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

Five hundred and thirty-three patients in the Oxford renal unit were reviewed to determine the incidence of infection in one calendar year. There were 310 patients who received dialysis, 53 with acute renal failure and 211 with chronic renal disease. Renal transplant patients were not included in the study. Apart from infections related to dialysis access, patients on maintenance haemodialysis or continuous ambulatory peritoneal dialysis developed few serious infections unless they had another disease causing suppression of immune function. A total of 97 urinary tract infections were seen; in patients with chronic renal disease not receiving dialysis the incidence of urinary tract infection was significantly associated with increasing uraemia, with diabetes, and with treatment with azathioprine or cyclophosphamide. In patients with acute renal failure, Gram-negative septicaemia and fungal infections were important causes of morbidity and mortality, but cardiovascular disease caused 42 per cent of the deaths unlike results from other series where sepsis has been by far the commonest cause of death.
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PMID:Infections in a renal unit. 259 47

The best definition of risk factors for renal injury, irrespective of the aetiological agent, comes from observations in patients with acute renal failure. From such observations, two subdivisions have evolved, i.e., acute insults and host risk factors. Acute renal insults include: hypertension, sepsis, use of nephrotoxic drugs (e.g., aminoglycoside antibiotics and contrast media), haemoglobinuria or myoglobinuria, liver disease and extracellular volume depletion. Host risk factors include: advanced age, hypertension, gout and hyperuricaemia, diabetes mellitus, chronic renal failure and use of diuretics. Furthermore, the mechanism of acute renal injury can be correlated with different risk factors: for a tubular toxic agent, acting either directly on the cells or haemodynamically, a dose-dependency is characteristic; while for immunologically mediated injury, genetic predisposition is more important. The identification of risk factors for chronic toxic injury is confounded by the possibilities of multiple episodes of subclinical renal injury, the distinct possibility that a major component of the ageing process may be a loss of renal reserve, and a progressive body burden, of, e.g., cadmium, which may deplete intrinsic protective mechanisms. However, clinically relevant risk factors can alert the clinician to exercise additional caution when prescribing medications that are potentially nephrotoxic. Such factors include dehydration, pre-existing renal disease, age, co-existing diseases that cause renal ischaemia, gender, concomitantly administered drugs, and electrolyte abnormalities.
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PMID:Risk factors for toxic nephropathies. 265 33

Cyclosporin (CYA) is now recognized as an effective immunosuppressant to lead to a marked improvement in graft survival in organ transplant recipients. Although the incidence of infection in the CYA group has been decreased compared with that in the azathioprine group, infectious diseases in 400 kidney transplant recipients treated with CYA were noted in our single center. Treatment strategy for infectious diseases: Antibiotics and/or gamma-Globulin were administered to all recipients with bacterial infections. Aciclovir was added in recipients with herpes simplex virus (HSV) infection or varicella zoster virus (VZV) infection. Human interferon-beta (HuIFN-beta) was used in recipients who had life-threatening viral infection, especially cytomegalovirus (CMV) pneumonitis. Glycyrrhizin was used for acute hemorrhagic cystitis and nephropathy due to adenovirus (AV). Trimethoprim sulfamethoxazole and/or pentamidine were added in recipients complicated with Pneumocystis carinii (Pc) pneumonitis or in order to prevent Pc pneumonitis. Infectious diseases: One hundred and six recipients had infectious diseases 129 times in this series, seventy-six percent of all infections occurred during the first 4 months after the transplantation. Urinary tract infection (UTI), herpes zoster and pulmonary infection were the most common infectious diseases, occurring in 28.7%, 24.0% and 23.2%, respectively. Septicemia or bacteremia developed in 9 recipients, secondary to UTI in 8 and to surgical wound infection in one. Sixty-one symptomatic viral infections occurred in 57 recipients. A total of 5 recipients (1.3%) died of interstitial pneumonitis. Infectious organisms: Viral and bacterial infections were most common, occurring in 47.3% and 41.9%, respectively. Viral species detected in these recipients with the frequency were HSV 14 times, CMV 9 times, VZV 31 times and AV 7 times. 1) The incidence of viral infections in kidney transplant recipients treated with CYA is relatively high compared to bacterial infections. 2) HuIFN-beta therapy is effective in the treatment of serious opportunistic herpes virus infections, especially CMV pneumonitis. 3) Glycyrrhizin therapy is effective in the treatment of acute hemorrhagic cystitis and nephropathy due to AV and hepatic dysfunction. 4) Aerosolised pentamidine therapy is very useful for prophylaxis of Pc pneumonitis.
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PMID:[Infectious diseases in kidney transplant recipients treated with cyclosporin]. 266 94

The peculiarities of the diagnosis of sepsis in 24 patients with local purulent processes are presented. The DIC-syndrome, pulmonary syndrome, toxic nephropathy are of most importance in diagnosis of the disease.
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PMID:[Diagnosis of infection]. 273 63

