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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The systemic manifestations of sepsis are associated with increased cardiac output, peripheral vasodilatation, and mesenteric vasoconstriction. Our objective was to determine whether tumor necrosis factor (TNF)-alpha regulates small intestinal microcirculatory changes observed during sepsis. An intact loop of terminal ileum of an anesthetized rat was exteriorized into modified Krebs solution and then topically suffused with varying concentrations of TNF-alpha (10(-4) ng/ml to 10(2) ng/ml), norepinephrine (10(-4) M), and sodium nitroprusside (10(-5) M). Videomicroscopy was used to measure arteriolar (A1, A2, A3) and venular (V1, V2) diameter changes in response to topical TNF-alpha. First order vessel diameters did not change in response to TNF-alpha. However, second and third order arterioles dilated maximally by 35 +/- 16 and 52 +/- 12 per cent, respectively, in a dose dependent manner in response to TNF-alpha. Higher order vessels were more sensitive to TNF-alpha than lower order vessels. Norepinephrine (10(-4) M) produced vasoconstriction in all vessels tested (A2 18 +/- 3 per cent, p < 0.05; A3 6 +/- 6 per cent; V2 13 +/- 4 per cent, p < 0.05). Topical TNF-alpha caused dilation in preconstricted vessels as in the nonpreconstricted vessels. TNF-alpha induced vasodilation was prolonged and not reversed by removal of TNF-alpha. These data demonstrate statistically significant dilation in response to TNF-alpha in second and third order arterioles and venules of the small intestine. Persistent vasodilation suggests an induced mechanism of vasodilation in response to TNF-alpha that remains active even after removal of exogenous TNF-alpha. We, therefore, conclude that TNF-alpha causes persistent vasodilatation beyond the period of actual exposure to TNF-alpha in the small intestinal microcirculation. This effect is not altered by the presence of norepinephrine. These data suggest that small intestinal vasoconstriction observed during clinical conditions such as sepsis is unlikely to be mediated by TNF-alpha.
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PMID:Role of tumor necrosis factor-alpha in small intestinal microcirculation. 952 Aug 8

Struvite stones constitute only about 2-3% of the stones reaching the laboratory for analysis, but the clinical problems they create including sepsis and even renal demise are greater than with any other stone type. This article reviews the evidence that bacterial urease, usually from a Proteus species, is responsible for the chemical changes in urine which result in struvite formation. Available urease inhibitors and other forms of medical management of patients with these stones are discussed. A patient with struvite stones should be assumed to have a progressive disease which cannot be ignored. Even after seemingly successful elimination of stones with lithotripsy and/or percutaneous nephrolithotomy, careful medical follow-up is critical. The medical profession is probably underutilizing postprocedure hemiacidrin irrigation because of shortsighted financial considerations. Primary-care physicians need to be educated in the importance of aggressive management of Proteus and other urea-splitting infections.
Nephron 1999
PMID:Struvite stones. 987 15

Septic shock is often complicated by systemic hypotension despite normal or increased cardiac output. Restoration of arterial pressure usually requires the administration of systemic vasopressor agents, such as norepinephrine. However, because norepinephrine induces vasoconstriction in other vascular beds, it may decrease visceral blood flow, impairing visceral organ function. Because sepsis is often associated with impaired peripheral vascular responsiveness, we hypothesized that, unlike in normal circulatory conditions, norepinephrine would improve visceral organ blood flow in sepsis by selectively increasing organ perfusion pressure. Thus, in nine pentobarbital-anesthetized, mechanically ventilated dogs, we measured the effect of norepinephrine infusion (0.3 microgram/kg/min) on renal, hepatic, and portal steady-state pressure-flow relations (P/Q) and the dynamic vascular P/Q, created by transient inferior vena caval occlusion, under basal and endotoxic conditions. Norepinephrine increased organ perfusion pressures during both control and endotoxemic conditions. However, even after controlling for the pressure effect using a general linear model, NE was associated with an increase in renal blood flow both before and after endotoxin administration. We conclude that, unlike the effects of administering norepinephrine under baseline conditions, norepinephrine infusion during endotoxic shock actually increases renal blood flow and that this effect is not the result of an increase in perfusion pressure alone.
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PMID:Effects of norepinephrine on the renal vasculature in normal and endotoxemic dogs. 1019 64

Following bone marrow transplantation, acute renal failure and proteinuria are common complications with a high mortality, particularly in patients requiring hemodialysis. Incidence, potential predisposing factors, and outcome of acute renal complications in patients with hematological malignancies receiving autologous peripheral blood stem cell transplantation were prospectively studied in 53 patients. Eight patients developed acute renal failure. Three of them required hemodialysis. Of all patients with acute renal failure, only those requiring hemodialysis died, due to nonrenal causes. Only 1 of the 45 patients without renal failure died. Mild proteinuria of predominantly tubular origin occurred in 16 patients, in 3 with and in 13 without acute renal failure. As predisposing factors for acute renal failure were identified: renal hypoperfusion due to systemic inflammatory response syndrome, sepsis or septic shock, and combined administration of nephrotoxic drugs. Especially those patients receiving high numbers of nephrotoxic drugs in combination with renal hypoperfusion were likely to develop acute renal failure. These results suggest that patients receiving high-dose chemotherapy and autologous peripheral blood stem cell transplantation have a low risk of developing acute renal failure and proteinuria.
Nephron 2000 Feb
PMID:Renal complications of high-dose chemotherapy and peripheral blood stem cell transplantation. 1065 14

