[Granulomatous interstitial nephritis in a patient with Behçet's disease treated with infliximab].

The patient is a 41-year-old man diagnosed with uveitis in 2004. Although the patient was positive for HLA-B51, the primary disease could not be identified, and oral administration of prednisolone (PSL) was initiated. A subsequent gradual decrease in the PSL dose was accompanied by the development of recurrent spasmodic chorioretinopathy and hypopyon. In November 2007, the patient was diagnosed with Behçet's disease based on the findings of erythema nodosum, acneiform eruption, and oral aphtha. In order to control the ocular symptoms, infliximab was administered. However, the patient's renal function began to deteriorate in November 2011, and he was transferred to our department after 6 months. At that time, his creatinine level was 8.56 mg/dL. Renal biopsy examination revealed granulomatous interstitial nephritis. Moreover, only infliximab yielded a positive result in a drug-induced lymphocyte stimulation test (DLST). Following initiation of PSL administration at 60 mg/day, his renal function improved. His creatinine level remained constant at approximately 3 mg/dL. In the present case, Behçet's disease, sarcoidosis, and infection were excluded as the underlying disease causing granulomatous interstitial nephritis. Moreover, infliximab is reportedly involved in the development of granulomas. Recent reports have stated that administration of TNF-alpha inhibitors occasionally results in the development of granulomas in the lungs and skin, and sometimes, in the kidneys as well. When renal dysfunction occurs in patients receiving TNF-alpha inhibitors, we believe that it is essential to include adverse events associated with TNF-alpha inhibitors in the differential diagnoses.

The association between intensive care unit-acquired hypernatraemia and mortality in critically ill patients with cerebrovascular diseases: a single-centre cohort study in Japan.

OBJECTIVES: Hypernatraemia is one of the major electrolyte disorders associated with mortality among critically ill patients in intensive care units (ICUs). It is unclear whether this applies to patients with cerebrovascular diseases in whom high sodium concentrations may be allowed in order to prevent cerebral oedema. This study aimed to examine the association between ICU-acquired hypernatraemia and the prognosis of patients with cerebrovascular diseases. DESIGN: A retrospective cohort study. SETTING: The incidence of ICU-acquired hypernatraemia was assessed retrospectively in a single tertiary care facility in Japan. PARTICIPANTS: Adult patients (≥18 years old) whose length of stay in ICU was >2 days and those whose serum sodium concentrations were 130-149 mEq/L on admission to ICU were included. OUTCOME MEASURES: 28-day in-hospital mortality risk was assessed by Cox regression analysis. Hypernatraemia was defined as serum sodium concentration ≥150 mEq/L. Using multivariate analysis, we examined whether ICU-acquired hypernatraemia and the main symptom present at ICU admission were associated with time to death among ICU patients. We also evaluated how the maximum and minimum sodium concentrations during ICU stay were associated with mortality, using restricted cubic splines. RESULTS: Of 1756 patients, 121 developed ICU-acquired hypernatraemia. Multivariate Cox proportional hazard analysis revealed an association between ICU-acquired hypernatraemia and 28-day mortality (adjusted HR, 3.07 (95% CI 2.12 to 4.44)). The interaction between ICU-acquired hypernatraemia and cerebrovascular disease was significantly associated with 28-day mortality (HR, 3.03 (95% CI 1.29 to 7.15)). The restricted cubic splines analysis of maximum serum sodium concentration in ICU patients determined a threshold maximum of 147 mEq/L. There was no significant association between minimum sodium concentration and mortality. CONCLUSIONS: ICU-acquired hypernatraemia was associated with an increased mortality rate among critically ill patients with cerebrovascular diseases; the threshold maximum serum sodium concentration associated with mortality was 147 mEq/L.

Fanconi Syndrome Associated with Hyponatremia in Two Patients with Legionella Pneumonia.

Legionella pneumophila is a cause of community-acquired pneumonia that is reported to induce electrolyte disorders, including hyponatremia, hypokalemia, and hypophosphatemia. We herein report two Japanese men with Legionella pneumonia and hyponatremia and hypophosphatemia. These findings were associated with an elevation of urinary low-molecular-weight tubular protein, including urinary ß2-microglobulin, N-acetyl-ß-D-glucosaminidase, the fractional excretion of phosphate and uric acid, and the presence of glycosuria and panaminoaciduria, suggesting that their electrolyte disorders had been caused by Fanconi syndrome. In these two cases, hyponatremia was probably due to salt wasting. Electrolyte disorders caused by Legionella pneumonia are corrected by treatment of the primary disease and fluid administration.