RESUMEN
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.
Asunto(s)
Artritis Infecciosa/etiología , Infecciones por Escherichia coli , Inmunosupresores/uso terapéutico , Trasplante de Riñón , Articulación de la Rodilla , Infecciones Urinarias/etiología , Adulto , Cadáver , Femenino , HumanosRESUMEN
Hyperchloremic metabolic acidosis can be seen in advanced chronic renal failure (CRF). To study this further, we measured acid excretion under controlled conditions in 19 patients with severe but stable CRF. Twelve patients had a hyperchloremic metabolite acidosis, 3 had an elevated anion gap acidosis ('delta acidosis'), while the 4 remaining patients had a slightly decreased tCO2 with a normal anion gap and serum chloride level ('mild acidosis'). Ammonium excretion was markedly reduced in CRF patients (11 +/- 1 vs. 32 +/- 2 mEq/day in normal subjects, p less than 0.005), and likewise urinary titratable acid was diminished (18 +/- 2 mEq/day in patients, vs. 28 +/- 3 mEq/day in normal subjects; p less than 0.005). When expressed per 100 ml GFR, ammonium and titratable acid excretion were markedly increased in all groups of patients compared to normal subjects. The Tm for bicarbonate was 22.5 +/- 3.7 mEq/l for all CRF patients and 24 +/- 1 mEq/l for the patients with a hyperchloremic metabolic acidosis. We conclude that the hyperchloremic metabolic acidosis in advanced renal failure is due to diminished excretion of ammonium and titratable acid and is not due to an increased bicarbonate leak. As renal failure advances and renal mass declines, the remaining functioning nephrons hypersecrete acid.