Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 20-year-old man developed a massive nephrotic syndrome, rapidly complicated by pulmonary embolism and septicemia. Two renal biopsies taken 3 months apart showed minimal change glomerulonephritis. Treatment with prednisolone 1.5 mg/kg/day failed to induce a sustained remission, then monotherapy with cyclosporin A (CsA, 5 mg/kg/day) was started. Complete remission was obtained after 15 weeks. CsA was gradually tapered to 3 mg/kg/day. Twenty-two months after starting CsA, a routine examination disclosed a right sub-clavicular lymph node, of which histological examination showed a class 4 large cell Hodgkin's lymphoma. CsA was abruptly withdrawn and a polychemotherapy resulted in lymphoma remission after four courses. Ten months later, Hodgkin's disease is currently in remission and there is no relapse of proteinuria.
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PMID:Cyclosporin A-sensitive nephrotic syndrome preceding Hodgkin's disease by 32 months. 238 97

Cases with a pathological diagnosis of renal venous thrombosis (RVT) associated with nephrotic syndrome (NS) were studied retrospectively for clinicopathological evaluation. The material consisted of 21 RVT cases which were diagnosed in 2000 consecutive pediatric necropsies, with an overall incidence of about one percent. Eight of the 21 RVT cases were associated with nephrotic syndrome (34%), and this group formed 0.4 percent of the total necropsies in our pediatric center. The glomerulopathies of these nephrotic patients consisted of three cases of Finnish-type congenital NS (FCNS), three cases of renal amyloidosis secondary to familial Mediterranean fever, and two cases of membranoproliferative glomerulonephritis (MPGN). The presence of sepsis associated with disseminated intravascular coagulation, and the morphological age of the thrombi suggested that the RVT was secondary to sepsis in the FCNS cases. In the MPGN and secondary renal amyloidosis cases, the long duration of both the nephrotic state and the administration of diuretics along with glucocorticoid treatment and also the newly formed thrombi without infarction are strong evidences, although not definite, that the RVT developed as a complication of the glomerulopathy. Even though there were no definite clinical criteria for the diagnosis of most of the RVT cases, we would like to emphasize the importance of flank pain, the rapid deterioration of renal functions in a stable nephrotic patient, as well as the hypercoagulable state in the consideration of the development of RVT which indicate the need for appropriate radiological studies for confirmation of this condition during life.
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PMID:The association of nephrotic syndrome and renal vein thrombosis: a clinicopathological analysis of eight pediatric patients. 260 31

In December, 1984, an outbreak of pyoderma affected five scrum players in the St Thomas' Hospital rugby team. The causative organism, Streptococcus pyogenes, was acquired during a match against a team experiencing an outbreak of impetigo, and was transmitted to two front row players of another team a week later, and to two girlfriends of affected St Thomas' players a month later. The strain was M-type 49, tetracycline-resistant, and virulent. It caused salpingitis in a girlfriend and acute glomerulonephritis in one rugby player. No case of subclinical glomerulonephritis was detected in eight patients with pyoderma. Screening of the St Thomas' Hospital team revealed four further cases of non-streptococcal skin infection, with evidence for contemporaneous spread of Staphylococcus aureus. Teams should not field players with sepsis, and it may be advisable to apply a skin antiseptic to traumatised skin after the match.
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PMID:Scrum kidney: epidemic pyoderma caused by a nephritogenic Streptococcus pyogenes in a rugby team. 287 37

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

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

Three unrelated severe infections with Streptococcus zooepidemicus occurred in England in 1985. The first patient developed septic arthritis, which has not been recorded before with this organism. The second died with septicaemia, pneumonia and post-streptococcal glomerulonephritis, the only record so far of nephritis following sporadic S. zooepidemicus infection and of nephritis and systemic sepsis in the same patient. The third patient experienced septicaemia during pregnancy but recovered without complications. A likely animal source of infection was found in only one case.
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PMID:Human infection with Streptococcus zooepidemicus (Lancefield group C): three case reports. 355 45

Diffuse crescentic glomerulonephritis was observed in a 40-year-old male patient who had a ventriculoatrial shunt implanted after a traffic accident 10 years previously. Immediately after treatment with immunosuppressants and plasma pheresis, signs of meningitis and septicemia developed. The responsible organism isolated was Staphylococcus albus. After the shunt was removed, clinical signs and renal function improved, associated with normalization of hypocomplementemia and disappearance of cryoglobulin and circulating immune complexes. Repeat renal biopsy performed 5 months after the removal of the shunt revealed mild mesangial proliferative and sclerotic glomerulonephritis with fibrous crescents. No apparent deposits observed in the initial biopsy were found on ultrastructural and immunofluorescent examinations. The reported cases with serial renal biopsies before and after the removal of the shunt were reviewed.
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PMID:Shunt nephritis: histological dynamics following removal of the shunt. Case report and review of the literature. 400 Mar 30

Seventy-five black children from 0 to ten years old with pneumococcal bacteraemia, who were hospitalized during a one-year period, were studied retrospectively from case records. Half the children were under one year and 68% under two years of age. Sixty-seven per cent were malnourished, 34% severely so. The overall case-fatality-rate was 26.7% being highest in children presenting in autumn (52.4%) and in those with meningitis (54.5%), severe protein-calorie malnutrition (42.8%) or associated infections (61.5%). Host defences against the pneumococcus are discussed, especially in relation to their deficiencies in malnourished and young children. Special mention is made of early-onset neonatal sepsis due to the pneumococcus and of the association between pneumococcal bacteraemia and acute post-streptococcal glomerulonephritis. This study indicates that pneumococcal bacteraemia is a serious infection in children, especially in those with malnutrition and other infections. In view of the emergence of penicillin-resistant strains, its treatment may become more difficult in the future.
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PMID:Pneumococcal bacteraemia--a study of 75 black children. 618 74

Thirty-nine cadaveric renal allografts were performed in 28 children under 6 years of age. Common primary renal diseases were glomerulonephritis, dysplasia/hypoplasia, and reflux/obstructive nephropathy. After a mean follow-up of 40 months of patients with surviving grafts, 19 patients had functioning grafts, 3 had returned to dialysis, and 6 had died. These children required an extraordinary amount of care postoperatively because of anorexia, diarrhea, and ileus. Their psychomotor and physical development was retarded prior to transplant; this reversed dramatically after transplant, but catch-up growth occurred in only 4 patients. Many patients were noticeably more active and distractible for 1 to 2 years post-transplant. Major causes of graft failure were primary nonfunction of 5 donor kidneys (4 from donors under 1 year old) and renal vessel thrombosis in 5 recipients (3 with native kidneys in place who received kidneys from donors over 10 years old). Other causes were recurrence of hemolytic uremic syndrome and Wilms tumor, rejection, and sepsis. Kidneys from donors under 1 year old proved unsatisfactory, and large donor kidneys in small children tended to thrombose, especially when native kidneys with high urine output were left in situ.
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PMID:Cadaveric renal transplants in children under 6 years of age. 636 47


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