Norepinephrine stimulates growth of Escherichia coli, Yersinia enterocolitica, and Pseudomonas aeruginosa in serum-supplemented media, and in vivo increases in norepinephrine may be important in the pathogenesis of sepsis by gram-negative bacteria. Because salmonellosis often is associated with stress, the effects of norepinephrine on in vitro growth, and in vivo pathogenicity of the swine pathogen Salmonella choleraesuis were investigated. When RPMI 1640 with and without pig serum was inoculated with fewer than 100 S. choleraesuis/ml and incubated overnight, bacterial numbers were 10(4) to 10(6) lower in RPMI containing serum. Norepinephrine restored bacterial growth in RPMI with serum to normal levels, but it did not increase growth in serum-free RPMI. Similar results were obtained with SAPI, a nutrient-poor medium previously used to study the effect of norepinephrine on growth of gram-negative bacteria. Conditioned media were produced by growing S. choleraesuis in RPMI containing serum with and without norepinephrine and filter sterilizing. Conditioned medium produced with norepinephrine stimulated growth of S. choleraesuis but not E. coli, whereas conditioned medium produced without norepinephrine stimulated growth of both bacteria. To determine the in vivo effects of norepinephrine, rats were implanted with tablets that secrete norepinephrine for 20 to 24 hours or with identical tablets without norepinephrine and infected intraperitoneally with graded doses of S. choleraesuis. The LD-50 of S. choleraesuis was the same in both groups, and norepinephrine did not affect the carrier rate at 30 days after infection. We concluded that although norepinephrine stimulates in vitro growth of S. choleraesuis in serum-based media, the increase in norepinephrine levels in the present in vivo system was probably not sufficient to influence the pathogenesis of S. choleraesuis infection.
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PMID:Norepinephrine stimulates in vitro growth but does not increase pathogenicity of Salmonella choleraesuis in an in vivo model. 1065 66

Persistent vasodilation characteristic of septic shock may result from overproduction of nitric oxide and can lead to pressor-refractory hypotension and death. To evaluate the significance of cytokine-inducible nitric oxide synthase (iNOS) in the pathogenesis of sepsis, we used a clinically relevant mouse model of sepsis and compared mortality and microvascular reactivity in wild-type (WT) mice and transgenic mice deficient in iNOS. WT C57BL/6 and iNOS-deficient mice were made septic by cecal ligation and puncture. Treated mice were given fluids and antibiotics every 6 hours. Microvascular vasoconstriction in response to topical norepinephrine was measured in cremasteric arterioles (15 to 30 microm) by videomicroscopy. Mortality at 48 hours was significantly lower in treated septic iNOS-deficient mice (45%) than in treated septic WT mice (76%), untreated septic iNOS-deficient mice (87%), or untreated WT mice (100%) (P<0.01). Norepinephrine-induced vasoconstriction was decreased in WT septic mice (EC(50) 200+/-56 nmol/L) compared with WT and iNOS-deficient shams (16+/-4 and 13+/-6 nmol/L), and vasoconstriction was significantly improved in septic iNOS-deficient mice (35+/-13 nmol/L, P<0.01). Microvascular catecholamine responsiveness and survival were improved in iNOS-deficient mice in a clinically relevant model of sepsis, suggesting that iNOS plays an important, but not exclusive, role in refractory vasodilation in patients with septic shock.
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PMID:Increased microvascular reactivity and improved mortality in septic mice lacking inducible nitric oxide synthase. 1076 11

Nitric oxide (NO) plays an important regulatory/modulatory role in a variety of inflammatory conditions. NO is a small, short-lived molecule that is released from a variety of cells in response to homeostatic and pathologic stimuli. It may act as a vasodilator and a platelet inhibitor and may interfere with adhesion molecules to prevent neutrophil adhesion. NO release may also lead to the formation of highly reactive species such as peroxynitrite and stable nitrosothiols and may cause mitochondrial damage and nitration of protein tyrosine residues. In addition, NO inhibits cell proliferation via inhibition of polyamine synthesis and cell uptake and may well act as a 'brake' on the proliferative response following cytokine exposure. All three isoforms of nitric oxide synthases are found in the kidney during inflammation. The site of NO release impacts significantly on its net function and structural impact. NO plays a protective role in many forms of immune injury, such as nephrotoxic serum-induced glomerulonephritis, autoimmune tubular interstitital nephritis, and experimental allergic encephalomyelitis. NO overproduction in sepsis, after cytokine exposure, inducible NO synthase transcription, and local inflammation can autoinhibit endothelial NO synthase, leading to selective renal and mesenteric vasoconstriction.
Nephron 2002 Apr
PMID:Role of nitric oxide in inflammatory conditions. 1196 94

