Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

KW-3902 [8-(noradamantan-3-yl)-1,3-dipropylxanthine] is a novel potent and selective adenosine A1-receptor antagonist. In anesthetized rats, KW-3902 (0.1 and 1 mg/kg p.o.) antagonized the 5'-N-ethylcarboxamidoadenosine (NECA) induced bradycardic response, which is thought to be mediated via adenosine A1-receptors. However, the hypotensive response to NECA, which is predominantly due to adenosine A2-receptor activation, was not affected by KW-3902. Diuretic and renal protective effects of KW-3902 were investigated in normal and pertussis toxin (IAP; 10 micrograms/kg i.v.)-treated rats. KW-3902 (0.001-1 mg/kg p.o.) caused significant increases of urine volume and sodium excretion with little change of potassium excretion in saline-loaded normal rats. In anesthetized normal rats, KW-3902 (0.01 and 0.1 mg/kg i.v.) caused significant diuresis and natriuresis with no change in renal plasma flow and glomerular filtration rate. These findings suggest that KW-3902 caused the diuretic effect not by the change in the renal hemodynamics, but by the inhibition of water and sodium reabsorption in tubular sites. KW-3902 (0.01-1 mg/kg p.o.) significantly attenuated increases of serum creatinine and urea nitrogen and renal tubular damage in glycerol-induced acute renal failure rats. Neither diuretic nor renal protective effects of KW-3902 were affected by pretreatment of rats with IAP, which totally abolished the bradycardic response to NECA. These results are compatible with the hypothesis that diuretic and renal protective effects by adenosine A1-receptor blockade are mediated via IAP-insensitive mechanism.
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PMID:Diuretic and renal protective effects of 8-(noradamantan-3-yl)-1,3-dipropylxanthine (KW-3902), a novel adenosine A1-receptor antagonist, via pertussis toxin insensitive mechanism. 833 58

Reported here is the case of a 6-week-old female infant with a severe Bordetella pertussis infection requiring supportive pressure-positive ventilation in the intensive care unit. After being discharged from the intensive care unit, she developed hemolytic anemia, thrombocytopenia and acute renal failure, which suggested a diagnosis of hemolytic uremic syndrome. The clinical outcome was favorable with no renal consequences. This case suggests there may be a direct cause-effect relationship between B. pertussis infection and hemolytic uremic syndrome.
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PMID:Hemolytic uremic syndrome in an infant following Bordetella pertussis infection. 1687 74

We showed previously that activation of A(1) adenosine receptors (AR) protects against renal ischemia-reperfusion (IR) injury in rats and mice. In the heart, transient A(1)AR activation produces biphasic protective effects: acute protection wanes after several hours but protective effects return 24-72 h later (second window of protection). In this study, we determined whether A(1)AR activation produces delayed renal protection and elucidated the mechanisms of acute and delayed renal protection. A(1)AR wild-type mice were subjected to 30-min renal ischemia and 24 h of reperfusion to produce acute renal failure. Pretreatment with a selective A(1)AR agonist 2-chloro-N(6)-cyclopentyladenosine (CCPA; 0.1 mg/kg bolus ip) either 15 min or 24 h before renal ischemia protected against renal IR injury and reduced renal corticomedullary necrosis, apoptosis, and inflammation. Transient A(1)AR activation led to phosphorylation of extracellular signal-regulated protein kinase mitogen-activated protein kinase (ERK MAPK), Akt, and heat shock protein 27 (HSP27). Moreover, induction of HSP27 and Akt occurred with CCPA treatment. Inhibition of PKC with chelerythrine prevented acute but not delayed renal protection with A(1)AR activation. Moreover, deletion of PI3Kgamma or inhibition of Akt, but not inhibition of ERK, prevented delayed and acute renal protection with A(1)AR activation. Inhibition of G(i/o) with pertussis toxin obliterated both acute and delayed A(1)AR-mediated renal protection. In contrast to renal protection with delayed ischemic preconditioning, nitric oxide synthase activity was not induced with delayed A(1)AR-mediated renal protection. Therefore, transient activation of renal A(1)AR led to acute as well as delayed protective effects against renal IR injury via distinct signaling pathways.
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PMID:Acute and delayed renal protection against renal ischemia and reperfusion injury with A1 adenosine receptors. 1792 14

We report the case of a 4-week-old infant with severe Bordetella pertussis infection resulting in hemolytic anemia, thrombocytopenia, and acute renal failure leading to a diagnosis of hemolytic uremic syndrome (HUS) associated with pertussis. In addition to antibiotic and supportive therapy, he was treated with plasma transfusions based on the possibility of underlying complement defect, and he improved. The association of B. pertussis infection and HUS has previously been described in a patient with a mutation in the gene encoding complement factor H (CFH). However, whereas a genetic workup for complement regulator mutations was performed, no mutation was found in our patient. This case demonstrates the possible association between pertussis infection and HUS and highlights the need for increased vigilance for renal complications in this diagnosis. Despite negative results in this case, in-depth workup of the complement system may be important to guide treatment efforts and strategies.
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PMID:Hemolytic uremic syndrome caused by Bordetella pertussis infection. 2014 55