Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0032285 (pneumonia)
54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the rate of recurrence of focal segmental glomerulosclerosis (FSGS) in renal transplant patients treated with cyclosporine, we reviewed the outcome of 25 renal Tx performed in 24 patients who had FSGS as their original renal disease. After Tx, 6 patients were treated with steroids and azathioprine (follow-up: 42 +/- 34 months) and 19 with CsA (follow-up: 30 +/- 31 months). Two of 6 Aza treated patients (33%) developed recurrence of FSGS and nephrotic syndrome (NS). Both patients lost their graft because of FSGS 24 and 25 months after Tx. Ten of 19 patients (55%) given CsA showed recurrence of FSGS; one of them had had recurrence in the first graft treated with Aza. One patient lost his graft a few weeks after Tx because of acute rejection and 3 lost their graft because of FSGS 4-28 months after NS developed. One patient with NS died from pneumonia 14 months after Tx when his plasma creatinine was 2.7 mg/dl. Three other patients now have NS and plasma creatinine between 1.9 and 2.4 mg/dl 15-37 months after Tx. The last two patients have NS and normal renal function 10 and 31 months after Tx. In both groups, most patients developed NS within the first week after Tx. The patients with recurrence, given Aza or CsA, tended to be younger at the onset of the disease and to have a shorter duration of the disease, when compared with those without recurrence, but the differences were not statistically significant. In our experience neither CsA nor Aza showed any effect on the outcome of FSGS recurring in the graft.
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PMID:The recurrence of focal segmental glomerulosclerosis in kidney transplant patients treated with cyclosporine. 221 81

9 consecutive cases of Legionnaires' disease are presented, all of which involved either a pathological urinary sediment or acute renal insufficiency. Diabetic glomerular sclerosis and terminal septic shock in one patient accounted per se for the urinary findings and terminal oliguric renal failure. In the remaining 8 patients the renal abnormalities are interpreted as manifestations of Legionnaires' disease: these were acute renal insufficiency in 6, requiring dialysis treatment in 4, proteinuria in 7, hematuria in 5, leukocyturia in 5 and cylindruria in 3 patients. One patient died of pneumonia and one patient, without Legionella-related renal involvement, of septic shock. Renal histology of 5 patients showed acute interstitial nephritis in one and diffuse sclerosing interstitial nephritis in a second patient, whose biopsy was obtained after 3 months' hemodialysis treatment. In 3 patients renal biopsy findings were explained by preexisting renal pathology, i.e. diabetic nephropathy, chronic transplant rejection and shock kidney respectively. Renal failure requiring hemodialysis and urinary abnormalities were largely reversible.
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PMID:[Renal involvement in Legionnaires' disease]. 381 99

We describe a rare case of a rapidly progressive glomerulonephritis (RPGN) superimposed on diabetic nephropathy. A 68-year-old woman with non-insulin-dependent diabetes mellitus (NIDDM) complicated with diabetic triopathy demonstrated a rapid deterioration of renal function. Her urinary sediment contained many red blood cell (RBC) cells and casts, suggesting an additional renal disease accompanying diabetic nephropathy. Renal biopsy revealed crescent formation in many glomeruli characteristic of the pauci-immune type of RPGN. Steroid pulse therapy transiently halted the deterioration in renal function, but the patient died of pneumonia complicated with methicillin-resistant staphylococcus aureus (MRSA) infection. The unusual findings in diabetic nephropathy indicated the coexistence of primary glomerulonephritis and diabetic glomerulosclerosis in this case.
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PMID:Rapidly progressive glomerulonephritis concomitant with diabetic nephropathy. 947 49

A considerable permeability factor (or factors) derived from circulating T cells has a crucial role in proteinuria of nephrotic syndrome (NS). We attempted to remove pathogenic T cells through lymphocytapheresis (LCAP) in 6 patients with primary NS, 2 patients with minimal change nephrotic syndrome (MCNS), 2 patients with focal segmental glomerulosclerosis (FSGS), 1 patient with membranous nephropathy (MN), and 1 patient with MN and FSGS using Cellsorba (Asahi Medical Co., Osaka, Japan). LCAP was performed 2 times in 2 consecutive weeks and was followed with corticosteroid therapy with or without cyclosporine A in 5 patients. Two patients with MCNS, 1 with FSGS, and 1 with MN and FSGS showed a dramatic decrease of proteinuria (-30% and -94%) in their urine protein/creatinine ratio. Three out of 4 patients had a complete or partial remission (proteinuria <1g/day) within 8 weeks following immunosuppressive therapy. During the LCAP, T cells, especially activated T cells, decreased significantly in the response group. The other 2 patients, 1 with FSGS and 1 with MN, however, had no response to LCAP and following immunosuppressive therapy or low-density lipoprotein apheresis and suffered from end-stage renal failure or death by pneumonia. These results suggested that LCAP might have a beneficial effect on the treatment of NS, especially MCNS and in some patients with FSGS, despite varying responses to LCAP and concomitant immunosuppressive therapy.
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PMID:The beneficial effects of lymphocytapheresis for treatment of nephrotic syndrome. 1198 60