Anderson-Fabry disease (AFd) is a rare X-linked disorder characterized by deficiency of alpha-galactosidase A that leads to systemic accumulation of neutral glycosphingolipids, predominantly globotriaosylceramide (Gb3), in body fluids and visceral tissues, including the kidney. End-stage renal failure is a common manifestation in hemizygous males that often occurs by the third to fourth decade of life. Usually transplanted patients exhibit improvement in clinical symptoms of the disease, probably related to the production of alpha-galactosidase A from the grafted kidney, but mainly related to the increase in Gb3 clearance by the functioning kidney, and increased survival of red cells due to the correction of the uremic status with an evident decrease in the production of Gb3 depending from hemolysis. Several Fabry patients with successful kidney graft survived for 10-15 years and died for cardiovascular complications related to the metabolic disease. The loss of grafted kidney is due to rejection, thrombosis or sepsis. An important issue considering renal transplantation in AFd is the recurrence of the disease in the kidney graft; however, no evidence regarding this possibility has occurred up to now. We report herein the ultrastructural study of the urinary sediment of a 35-year-old male Fabry patient with a severe clinical form of the disease with progression to ESRF at age 29, and submitted to renal transplantation at 33 years. Ultrastructural findings of the urinary sediment documented several cells, probably tubular epithelial cells, with typical accumulation of myelinic bodies resulting from intracellular storage of neutral glycosphingolipids. This morphological evidence arises the problem of the possible recurrence of AFd in the kidney graft in patients with severe phenotype of the metabolic disease.
Nephron 2002 Jun
PMID:Renal transplantation in patients with Fabry disease. 1205 80

Infection, mainly related to vascular access, is one of the main causes of morbidity and a preventable cause of death in hemodialysis patients. From January 1994 to April 1998 we conducted a prospective study to assess the incidence and risk factors of catheter-related bacteremia. One hundred and twenty-nine tunneled dual-lumen hemodialysis catheters were inserted percutaneously into the internal jugular vein in 89 patients. Bacteremia (n = 56) occurred at least once with 37 (29%) of the catheters (an incidence of 1.1/1,000 catheter-days); local infection (n = 45, 1/1,000 catheter-days) was associated with bacteremia in 18 cases. Death in 1 case was directly related to Staphylococcus aureus (SA) septic shock, and septicemia contributed to deaths in 2 additional cases. Catheters were removed in 48% of the bacteremic episodes. Treatment comprised intravenous double antimicrobial therapy for 15-20 days. Bacteriological data of bacteremia showed 55% involvement of SA. Nasal carriage of SA was observed in 35% of the patients with catheters. Bacteremic catheters were more frequently observed in patients with diabetes mellitus (p = 0.03), peripheral atherosclerosis (p = 0.001), a previous history of bacteremia (p = 0.05), nasal carriage of SA (p = 0.0001), longer catheter survival time (p = 0.001), higher total intravenous iron dose (p = 0.001), more frequent urokinase catheter infusion (p < 0.01), and local infection (p < 0.001) compared with non-bacteremic catheters. Monovariate survival analysis showed that significant initial risk factors for bacteremia were nasal carriage of SA (p = 0.00001), previous bacteremia (p = 0.0001), peripheral atherosclerosis (p = 0.005), and diabetes (p = 0.04). This study confirms the relatively high incidence of bacteremia with tunneled double-lumen silicone catheters and its potential complications. Possible preventive actions are discussed according to the risk factors.
Nephron 2002 Jul
PMID:Risk factor analysis for long-term tunneled dialysis catheter-related bacteremias. 1211 69

A 72-year-old non-diabetic uremic woman underwent right nephrectomy for urolithiasis at the age of 50. Because pyuria, fever, chilliness and left flank pain developed during preparing for arteriovenous fistula, she was admitted to National Cheng Kung University Hospital. Renal cell carcinoma (RCC) complicated with emphysematous pyelonephritis (EPN) was diagnosed and immediately treated with antibiotics and CT-guided percutaneous catheter drainage. Cultures of pus and blood yielded Escherichia coli. She received left radical nephrectomy later for the control of persistent sepsis and removal of left renal tumor. The pathology of the tumor was composed of a glandular arrangement of granular cells with the occasional atypism, and renal parenchyma had been totally replaced by RCC. The non-tumor part of the kidney showed chronic pyelonephritis. Five months later, multiple metastases developed. We reported this first uremic case with EPN and RCC, but without diabetes mellitus and urinary tract obstruction. The gas formation may be due to large RCC, which caused impaired tissue perfusion and E. coli infection.
Nephron 2002 Sep
PMID:Renal cell carcinoma complicated by emphysematous pyelonephritis in a non-diabetic patient with renal failure. 1218 10


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