Trimethoprim-sulfamethoxazole in cyst fluid from autosomal dominant polycystic kidneys

Trimethoprim-sulfamethoxazole in cyst fluid from autosomal dominant polycystic kidneys. Cyst infection in patients with autosomal-dominant polycystic kidney disease (ADPKD) is often refractory to therapy, in part because of the limited entry of commonly used antibiotics into cyst fluid. To study the efficacy of trimethoprim-sulfamethoxazole in cyst infection, cyst fluid was obtained by percutaneous aspiration or at surgery from eight patients with ADPKD receiving trimethoprim-sulfamethoxazole. Cysts were categorized as nongradient or gradient by cyst-fluid sodium concentration. Trimethoprim-sulfamethoxazole concentrations within cysts were determined and cyst fluid inhibitory and bactericidal titers were assessed in vitro against Escherichia coli, Proteus mirabilis and Streptococcus fecalis. The mean cyst fluid trimethoprim and sulfamethoxazole concentrations were 15.2 µg/ml and 42.5 µg/ml, respectively. Preferential accumulation of trimethoprim was observed in gradient cysts, exceeding serum levels more than eightfold. Sulfamethoxazole penetrated cysts to a lesser extent, with. concentrations ranging from 10 to 70 percent of the serum level. Cyst fluid sampled prior to trimethoprim-sulfamethoxazole administration (control) demonstrated no antibacterial activity, while cyst fluid inhibitory and bactericidal titers following antibiotic administration were 1:32 or greater in most instances. These studies indicate that trimethoprim-sulfamethoxazole is likely to be efficacious in the treatment of cyst infection in polycystic kidneys

Intermittent Auditory Imperception: Clinical Characteristics and Implications for Treatment

TB

Amino acid losses during sustained low-efficiency dialysis in critically ill patients with acute kidney injury

Objective: Sustained low-efficiency dialysis (SLED) involves the use of standard dialysis machines for prolonged intermittent renal replacement therapy in critically ill patients. In this study we aimed to quantify dialysate amino acid (AA) and albumin losses in 5 patients who underwent successful SLED treatment. Design: This was a prospective observational study. Setting: The study was performed in a general intensive care unit. Subjects: The study was performed in critically ill patients with acute kidney injury undergoing SLED using low-flux hemodialyzers. Intervention: We performed total dialysate collection and measured dialysate AA profiles by reverse-phase high-pressure liquid chromatography using an automated AA analyser. Main outcome measure: Individual and total amino acid losses. Results: Albumin was undetectable in dialysate. The median (mean +/- SD) total amino acid loss was 15.7 (23.4 +/- 19.2) g/treatment, or 122.1 (180.6 +/- 148.5) mmol/treatment. Two patients were receiving intravenous nutrition. One patient had severe hepatic failure with encephalopathy, and had high dialysate AA levels with a total loss of 57 g/treatment. Conclusions: During SLED with low-flux hemodialyzers, albumin losses are negligible but AA losses to dialysate are comparable to those during continuous renal replacement therapy. Patients' nutritional protein prescriptions should be augmented to account for this