The clinical significance of the glomerular tip lesion, characterized by podocyte prominence, capsular adhesion, and/or intracapillary foam cells at or adjacent to the urinary pole, remains unclear. It has been postulated that this lesion simply represents a response to heavy proteinuria, and cases of nephrotic syndrome with tip lesions, but no other histological abnormalities, may represent a form of minimal change nephropathy (MCN). However, others have reported that such lesions have a clinical course similar to that of primary focal segmental glomerulosclerosis (FSGS), and the tip lesion often is included among histological variants of FSGS. To determine whether tip lesions may be seen in MCN, we examined histological slides of kidneys from pre-1950 autopsies of patients with a diagnosis of lipoid nephrosis, a term that at that time comprised MCN and FSGS. Before the introduction of antibiotics and corticosteroid therapy, patients with nephrotic syndrome frequently died of sepsis. Eight such cases, with autopsies performed from 1924 to 1943, were identified in which no glomeruli had changes typical of classic FSGS or membranous nephropathy. More than 400 glomeruli were present in each case. Patient ages ranged from 3 to 45 years (six patients <11 years), all had marked edema (duration, 2 weeks to 21 months) and heavy proteinuria, and each died of sepsis and/or pneumonia (pneumococcal in six patients). Glomerular tip lesions were found in five of these eight cases (range, 3 to 26 lesions per case; 0.3% to 4.4% of total glomeruli present), with no predilection for the deep, middle, or superficial cortex. No tip lesions were seen in kidneys from autopsies of age-matched patients without a history of glomerular disease. These findings suggest that the glomerular tip lesion can occur in MCN and most likely represents a response to heavy proteinuria that is not disease specific.
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PMID:Glomerular tip lesion in minimal change nephropathy: a study of autopsies before 1950. 1204 27

Mycophenolate mofetil is an immunosuppressive agent in transplantation which inhibits the purin neogenesis. Proliferating lymphocytes are suppressed and antibody production is decreased. Many cases of successful therapy in different kidney diseases are reported, such as diffuse proliferative lupus nephritis, pauci-immune necrotizing glomerulonephritis, focal segmental glomerular sclerosis and IgA nephropathy. We report 3 patients with IgA nephropathy who were treated with mycophenolate mofetil for more than 1 year. In all patients, proteinuria decreased significantly and the renal function remained stable. In 2 patients, kidney biopsy was repeated after 12 months and 18 months, respectively. There were no histological signs of progression of the disease. Two patients developed infections during treatment. One patient had a pneumonia, and a second patient an infection with varizella zoster. Based on our data, mycophenolate mofetil can be a potential treatment of IgA nephropathy. Further controlled studys are warranted to investigate the role of mycophenolate mofetil in IgA nephropathy.
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PMID:Therapy of IgA nephropathy with mycophenolate mofetil--report of 3 cases. 1507 72

Microscopic polyangiitis (MPA) is well known as a life-threatening member of a group of systemic vasculitis diseases. We report two cases of MPA. Case 1 was a 79-year-old-man who had been diagnosed with anti-neutrophil-cytoplasmic-antibody associated vasculitis (ANCA associated vasculitis) with alveolar hemorrhage and crescentric glomerulonephritis (CrGN). He presented with urticarial erythema in the abdomen, legs and back. The skin biopsy specimens showed leukocytoclastic vasculitis on the upper dermis. Case 2 was a 74-year-old-man, who presented with purpura on the abdomen, buttocks and legs that were similar to Henoch-Schonlein purpura (HSP). He also suffered from interstinal pneumonia. His renal biopsy specimens showed glomerulosclerosis and the peripheral pattern anti-neutrophil cytoplasmic antibody (P-ANCA) was positive. We reviewed the skin eruptions that had been reported with MPA, including our cases.
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PMID:Microscopic polyangiitis presenting urticarial erythema and Henoch-Schonlein purpura: two case reports. 1549 39