A poor prognosis was observed in patients who had end-stage renal disease (ESRD) as a result of systemic lupus erythematosus (SLE). This was true even in patients in whom SLE disease activity was transiently quiescent during the period of hemodialysis. Six of 9 patients with ESRD and SLE died with active SLE and/or sepsis 1-28 months following the onset of dialysis. In 5 of the 6 patients, acute inflammatory activity of SLE flared within 1 month of the patient's death. Four patients died with superimposed sepsis, but only 2 of the 4 were receiving high-dose concomitant immunosuppressives for more than 1 week prior to death. Infected hemodialysis vascular access sites were implicated as the source of septicemia in 3 of 4 infectious deaths. The 3 surviving patients had minimal lupus activity prior to the development of ESRD, a possible marker for stability in SLE patients who require hemodialysis. Our results suggest that hemodialyzed lupus patients with nonautologous vascular access sites may be at continued increased risk for life-threatening inflammatory and septic complications.
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PMID:Poor prognosis in end-stage lupus nephritis due to nonautologous vascular access site associated septicemia and lupus flares. 281 17

The clinical manifestations of a genetically determined deficiency of C3 were examined in a closed colony of dogs. One hundred and twelve dogs, including twenty C3-deficient dogs, were studied over a period of 6 years. Five of the C3-deficient dogs developed significant bacterial infections, such as pneumonia, sepsis, and pyometra, which were caused by Clostridium spp., Escherichia coli, and Klebsiella spp. Two of the C3-deficient dogs who had had significant infections also subsequently developed renal disease. Secondary amyloidosis was the predominant renal lesion in one dog. The predominant renal lesion in the second dog was membranoproliferative glomerulonephritis, although some amyloid was also present. The two dogs with renal disease also had positive rheumatoid factors. No other clinical or serological evidence of autoimmune disease or immune complex disease has been found. None of the dogs heterozygous for C3 deficiency, and none of the homozygous normal dogs in the colony has developed significant bacterial infections or renal disease. Thus, dogs deficient in C3, like C3-deficient humans, demonstrate both an increased susceptibility to infection and renal disease.
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PMID:The clinical manifestations of a genetically determined deficiency of the third component of complement in the dog. 298 27

Renal disease with distinctive pathologic features developed in two young women who had placental site trophoblastic tumors. The renal abnormalities were manifested by proteinuria in both cases and by hematuria in one case; blood pressure was elevated in one of the patients. Pathologic examination of the kidneys showed distinctive glomerular abnormalities, characterized mainly by the presence of occlusive eosinophilic deposits in many of the glomerular capillary lumina, most of which stained for fibrinogen-related antigens and IgM by immunohistochemical techniques. Ultrastructural examination showed the deposits to consist mainly of granular material that contained packets of fibrillar material with the appearance of fibrin. The uterine tumors were composed of mononucleated and multinucleated cells with abundant cytoplasm that infiltrated between the muscle bundles of the myometrium; in both tumors there was prominent deposition of eosinophilic material that had the tinctorial properties of fibrin and that stained for fibrinogen and IgM in immunoperoxidase studies. The renal abnormalities disappeared after hysterectomy in one case; the other patient, who was receiving chemotherapy and had disseminated intravascular coagulation, died with leukopenia and sepsis. The clinical and pathologic features in these cases suggest that the renal abnormalities were related to the uterine tumors and that the production of immune complexes and/or the activation of intravascular coagulation by the tumors were pathogenetic mechanisms.
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PMID:A distinctive glomerular lesion complicating placental site trophoblastic tumor: report of two cases. 298 14

Initially, poor long-term prognosis in patients with SLE and fear of recurrent disease dissuaded renal transplantation in this group of patients. However, in 1975 the Advisory Committee to the Renal Transplant Registry reported satisfactory 1-2-year results in 56 patients with SLE from 36 institutions. Subsequently, renal transplantation for SLE patients with end-stage renal disease has become more accepted, though it has been recommended that transplantation be postponed for at least one year after initiating dialysis. Five cases of recurrent lupus nephritis have been reported in the literature. However, since the long-term outcome after transplantation in this group of patients is not well established, we have examined the long-term outcome in SLE patients who underwent renal transplantation at the University of Minnesota. Thirty-two SLE patients receiving 33 transplants between December 1969 and December 1987 were studied retrospectively and compared with controls matched for age, sex, donor source, HLA match, date of transplant, and diabetic status. A total of 69% (22/32) of patients underwent less than 1 year of dialysis prior to transplantation, and 50% (16/32) experienced biopsy-proved acute rejection, which was reversible in 67% (11/16). Actuarial graft function and patient survival rate in SLE patients were not significantly different from those in the matched control group. Duration of prior dialysis did not affect outcome. Surviving grafts have excellent function as measured by serum creatinine (1.3 +/- 0.4 mg/dl, means +/- SD). Causes of death were sepsis (5) and myocardial infarction (1). One patient lost the graft from rejection after withdrawal of immunosuppression because of a malignancy one month posttransplant. Three patients lost graft function due to chronic rejection. To date no patients have had evidence of recurrent SLE nephritis.
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PMID:Single-center 1-15-year results of renal transplantation in patients with systemic lupus erythematosus. 305 93

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.
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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.
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PMID:Allograft membranous glomerulonephritis and renal-vein thrombosis in a patient with a lupus anticoagulant factor. 314 30


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