Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathophysiology, clinical aspects, medical, and surgical management of endotoxin shock are reviewed. In the primate, the pathophysiology of endotoxin shock is contributed to by selective vasopasm, disseminated intravascular coagulation, and reduced myocardial response to sympathetic stimuli. Studies in the baboon measured various parameters of hemodynamics and coagulation, catecholamines, and some biochemical changes following the injection of a single bolus of endotoxin. Hemodynamic studies pointed to the kidney as a primary target organ. Coagulation changes included alterations in factor XII and XIII (and others) and plasminogen. Deposition of fibrin was also noted. Neurohormonal studies using tritiated norepinephrine showed a sharp rise in catecholamines 3 minutes after injection of endotoxin followed by a return to normal within 120 minutes, confirming the role of vasopasm in reducing renal perfusion early in shock. Prevention of septic shock is the best way to eradicate the extremely high reported mortality rates; infected abortion, chorioamnionitis, and pyelonephritis should all be warning signals. Methods of monitoring the patient in septic shock with special attention to blood pressure, central venous pressure, blood volume changes, and urinary output are discussed. Early surgical intervention and the proper use of vasomotor drugs and corticosteroids enhance patient survival.
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PMID:Septic shock (endotoxic shock). 419 24

Acute pyelonephritis, frequently caused by Escherichia coli, is a substantial health problem. Plasminogen activator inhibitor type-1 (PAI-1) not only inhibits plasminogen activation but is also involved in cell migration. To determine if it has a role in host defense, we induced pyelonephritis in PAI-1 gene knockout and wild-type mice by intravesical inoculation with uropathogenic E. coli 1677. Bacterial growth was determined on blood agar plates in portions of the kidneys homogenized in sterile saline. Kidney levels of PAI-1 were increased in infected compared to control mice, suggesting a physiological role for PAI-1 during pyelonephritis. The knockout mice had significantly more bacterial outgrowth in kidney homogenates compared to the wild-type mice. Strikingly, higher colony-forming units were accompanied by increased levels of the cytokines TNF-alpha, IL-1beta, and IL-6 in the kidneys of knockout mice, but levels of the chemokines KC and MIP-2 were not different. Remarkably, plasma levels of KC were higher, but renal neutrophil influx was significantly lower, in the knockout than in the wild-type mice. Our study shows that PAI-1 is critically involved in host defense against E. coli-induced acute pyelonephritis, in part, by modulating neutrophil influx.
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PMID:Plasminogen activator inhibitor-1 regulates neutrophil influx during acute pyelonephritis. 1880 31