This investigation was carried out on 851 consecutive judicial autopsies of drug addicts who died mostly of heroin overdose from 1977 to 1996. Research of anti-HIV/HBV/HCV antibodies was performed, and histologic sections were retrospectively reviewed. More than 65% were HBV/HCV-positive and about 17% HIV-positive; females were HIV-positive more often than males. Intracranial microhemorrhages were frequently found; cerebral infectious diseases were rare. Inflammatory heart lesions, myocardial fibrosis, and acute ischemia were common. Interstitial nephritis (found in about 8%) was more frequent in females, in older patients, and in those carrying HIV infection; glomerular sclerosis was detected in about 12%. Acute bronchitis and/or pneumonia was demonstrated in 12%, without significant association with HIV infection; pulmonary hemorrhages, foreign body granulomas, and food aspiration were also commonly seen; hyperplasia of pulmonary perivascular lymphatic tissue was rather characteristic. Liver was carrying steatosis in 66.3% and/or hepatitis in 64.5%; acute hepatitis was more frequent in females, chronic hepatitis in older subjects and in those proven positive for hepatotropic viruses; cirrhosis occurred more often in older patients, in those carrying virus infection, and in consumers of nonnarcotics drugs such as ethanol. No pathologic finding was clearly related to drug abuse; therefore, during autopsy, drug addiction can be suspected, but anamnestic and circumstantial data are needed to lead pathologists to request toxicologic analysis to ascertain the cause of death. The present investigation emphasizes that, in addition to the risk of death by overdose, the high incidence of acute and chronic diseases could seriously undermine the health status of heroin and/or other drug consumers.
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PMID:Histopathological findings in 851 autopsies of drug addicts, with toxicologic and virologic correlations. 1589 41

Human immunodeficiency virus-associated nephropathy (HIVAN) is characterized by high-grade proteinuria and rapid progression to end-stage renal disease (ESRD). Despite the large numbers of HIV-infected cases in Asian countries, data on HIVAN in this area are limited. We report a 54-year-old Taiwanese man with HIVAN who presented with cytomegalovirus retinitis, renal insufficiency (serum creatinine, 3.8 mg/dL) and nephrotic range proteinuria with a daily protein loss of 10.8 g. Despite highly active antiretroviral therapy (HAART) for 31 months, renal failure developed requiring maintenance hemodialysis. Renal biopsy showed collapsing focal segmental glomerular sclerosis, podocyte proliferation and tubulointerstitial nephritis with mononuclear cell infiltration. These features were compatible with HIVAN. Although hemodialysis was instituted, he died 2 months later due to nosocomial pneumonia complicated with multiple organ failure. In summary, this case of HIVAN in a Taiwanese patient shows that the condition may progress to ESRD despite successful viral suppression with HAART.
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PMID:Human immunodeficiency virus-associated nephropathy. 1693 71

A 19-yr-old, 78.2-kg captive female Indochinese tiger (Panthera tigris corbetti) from the El Paso Zoo (El Paso, Texas, USA) with chronic renal disease was euthanized after a 10-day course of anorexia, depression, progressive rear limb weakness, muscle fasciculations, and head tremors. Postmortem findings included pericardial effusion, generalized lymphadenopathy, glomerulosclerosis, glomerular atrophy with membranous glomerulonephropathy, and pancreatic adenocarcinoma. Pyogranulomatous pneumonia, pericarditis, and lymphadenitis were associated with fungal spherules histomorphologically consistent with Coccidioides immitis. Rising antibodies to C. immitis were detected on samples obtained perimortem and 2 mo before euthanasia. Retrospective serology was negative for two additional Indochinese tigers, two Iranian leopards (Panthera pardus saxicolor), two jaguars (Panthera onca), two bobcats (Lynx rufus texensis), two ocelots (Leopardus pardalis), and three Amur leopards (Panthera pardus orientalis) housed at the zoo over an 8-yr period. Despite being located within the endemic region for C. immitis, this is only the second case of coccidioidomycosis reported from this institution.
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PMID:Disseminated coccidioidomycosis in a captive Indochinese tiger (Panthera tigris corbetti) with chronic renal disease. 1731 42


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