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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-seven patients with renal vein thrombosis were retrospectively studied to evaluate their long-term prognosis and relevant prognostic factors. Twenty-four patients presented with a nephrotic syndrome, and 15 had renal impairment (8 acute; 7 moderate). Ten patients had a previous history of proteinuria, and 14 of nephrotic syndrome. Renal biopsy performed in 20 patients, of whom 19 were nephrotic, showed membranous glomerulonephritis in 14, focal segmental glomerulosclerosis in three, minimal change glomerulonephritis in two, and periarteritis nodosa in one. Renal vein thrombosis was angiographically proven in all patients and was bilateral in 18, localised to the left renal vein in seven, and to the right in two. Thrombosis of the inferior vena cava was associated in seven patients. Ten patients were treated by anticoagulants alone, nine by surgical thrombectomy, seven by thrombolysis, and two did not receive any specific treatment. One patient underwent successively thrombectomy and then thrombolysis. Eleven patients died within the first 6 months, mainly from haemorrhagic complications (n = 5) or severe sepsis (n = 2). Survivors were followed up from 6 months to 19 years. Nephrotic syndrome improved or even disappeared in 12 patients, and renal function did not worsen throughout the follow-up in any patients. The main prognostic factors were initial renal function and type of nephropathy: patients with membranous glomerulonephritis had a significantly better renal function and a lower mortality rate than patients with other nephropathies. Initial renal insufficiency was significantly associated with a poor prognosis. There was no advantage, in terms of survival, kidney function and nephrotic syndrome, of either thrombectomy or thrombolysis over anticoagulants alone, despite two complete venous recanalisations after thrombolysis. Accordingly, patients with renal vein thrombosis from membranous glomerulonephritis should be treated by anticoagulants alone, since the long-term prognosis of this disease seems unaffected by intercurrent renal vein thrombosis. With respects to the risk-to-benefit ratio, thrombectomy should be avoided and thrombolysis considered only in patients with initial acute renal failure from acute renal vein thrombosis.
Nephrol Dial Transplant 1988
PMID:The prognosis of renal vein thrombosis: a re-evaluation of 27 cases. 314 96

A circulating lupus anticoagulant factor was detected in a 38-year-old man with end-stage renal disease and a 'lupus-like' syndrome with a diffuse proliferative glomerulonephritis. When treated with steroids, the 'lupus' complications were controlled and the anticoagulant factor disappeared; however, renal function did not recover and the patient commenced regular haemodialysis. Four months later the patient received a cadaver kidney transplant. At transplantation and during follow-up there was neither clinical nor laboratory evidence of lupus activity, but 19 months after transplantation, when steroids were tapered to a low dose, the lupus anticoagulant factor was detected, and renal-vein thrombosis complicated by sepsis led to the patient's death. A membranous glomerulonephritis was found on autopsy. This is the first time in which a (probably 'de novo') membranous glomerulonephritis has been detected in the allograft of a patient with circulating lupus anticoagulant factor.
Nephrol Dial Transplant 1988
PMID:Allograft membranous glomerulonephritis and renal-vein thrombosis in a patient with a lupus anticoagulant factor. 314 30

In a prospective study the diagnostic value of urinary thromboxane B2 (TXB2) and beta 2-microglobulin (beta MG) in renal allograft rejection was studied in 34 patients after transplantation. Twenty-four episodes of rejection were diagnosed by clinical symptoms. The clinical diagnosis of rejection was confirmed by an increase of urinary TXB2 in 21 (88%) cases. The augmented renal excretion of TXB2 proceded the clinical signs of rejection for 2.0 +/- 0.75 days. The symptoms in the remaining three (12%) cases of supposed allograft rejection without increased urinary TXB2 were caused by non-immunological events (urinary tract infection, acute tubular necrosis). No elevated TXB2 excretion was observed during urinary tract infection, sepsis, and acute tubular necrosis whereas urinary beta MG increased during these events as during transplant rejection. Urinary TXB2 was found to be an early, specific, and sensitive marker of renal allograft rejection with greater reliability than beta MG excretion or clinical signs of rejection.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Thromboxane B2 and beta 2-microglobulin as early indicators of renal allograft rejection. 388 70

Generalised sepsis was induced in sheep by caecal perforation. Serial measurement of haemodynamic parameters revealed that the subsequent generalised sepsis induced increased cardiac output and decreased systemic resistance comparable to that known to occur in man. Glomerular filtration rate in these animals fell significantly 48 hours after induction of sepsis and there was evidence of tubular damage in the finding of low molecular weight proteinuria and increased clearance of lysozyme. Pathological examination of the kidney revealed normal glomeruli, no consistent changes in tubular cells on light microscopy, negative immunofluorescence, but structural changes in proximal tubular cells on EM. In this model, non-hypotensive sepsis predictably produces damage to proximal tubular cells accompanied by reduction in GFR.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Acute renal failure and tubular damage due to sepsis in an animal model. 399 81

Sixty four patients who developed acute renal failure at The New York Hospital between July 1981 and June 1982 were studied. The average age was found to be 59.5 years. The overall mortality rate was 62.5%. Patients with non-oliguric renal failure had a lower mortality rate (25%) than those with oliguric renal failure (79%). Those patients with non-oliguric renal failure were more likely to have a discrete cause of renal failure (drugs) and to be in a more stable cardiovascular status. Tachycardia, hypotension, respiratory failure, and documented (or presumed) sepsis all adversely affected prognosis.
Clin Exp Dial Apheresis 1983
PMID:Prognostic patterns in acute renal failure: the New York Hospital, 1981-1982. 688 3

