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)

During the last 3.5 years we have had facilities to perform effective plasma exchange treatment (PE). During this period of time 12 patients of idiopathic and 19 patients of collagenous rapidly progressive glomerulonephritis (RPGN) appeared, Goodpasture's syndrome excluded. In an attempt to evaluate the separate effect of immunosuppression (IS) and PE, PE was if possible withheld for two weeks. In 3 patients IS alone had a satisfactory effect and therefore no PE was performed. In 2 severely ill patients IS and PE were instituted simultaneously. In 6 patients PE was started 5-12 days and in 17 patients at least 14 days after the start of IS. In 3 patients PE was started first because of suspected septicemia. 23 of the 31 patients improved; 6 from IS alone, 3 from IS and probably also from PE, 1 from PE and probably from IS, 5 both from IS and PE and 1 from PE alone. In 7 patients the individual effect of IS and PE could not be evaluated. At follow up 1-37 (median 13) months 13 patients had a S-creatinine below 200, 2 patients 200-300 and 1 patient 510 mumol/l. 3 patients went into RDT immediately and 7 after 4-22 months. 5 elderly patients died, only 1 from uremia, the others from cardiovascular diseases. The outcome was unpredictable from clinical and laboratory data. Addition of PE in the treatment of RPGN seems to have improved the outcome considerably.
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PMID:Improved outcome in rapidly progressive glomerulonephritis by plasma exchange treatment. 664 28

We have determined the level of persisting pneumococcal antibody in a group of nephrotic children vaccinated by us 5 years ago. Of the 19 vaccinated children, 2 have died and 1 has moved away. Sera from the remaining 16 patients were examined by radioimmunoassay to determine the antibody response to 11 of the 14 types contained in the polyvalent pneumococcal vaccine. The lowest protective level of geometric mean titre (GMT) of antibody in our laboratory is 300 ng antibody nitrogen per millilitre. 56% (9/16) of the patients showed adequate GMT 5 years after vaccination. All 9 patients had minimal change nephrotic syndrome. 44% (7/16) of the children had a GMT less than 300 ng antibody nitrogen per millilitre. 3 of these patients had focal sclerosis, 3 had membranoproliferative glomerulonephritis, and 1 patient had IgM nephropathy. Of these 7 patients, 1 with the lowest GMT (23 ng antibody nitrogen per millilitre) developed pneumococcal peritonitis. During this same period, in 20 other unvaccinated nephrotic patients followed continuously from 1976 to 1981, 7 cases of pneumococcal peritonitis occurred (p less than 0.05). Additionally, 1 unvaccinated child died of pneumococcal sepsis. Our study indicates that patients with minimal change nephrotic syndrome continue to maintain adequate amounts of antibody, but those with disease other than minimal change nephrotic syndrome are unable to maintain an adequate level of antibody.
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PMID:Persistence of protective pneumococcal antibody following vaccination in patients with the nephrotic syndrome. 673 97

The experience of the Peter Bent Brigham Hospital with 217 renal allografts functioning for more than 5 years is reviewed. Patient and graft survival were similar after 5 years, with patient survival being 88 and 66% at 10 and 15 years, respectively, and graft survival 85 and 75% at the same time intervals. Actuarial graft survival at 15 years was higher than patient survival because death with a functioning graft was not considered to be graft failure. No differences in patients or graft survival were found between living related and cadaver donor allografts. There were 33 deaths (15.2%), occurring from 5 1/2 to 20 1/2 years post-transplantation. Chronic liver failure and sepsis were the most common causes of death. Thirty-two patients (14.7%) lost their grafts after 5 years, most commonly from chronic rejection. Another 33 patients (15.2%) had evidence of graft dysfunction secondary to chronic rejection, recurrent glomerulonephritis, ureteral obstruction, or renal artery stenosis. Chronic rejection was generally not responsive to alterations in immunosuppressive medication. Complications of varying severity were common affecting 204 (94%) of the patients. The most frequent were hypertension, cataracts, avascular necrosis, malignancy, urinary tract infection, and pneumonia. These data demonstrate that transplant-related mortality and morbidity continue to occur in recipients of long-term renal allografts. These patients require careful and continuing care in medical centers experienced in transplantation.
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PMID:Late mortality and morbidity in recipients of long-term renal allografts. 681 39

