Gentamicin is well known to be a cause of vestibular toxicity. Despite this, gentamicin is often used to treat peritonitis and exit site infections in peritoneal dialysis patients because of the ease of intraperitoneal administration and the broad coverage of aerobic Gram-negative bacilli, including Pseudomonas aeruginosa. We report 4 cases of severe vestibular toxicity occurring in peritoneal dialysis patients treated with gentamicin. They were all treated as outpatients for peritonitis or an exit-site infection while on continuous ambulatory peritoneal dialysis (CAPD) or continuous cyclic peritoneal dialysis (CCPD). The drug was administered to 3 patients in each peritoneal exchange (5 mglL) after a loading dose. A fourth patient was given 1 mglkg of intraperitoneal gentamicin every other day. The mean length of treatment was 21 days. Levels were not used to adjust the doses. All developed severe vertigo from which there was incomplete or no recovery. We suggest that gentamicin and the other aminoglycosides should be used in peritoneal dialysis patients only when there is no suitable alternative antibiotic. When gentamicin is administered, levels should be carefully followed. Studies should be performed in peritoneal dialysis patients on the feasibility of dosing gentamicin intermittently, which may be less toxic than continuous intraperitoneal administration.

Infections are common causes of morbidity in the renal transplant population, but infectious arthritis is rarely encountered. Gram-negative joint infections in the nontransplant population are often associated with simultaneous urinary tract infections. We report a case of Escherichia coli monoarthritis and a concomitant urinary tract infection in a renal transplant recipient and consider the possible predisposing factors for the infection.

The goal of this study was to evaluate the relative contribution of the renin-angiotensin system and mean arterial pressure to sodium excretion and urine flow rate during an infusion of atrial natriuretic peptide (ANP) at physiologically relevant doses in humans. Eight normal volunteers were studied during five periods: (1) baseline in the supine position; (2) during an infusion of ANP at physiologic doses (0.01 micrograms/kg/min) in the supine position; (3) during ANP infusion and 60 degrees head-up tilt; (4) during ANP infusion, head-up tilt, and interruption of the renin-angiotensin axis with the angiotensin converting enzyme inhibitor (ACEI) enalaprilat; and (5) in the supine position during ANP infusion and ACEI. Infusion of ANP in the supine posture significantly increased urine flow rate and sodium excretion compared to baseline while mean arterial pressure and plasma renin activity were unchanged. During head-up tilt and ANP infusion, urine flow rate and sodium excretion were no longer significantly elevated over baseline while mean arterial pressure decreased and plasma angiotensin II levels increased. Addition of ACEI caused a marked diminution of urine flow rate and sodium excretion compared to baseline levels despite continued ANP infusion. Although mean arterial pressure after ACEI administration was lower than baseline, it was not significantly different from the non-ACEI head-up tilt state. Placing subjects in the supine position during ANP infusion and ACEI administration increased mean arterial pressure to levels that were no longer different from baseline, but urine flow rate and sodium excretion remained significantly depressed to the same degree as during head-up tilt with ACEI.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract