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

This study records our experience with 40 infants who developed acute renal failure in a tropical environment over a period of 2 years. All the patients required intermittent peritoneal dialysis. Septicaemia (88%) and acute gastroenteritis (55%) constituted the leading causes of acute renal failure. Haemolytic uraemic syndrome was present in six (18%) patients. An elevated serum creatinine (85%), metabolic encephalopathy (75%), uncompensated metabolic acidosis (75%) and hyperkalaemia (48%) were the major indications for dialysis, while fluid overload was present in only 18% of the infants. Intermittent peritoneal dialysis was used in all the patients and was found to be effective. Procedural complications were minor and infrequently encountered. The clinical course and laboratory data consistent with haemolytic uraemic syndrome was observed in six patients, and acute tubular necrosis was the predominant renal lesion in the remainder. Mortality was 75%. The aetiology of acute renal failure in infants in the tropics differs significantly from that in the West, and even within a given country marked regional variations exist.
Nephrol Dial Transplant 1989
PMID:Acute renal failure in infants in the tropics. 250 74

Plasma concentrations of carnitine and carnitine esters were determined in patients with multiple forms of acute renal failure with and without sepsis, and also before and after haemodialysis therapy. Total carnitine, free carnitine, short-chain and long-chain acylcarnitine values of both groups of acute renal failure patients were markedly elevated compared with healthy subjects and chronically uraemic patients undergoing regular haemodialysis treatment. Carnitine and carnitine esters did not differ between septic and non-septic patients before and after haemodialysis with dialysers made of cuprophane or polysulphone. Animal experiments with acutely uraemic rats were performed in order to determine whether the liver or the kidney may be responsible for elevated carnitine and carnitine esters in acute renal failure. Plasma and liver total carnitine, free carnitine, short-chain acylcarnitine and long-chain acylcarnitine were significantly elevated in sham-operated animals, and further in ureter ligated and bilateral nephrectomised rats. Skeletal muscle and heart muscle carnitine and carnitine esters remained the same as in sham-operated controls. Our data demonstrate markedly increased liver carnitine synthesis and carnitine acylation in an acute uraemic rat model even after binephrectomy and 48-h food depletion and in the presence of elevated serum carnitine concentrations. Furthermore, from our clinical study we conclude that there is no need for carnitine supplementation in patients who developed acute renal failure in the postoperative and post-traumatic state under adequate nutrition even when requiring daily haemodialysis.
Nephrol Dial Transplant 1989
PMID:Carnitine and carnitine esters in acute renal failure. 251 86

One hundred and seven Hickman catheters for haemodialysis were inserted in 90 end-stage chronic renal failure patients, and were used for 1-448 days (median 45 days). Sixty-nine per cent of the patients were treated without any problem for 1-165 days (median 34 days). Clinically evident complications occurred in 44 catheters inserted in 28 patients, and included outflow obstruction (16.8% of the catheters) and thrombosis (13.1% of the catheters). However, many episodes of clotting or insufficient flow could be corrected by simple manoeuvres. Other less frequent complications were recorded: sepsis, mainly in patients with increased risk factors (4.1% of the catheters), laceration of the catheter (3.7%) and occasional cases of jugular-vein phlebitis, transient palsy of a vocal cord, haematoma of the wound, and bleeding of the cutaneous orifice. No clinical sign of subclavian or innominate-vein thrombosis was observed. Nevertheless, a prospective study conducted in 50 asymptomatic patients demonstrated a 12% rate of anomalies of the venous system, although two-thirds of these alterations were mild and had no consequence. When the present series is compared to the results obtained with currently available percutaneous haemodialysis catheters, it is concluded that the Hickman catheter is a safe, comfortable and efficient vascular access device.
Nephrol Dial Transplant 1989
PMID:Central venous access for haemodialysis using the Hickman catheter. 251 92

The courses of 34 graft failures leading to graft nephrectomy in 19 patients were examined retrospectively. Cyclosporin (CsA) was the sole immunosuppressive in 70% of the cases, and azathioprine-prednisolone in 30%. Having diagnosed graft failure, the immunosuppressive treatment was continued for about 2-3 months and then tapered slowly. No deaths related to graft failure were recorded. In three cases a delay in graft nephrectomy caused complications such as sepsis and coagulopathy. We conclude that continuing immunosuppression a few months after having diagnosed graft failure may postpone or avoid graft nephrectomy while steroid withdrawal symptoms do not complicate the course at the time of graft failure.
Nephrol Dial Transplant 1987
PMID:Graft failure and graft nephrectomy without severe complications. 311 80

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


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