The use of 131I-orthiodohippurate (OIH) scintigraphy combined with the estimated renal plasma flow (ERPF) and excretion index (EI) has been beneficial in separating impaired renal function due to graft rejection from acute tubular necrosis, ureteral obstruction, urinary extravasation and in some instances renal artery occlusion. The radionuclide data accurately identified acute and chronic rejection, confirmed by the clinical course, increase in BUN and serum creatinine and on occasion renal biopsy. Reversible and irreversible acute tubular necrosis (ATN) were clearly differentiated from acute rejection. When the ERPF and EI were plotted on a graph, multiple sequential radionuclide studies accurately predicted graft survival when chronic rejection existed. The limitation of this technique was the inability to discriminate between renal artery stenosis, ureteral obstruction and inflammatory disease. Scintigraphic studies did not distinguish between renal artery stenosis and chronic rejection. In these circumstances arteriography was the diagnostic procedure of choice. Although ureteral obstruction often can be correctly diagnosed by scintigrams, the ERPF, EI and intravenous pyelogram remained the most accurate diagnostic procedures. Recurrent glomerulonephritis, gram negative septicemia and generalized viral illness (herpes zoster or cytomegalovirus) simulated acute rejection and had to be separated by renal biopsy or the clinical course. The most valuable features of the radionuclide technique included: 1) the noninvasive method, 2) the simplicity, 3) the rapidity and 4) the reproducibility.
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PMID:Diagnosis of impaired renal function after kidney transplantation using renal scintigraphy, renal plasma flow and urinary excretion of hippurate. 698 32

We have previously described (Medicine 56:493, 1977) 12 patients with diffuse lupus glomerulonephritis who had no clinical or laboratory evidence of renal involvement at the time of the initial biopsy. In this article we report the course of 10 of these patients followed for 5-11 yr (mean 83 mo). One patient died in renal failure and two others of related causes (septicemia and subarachnoid hemorrhage). Seven patients (Group I) had a benign course from a renal standpoint, with stable renal function and mild or no urinary abnormalities. Repeat biopsy in four patients in this group revealed near complete resolution of the original lesion in two and considerable improvement in two others, who now have primarily mesangial hypercellularity and a focal lesion, respectively. Renal function deteriorated in three patients (Group II), resulting in loss of congruent to 50% of GFR in two and renal death in the third. Repeat biopsy in one of these patients showed a more severe, albeit focal, glomerulonephritis. Prognosis for renal function appears better in patients with silent nephropathy, but larger numbers are required to substantiate this impression. Until definitive answers become available, we believe it prudent to biopsy SLE patients even in the absence of overt renal involvement and to treat those with diffuse proliferative glomerulonephritis.
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PMID:Silent diffuse lupus nephritis: long-term follow-up. 704 6

Attempts were made to evaluate the separate effect on kidney function of immunosuppressive treatment (IS) and plasma exchange (PE) in 27 patients with rapidly progressive glomerulonephritis (RPGN). Twenty-four of the patients were treated with PE. Initial IS was supplemented with PE within 6-12 days in 5 patients, and after at least 14 days in 13. Because of suspected septicemia, 2 patients were first treated with PE, and IS was not initiated until the possibility of septicemia had been excluded. In 4 severely ill patients wih rapid clinical deterioration, both treatments were started simultaneously. Twenty patients improved during one or both treatments, 4 with IS alone, 2 with IS and doubtfully with PE, 3 with IS and probably also with PE, 5 both with IS and PE and one with PE alone. In 5 patients the individual effects of IS and PE could not be evaluated. In another 2 patients the combined treatment seemed to influence the course favourably. In the remaining 7 patients the effect of the treatment was doubtful or nil. Two further patients with Goodpasture's syndrome were treated. They were admitted late, and both kinds of treatment were instituted simultaneously. One of them died in respiratory insufficiency, the other remained oliguric while the pulmonary changes faded. Thus, PE added a positive effect to IS in several patients with RPGN. The treatment had few and mostly mild side-effects.
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PMID:Immunosuppression and the additive effect of plasma exchange in treatment of rapidly progressive glomerulonephritis. 714 2

Circulating immune complexes were determined with the 125I-Clq binding assay and the conglutinin binding assay in a prospective, longitudinal study of 40 patients with infective endocarditis, 34 patients with endocardial defects and nonseptic fever and 25 patients with septicemia without endocarditis. Fourteen patients with uncomplicated valvular lesions constituted a control group. Upon admission, 63 percent of the patients with infective endocarditis had a positive 125I-Clq binding assay versus 9, 12 and 7 percent, respectively, of the other three groups (p less than 0.001). The incidence of positive conglutinin binding assays became significantly higher during the course of infective endocarditis (53 percent) than during the course of nonseptic fever (21 percent), but, upon admission, this difference was not significant. The high incidence of Clq-binding immune complexes among patients with infective endocarditis could be attributed mainly to those patients with the characteristic features of subacute endocarditis. The incidence of circulating immune complexes in acute endocarditis was low and did not contribute to making the clinically important distinction from septicemia without endocarditis. A rise in the 125I-Clq binding assay levels during the course of infective endocarditis correlated significantly (p less than 0.01) with failure of antibiotic treatment. With the 125I-Clq binding assay, significantly higher levels were found in patients with signs of renal involvement of cutaneous vasculitis than in patients without these extracardiac manifestations of endocarditis. These results show that the determination of circulating immune complexes has clinical implications for both the diagnosis and the management of infective endocarditis and that circulating immune complexes are probably involved in the development of glomerulonephritis and vasculitis.
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PMID:The clinical implications and the pathogenetic significance of circulating immune complexes in infective endocarditis. 724 77

