Current concepts of contrast-induced nephropathy: a brief review.

Contrast-induced nephropathy (CIN) is a common hospital-acquired acute kidney injury. Published studies on this condition have dramatically increased in recent years. This article aims to provide a brief literature review. English articles published from 1983 to 2012 were retrieved from PubMed by searching using the term "contrast-induced nephropathy." Patients with CIN were associated with increased resource utilization, prolonged hospital stay, and increased long-term mortality. CIN is defined as a ≥ 0.5 mg/dL rise in serum creatinine or a 25% increase, assessed within 48-72 hours after administration of contrast medium (CM). All patients receiving CM should be evaluated for their CIN risk, especially preexisting kidney disease. The CM should be prewarmed to 37 °C and injected at the lowest possible dose. Repeat injection within 72 hours should be avoided. Either iso-osmolar CM or low-osmolar CM, except ioxaglate or iohexol, can be used in all patients. Iso-osmolar CM iodixanol may be a better choice for high-risk patients with chronic kidney disease requiring intra-arterial administration. Nephrotoxic drugs should be stopped 2 days prior to when the patient undergoes a procedure. All patients receiving CM should be at an optimal volume status. Parenteral isotonic saline without any diuretic should be started 12 hours prior to CM at a rate of 1 mL/kg/h and continued for 24 hours if there is no contraindication. In patients who require shorter volume supplement periods or are at a higher risk, bicarbonate infusion (154 mEq/L, 3 mL/kg/h for 1 hour bolus prior to CM, followed by 1 mL/kg/h for 6 hours) may be used as an alternative to isotonic saline. Oral N-acetylcysteine (600 mg bid, starting on the day prior to the procedure) together with parenteral hydration is suggested for patients at risk. Hemodialysis/hemofiltration is only considered in chronic kidney disease stage 4/5 patients when an access is available. The other medications or techniques for reducing CIN risk are still unclear. CIN is a potentially preventable clinical condition. A careful review of published reports gives us a deeper understanding of CIN and a greater chance of decreasing its risk.

Vaccination with recombinant Mycobacterium avium subsp. paratuberculosis proteins induces differential immune responses and protects calves against infection by oral challenge.

We previously reported the in vitro cellular immune responses to recombinant antigens (rAgs) of Mycobacterium avium subsp. paratuberculosis (MAP). Here we report the differential immune responses and protective efficacy of four rAgs of MAP (85A, 85B, 85C, and superoxide dismutase (SOD)) used with two adjuvants (monophosphoryl lipid A (MPLA) containing synthetic trehalose dicorynomycolate, cell wall skeleton (MPLA) and bovine IL-12), against MAP challenge in calves. Group I was administered the four rAgs with MPLA and IL-12. Group II was administered the four rAgs and MPLA. Group III received MPLA and IL-12, and Group IV MPLA. rAgs induced significant lymphoproliferative responses in vaccinated animals (Groups I and II). All the rAgs induced significant IFN-gamma production from 11 to 23 wk after primary vaccination (APV), except for SOD. Significant increases were noted in CD3(+), CD4(+), CD8(+), CD21(+), CD25(+), and gammadelta(+) cells against all four rAgs in vaccinated animals. rAg-specific expression of IL-2, IL-12p40, IFN-gamma and TNF-alpha was significantly higher in the two vaccinated groups. Culture results found 4/8 animals in Group I, 3/8 animals in Group II, and 3/4 animals in Groups III and IV were positive for MAP in one or more tissues. Among the seven positive animals in Groups I and II, all but one had had <10CFU. Isolation was confined to one tissue in these animals, except in one animal in which MAP was isolated from two tissues. In the control groups (III and IV), MAP was cultured from up to five different tissues with >250CFU. Preliminary data from this study indicates that all four rAgs induced a good Th1 response and conferred protection against MAP infection in calves.

Cloning and characterization of the Actinobacillus pleuropneumoniae fur gene and its role in regulation of ApxI and AfuABC expression.

The ferric uptake regulation (fur) gene was cloned and characterized from Actinobacillus pleuropneumoniae and it exhibited 97% amino acid sequence identity to the Haemophilus ducrey fur gene. The flanking regions of the fur gene included an upstream putative flavodoxin (fldA) gene and a downstream possible transmembrane protein gene of unknown function. A single promoter was identified by 5' rapid amplification of cDNA ends (RACE), but there were no sequences homologous to an Escherichia coli Fur box in the 5' upstream sequence. The A. pleuropneumoniae fur clone complemented an E. coli fur deletion mutant. Transcriptional analysis of the divergent promoters of the A. pleuropneumoniae toxin I operon (apxICABD)--and the Actinobacillus ferric uptake operon (afuABC) showed that Fur and calcium together positively regulated the transcription of apxICABD while Fur was a repressor for afuABC. Hemolytic activity was significantly induced by iron and calcium and Fur appeared to act as an activator under high calcium conditions and as a repressor under low calcium conditions. A possible regulator-binding site was suggested by the properties of a point mutation in 33 bp upstream of the apxIC gene. This point mutation affected ApxI and Afu expression in response to iron, calcium, or Fur. These results provide further proof that calcium and the A. pleuropneumoniae Fur protein play a role in the expression of ApxI and Afu.

Antimicrobial susceptibility of Riemerella anatipestifer isolated from ducks and the efficacy of ceftiofur treatment.

The in vitro susceptibilities of 50 field isolates of Riemerella anatipestifer from ducks to ceftiofur and 16 other commonly used antimicrobials were determined. The MIC90 values (MIC refers to minimum inhibitory concentrations) for the antimicrobials used in this study are as follows: penicillin was 16 microg/ml; ceftiofur was 32 microg/ml; cephalothin, chloramphenicol, flumequine, and kanamycin were 64 microg/ml; nalidixic acid, nitrofurantoin, and sulfamethoxazole were 128 microg/ml; amikacin, ampicillin, gentamicin, lincomycin, spectinomycin, streptomycin, tetracycline, and trimethoprim were > or = 256 microg/ml. The therapeutic efficacy of ceftiofur against a highly lethal experimental R. anatipestifer infection in ducks was also evaluated. All experimental ducks were infected through the infraorbital sinus with 1 ml of 9 x 10(9) CFU of R. anatipestifer. Ceftiofur (0, 0.25, 0.5, 1, and 2 mg/kg) was injected subcutaneously 5 hours after infection. A single dose of 2 mg/kg resulted in 73% survival as compared with 10% survival in the infected, but untreated controls.