RESUMO
Spotted fever rickettsiosis is rarely observed in solid organ transplant recipients, and all previously reported cases have been associated with tick bite months to years after transplantation. We describe a kidney transplant recipient in North Carolina, USA, who had a moderately severe Rickettsia parkeri infection develop during the immediate posttransplant period.
Assuntos
Transplante de Rim , Infecções por Rickettsia , Rickettsia , Humanos , Pessoa de Meia-Idade , Antibacterianos/uso terapêutico , Transplante de Rim/efeitos adversos , North Carolina , Rickettsia/genética , Rickettsia/isolamento & purificação , Infecções por Rickettsia/diagnóstico , Infecções por Rickettsia/microbiologia , TransplantadosRESUMO
Two and a half centuries have passed since the therapeutic use of peritoneal cavity for the treatment of ascites by peritoneal lavage was reported. George Ganter was the first to describe the use of peritoneal dialysis (PD) in humans. This chapter will describe the various milestones in the field of PD achieved over the years. These include the understanding of solute and water transport across the peritoneal membrane, developments in PD technique and technology, progress in the prevention and treatment of infections, and other important milestones.
RESUMO
BACKGROUND: Vancomycin-associated (VA) acute kidney injury (AKI) is being increasingly recognized. A distinct pattern of rapid rise in serum creatinine (sCr) during VA-AKI has occasionally been observed. However, such scenarios remain underreported. METHODS: We conducted an online survey at the American Society of Nephrology Communities forum and reviewed publications of VA-AKI via PubMed or Google searching for cases of precipitous AKI (those with rise in sCr ≥1.5 mg/dL/day) attributable to vancomycin. RESULTS: We identified 12 original cases compiled from 6 different hospitals and 4 published cases (n = 16; 38% women, age 43.5 ± 16 years, weight 108 ± 23 kg, body mass index 35 ± 7 kg/m2) of precipitous AKI observed shortly after large cumulative doses of VA (8.8 ± 5 g). The median steepest 24-h rise in sCr was 2.6 mg/dL (range 1.5-3.5 mg/dL) and the slope of the initial 48-h sCr rise was greater than that of a control AKI (non-VA, n = 48) group (2.03 ± 0.1 vs. 0.62 ± 0.0 mg/dL/day; p < 0.0001). The steep rise in sCr in the VA-AKI was not accompanied by anuria. Overt rhabdomyolysis was absent in all cases. Further, in 3 precipitous VA-AKI cases, simultaneous serum cystatin C values did not rise precipitously, suggesting that the reductions in glomerular filtration rate were overestimated by the sCr increase. CONCLUSIONS: VA-AKI can manifest with a precipitous rise in sCr shortly after a high cumulative dose of vancomycin. True toxic tubular injury overrepresented by the sCr rise is postulated.