A 16-year-old student was admitted with acute, oliguric renal failure complicating staphylococcal sepsis. During treatment with methicillin drug hypersensitivity was suspected, and antibiotic was changed to vancomycin; by day 19 hemodialysis was discontinued. Renal biopsy showed two pathologic processes: acute exudative glomerulonephritis and widespread tubulointerstitial nephritis. In addition to glomerular immunoglobulin and C'3 deposits, interstitial and focal tubular basement membrane deposits of IgG were seen. Antiserum to DPO (methicillin) haptens localized apparently to the same tubular sites, as did fluorescein-conjugated antibodies from the patient's serum. The data suggest that interstitial nephritis was caused by serum antibodies to methicillin which bound to sites in renal tubules to which methicillin also had fixed. The acute tubulointerstitial nephritis complicated acute oliguric glomerulonephritis of staphylococcal sepsis.
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PMID:Interstitial nephritis caused by methicillin. Studies in a case complicating staphylococcal sepsis with acute glomerulonephritis. 728 31

We reported a case of type II cryoglobulinemia involving glomerulopathy associated with HCV-induced liver cirrhosis. The patient was a 57-year-old woman. Her past history included chronic hepatitis at 51 years and rheumatoid arthritis at 53 years of age. At 46 years, an erythematous lesion appeared on her legs, which was diagnosed as allergic vasculitis by skin biopsy. At 50 years, proteinuria, hematuria and hypertension were recognized. The next year, the first renal biopsy was performed and showed membranoproliferative glomerulonephritis (MPGN). Recently, the edema of her legs has progressed, and the laboratory data showed proteinuria, hematuria, hypocomplementemia, rheumatoid factor positivity, and increase of monoclonal IgG kappa chain. The second renal biopsy revealed an endocapillary proliferative glomerulonephritis-like lesion with marked infiltration of monocytes and macrophages. The subendothelial deposit showed a fine fibril-like pattern. She was treated with steroids and double filtration plasmapheresis (DFPP) therapy, but the treatment was not very effective. She died of liver cirrhosis, which was probably induced by hepatitis C virus (HCV), and sepsis. Generally, the patients of type II cryoglobulinemia often showed HCV antibody positivity, pointing to HCV as an etiological factor. In this case, renal biopsy was performed twice in the same patient, and the histologic findings suggest the clinicopathological course of cryoglobulinemia.
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PMID:[A case of type II cryoglobulinemia involving glomerulopathy associated with hepatitis C antibody]. 750 47

Before the introduction of antibiotics, serious infections caused by Streptococcus pyogenes (Lancefield Group A streptococci) were common. Before World War II, this bacterium was responsible for as many as 50% of postpartum deaths and was the major cause of death in patients with burns. Also common were the sequelae of streptococcal infections-rheumatic fever and post-streptococcal glomerulonephritis. With the use of penicillin, however, Streptococcus pyogenes was believed to be virtually eliminated as a pathogen. The organism was consigned to the history books, but not for long. In the mid-1980s, focal resurgences of rheumatic fever began to be reported from different areas in the USA, such as Salt Lake City, Utah. In such communities, where increases in cases of rheumatic fever had been reported, the serotypes M-1, 3, 5, 6 and 18 were isolated which, on culture, produced characteristic mucoid colonies. At the same time, reports of increases in invasive streptococcal disease began to surface in both the USA and Europe. Two syndromes were described; invasive streptococcal infection, occurring in previously healthy children and adults, commonly associated with septicaemia resulting from a deep focus of infection such as bone or lung; and streptococcal toxic shock syndrome, involving a cutaneous focus, accompanied by necrotizing or bullous soft tissue changes. Septicaemia is rare in streptococcal toxic shock syndrome, but the most characteristic feature is one of rapidly progressing multi-organ failure. A high proportion of the strains of Streptococcus pyogenes associated with this condition are serotype M-1, and fatality rates approaching 50% have been reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Invasive streptococci. 772 68


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