Previous studies of experimental sepsis suggested that excessive systemic vasodilatation might be the stimulus to renal hypofiltration and fluid retention in sepsis. Successful therapy for this syndrome requires agents that either act to improve systemic haemodynamics without adverse renal effects, or that act directly on the kidney without impairing circulatory homeostasis. The plasma kallikrein-kinin system is a potent vasodilator pathway, activated by endotoxin. We studied the effect of aprotinin (Trasylol), which inhibits plasma kallikrein, in an ovine model of surgically-induced intra-abdominal sepsis. Given either as an early or late intervention, aprotinin was associated with increased mean arterial pressure and systemic vascular resistance, improved glomerular filtration rate, and increased urinary sodium excretion. In further studies, treatment with the thromboxane synthetase inhibitor, U63,557A (Upjohn), either before or after the surgical induction of peritonitis, was associated with increased glomerular filtration rate and sodium excretion, without any effect on systemic haemodynamics. Logical use of specific antagonists, based on an understanding of the pathophysiology of the septic ARF syndrome, is a desirable strategy.
Nephrol Dial Transplant 1994
PMID:Acute renal failure and sepsis: therapeutic approaches. 752 64

We reviewed our experience with patients suffering from civilian trauma to identify risk factors for the development of acute renal failure (ARF) and ARF outcome. Of the 437 patients consecutively admitted to a surgical intensive care unit (SICU), 206 had a SICU stay of at least 1 day and ARF developed in 30 of these patients. All ARF patients had additional organ system failure (OSF). Pre-existing chronic disease (including chronic renal failure), malnutrition, injury severity score (ISS), number of organs injured, sepsis, and all OSFs before the onset of ARF were factors predisposing to ARF. Mortality was 40%. Chronic disease, malnutrition, ISS, failure of cardiovascular, pulmonary, hepatic, and neurological systems (either before and after ARF) were significantly associated with mortality. When OSFs were considered in their temporal relationships to ARF, only cardiovascular and pulmonary failure before, and gastrointestinal failure after, the onset of ARF were related to mortality. An increasing number of OSFs increased mortality, both before and after the development of ARF. However, the number of OSFs before was significantly greater than after ARF. Sepsis was not associated with increased mortality. Thus, the outcome of ARF patients with critical trauma seems to be dependent on factors predisposing to ARF. Our results suggest that more attention must be paid to prevention of these precipitating conditions.
Nephrol Dial Transplant 1994
PMID:Acute renal failure in patients with severe civilian trauma. 780 Feb 44

Acute renal failure (ARF) is a common manifestation of a septic condition which very often complicates surgical and traumatic events. The release of endotoxin, a lipopolysaccharide (LPS) from the cell wall of Gram-negative bacteria, and subsequently of numerous host mediators, is the initiating event of sepsis syndrome and eventually of septic shock. Particularly interesting is the observation that not only endotoxins but also Staphylococcus aureus which does not produce endotoxins induce the same cardiovascular changes of septic shock. The main aspect of septic shock is the inadequate oxygen supply to the body tissues. However, despite the documented myocardial depression in the course of septic shock, myocardial ischaemia is not to be considered a contributing factor, and the coronary blood flow is normal or even increased. Protein hypercatabolism can be at best only limited; in any case the optimal protein-sparing effect was observed with 1.5 g/kg proteins. Recently monoclonal antibodies to endotoxin core glycolipid have been developed; they are: (a) E5, a murine IgM anti-lipid A monoclonal antibody; (b) HA-1A, a human monoclonal antibody to endotoxin core glycolipid. In conclusion, hypercatabolic septic patients should be managed in an intensive care environment where a continuous monitoring of fluids, electrolytes, and acid-base disorders can be achieved. Surgical search of septic foci, and wide-spectrum antibiotic therapy are fundamental measures to combat cytokine and vasodilator production which impair tissue perfusion and create the premise of a shock status complicated by lactic acidosis. Dialysis treatment is a further complementary but fundamental approach that allows a large fluid and nutritional intake and a continuous correction of electrolyte and acid-base disorders.
Nephrol Dial Transplant 1994
PMID:Basic therapeutic requirements in the treatment of sepsis in acute renal failure. 780 Feb 55

Acute renal failure (ARF) is often a component of multiple organ system failure in critically ill patients. Sepsis (i.e. systemic bacterial infection) is a major factor in the aetiology of ARF and this is primarily caused by sepsis-induced cardiovascular and pulmonary failure. This association suggests that systemic haemodynamic factors, leading to severe and persistent renal hypoperfusion, play a key role in the development of ARF. However, ARF in the course of sepsis or endotoxaemia may not be solely due systemic or renal haemodynamic changes, since humoral and cellular reactions may also have an adverse effect on renal function. This review will address the haemodynamic and non-haemodynamic factors and their interaction in the development of ARF during sepsis.
Nephrol Dial Transplant 1994
PMID:Pathogenesis of acute renal failure during sepsis. 780 Feb 69

A rapidly increasing body of evidence is implicating endothelin and TNF in the pathogenesis of septic acute renal failure. TNF causes renal damage by recruiting leukocytes, accelerating fibrin accumulation, promoting cell lysis, stimulating the release of vasoconstrictor substances, and other mechanisms. ET-1 causes renal dysfunction in sepsis and endotoxaemia primarily by evoking severe reductions in RBF and GFR. While these are only two of the many agents that mediate renal dysfunction during sepsis, they stand out by virtue of their combined ability to modulate numerous inflammatory pathways and to elicit marked alterations in renal function. Clearly the development of specific TNF and endothelin antagonists holds out promise for the treatment and prevention of septic acute renal failure.
Nephrol Dial Transplant 1994
PMID:Role of endothelin and tumour necrosis factor in the renal response to sepsis. 780 Feb 73


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