the colon ulcer base. This finding suggests that CMV infection may trigger fungal infection in the pathogenesis of colonic ulcer.
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The serum anion gap (serum [Na(+)]-Cl(-)]-[CO(2)]) is still the first-line approach to metabolic acidosis. However, while it is generally acknowledged that hypoalbuminemia mandates a downward adjustment of the expected anion gap, a specific correction factor for the anion gap in the face of low serum albumin has never been demonstrated. ⋯ For intensive care patients with normal or high serum tCO(2) (>21 mEq/l) a simple bedside adjustment of the anion gap by subtracting 1.5 times the difference between measured serum albumin and the 'normal' level of 4.0 g/dl gives a close estimate of the actual anion gap. For intensive care patients with serum tCO(2) <22 mEq/l, correction of the anion gap is well predicted by adding about twice the Delta (albumin) to the calculated gap.