Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To disclose the prevalence of thin membrane nephropathy (TMN) in China and its clinical and pathological features, we prospectively studied TMN cases including 722 cases of renal biopsies in 2 years. 27 cases (male 7 cases, female 20) were diagnosed as primary glomerulonephritis. The GBM thicknesses of TMN group (n = 27) and control group (n = 32) was 207 +/- 36 nm and 382 +/- 34 nm (P < 0.01) respectively. IF of TMN was negative or trace, near normal morphology or mild mesangial proliferative glomerulo nephritis was observed by LM. A few of them had global glomerular sclerosis or single crescent formation. All TMN patients had microscopic hematuria. About one third (9/27 cases) patients with TMN presented isolated persistent microscopic hemataria, 44.4% (12/27 cases) and 22.2% (6/27 cases) patients with TMN were accompanied with mildmoderate proteinuria and heavy proteinuria (> or = 3.5 g/24 h) or nephrotic syndrome. The patients with heavy proteinuria or nephrotic syndrome had good response to corticosteroid therapy. All patients with TMN had normal renal function, only a few of them had transient hypertension. The results showed that the prognosis of TMN would be regarded as good. The familial history of 15 patients with TMN was investigated, and 47% (7/15 cases) of them had > or = two members with microscopic hematuria in their families. TMN was found in 3.7% (27/722 cases) in total renal biopsies and 11.5% (9/78 cases) in the patients with isolated microscopic hematuria. It suggests that TMN isn't a rare kidney disease in China. Careful EM is a critical method for the correct diagnosis of TMN.
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PMID:[Thin membrane nephropathy: 27 cases]. 1045 44

Dissemination of gliomas outside the central nervous system without preceding neurosurgery is a rare phenomenon. Glial neoplasms presenting as bone lesions are even more rare. A case of glioblastoma multiforme (GBM) with initial presentation in the orbit following a single generalized seizure is described. Signs of intracranial hypertension resulted from subarachnoid tumor invasion. The patient was treated with whole-dose radiation therapy but survived for only 6 months following the initial presentation. An autopsy revealed a right temporal GBM with extensive subarachnoid spread and invasion in the left orbit and skull base. The literature on dissemination of primary tumors of the brain is reviewed.
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PMID:Right temporal lobe glioblastoma presenting in the left orbit. Case report. 1076 63

Over a 31-year period, we have encountered 13 children with a disease entity not reported by other clinics that leads to rapidly progressive crescentic glomerulonephritis. Gross hematuria, rapidly declining renal function, and a serum C3 level at the lower limit of normal or slightly depressed usually characterized the disease onset; hypertension and nephrotic syndrome were absent. Glomerular IgG was absent, but large C3-containing subepithelial deposits on the paramesangial basement membrane (GBM) were always present. Because of these deposits and because dense alteration of the GBM was found in 3 patients, the disease may resemble membranoproliferative glomerulonephritis type II, but is distinguishable on other morphological and clinical grounds. The absence of anti-neutrophil cytoplasmic antibody, tested for in 5 of 13 patients, is one of several ways the disease differs from the pauci-immune glomerulonephritis of adults. Clinically and by glomerular morphology, it also differs from severe poststreptococcal acute glomerulonephritis. Treatment with high-dose corticosteroids has been highly successful. Because in this series the disease occurred only in children under age 12 years and the amount of silver-positive mesangial matrix was normal, indicating absence of mesangial proliferation, it has been designated juvenile acute non-proliferative glomerulitis.
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PMID:Acute non-proliferative glomerulitis: a cause of renal failure unique to children. 1095 28

A 56-year-old male with DM and HTN presented with flank pain and nausea. Review of systems was negative, physical examination was notable for mild hypovolemia and laboratory revealed BUN 51 mg/dl, creatinine (Cr) 5.1 mg/dl (baseline 1.5), Westergren ESR 122 mm/h, fractional excretion of sodium 0.2% and UA positive for blood and protein. Despite volume resuscitation the Cr continued to rise. Urine sediment analysis revealed granular casts, renal tubular epithelial cells and a negative Hansel's stain. Hemodialysis was initiated with Cr 13.7 mg/ dl for dyspnea and dysgeusia. Subsequent laboratory data revealed 2 separate positive anti-GBM antibody titers and prednisone therapy was initiated. Renal biopsy was performed for further diagnostic, therapeutic and prognostic information and demonstrated interstitial nephritis with linear IgG and albumin deposition consistent with diabetic nephropathy. Follow-up antibody titers were negative. prednisone was discontinued and Cr stabilized with conservative therapy. Anti-GBM antibody disease is characterized by circulating IgG antibodies directed against the glomerular basement membrane, specifically the alpha-3 (IV) collagen chain. Anti-GBM nephritis is a rapidly progressive, isolated glomerulonephritis in association with circulating anti-GBM antibodies. A positive immunofluorescence (IF) test is considered diagnostic in the appropriate clinical setting. Therapies include immunosuppressive agents to suppress new antibody production and plasmapheresis to eliminate circulating antibodies. Anti-GBM antibody is not rapidly cleared by steroid therapy and the recovery of renal function is rare if initiation Cr is greater than 7 mg/dl. This case demonstrates that the current ELISA for alpha-3 (IV) collagen is not pathognomonic for anti-GBM nephritis and that renal biopsy with IF for IgG and albumin may be indicated to prevent administration of potentially toxic treatment.
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PMID:Diabetic nephropathy with interstitial nephritis presenting with a false-positive anti-GBM antibody. 1203 99

A previous placebo-controlled trial has shown that biodegradable 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) wafers (Gliadel wafers) prolong survival in patients with recurrent glioblastoma multiforme. A previously completed phase 3 trial, also placebo controlled, in 32 patients with newly diagnosed malignant glioma also demonstrated a survival benefit in those patients treated with BCNU wafers. Because of the small number of patients in that trial, a larger phase 3 trial was performed to confirm these results. Two hundred forty patients were randomized to receive either BCNU or placebo wafers at the time of primary surgical resection; both groups were treated with external beam radiation postoperatively. The two groups were similar for age, sex, Karnofsky performance status (KPS), and tumor histology. Median survival in the intent-to-treat group was 13.9 months for the BCNU wafer-treated group and 11.6 months for the placebo-treated group (log-rank P -value stratified by country = 0.03), with a 29% reduction in the risk of death in the treatment group. When adjusted for factors affecting survival, the treatment effect remained positive with a risk reduction of 28% ( P = 0.03). Time to decline in KPS and in 10/11 neuroperformance measures was statistically significantly prolonged in the BCNU wafer-treated group ( P </= 0.05). Adverse events were comparable for the 2 groups, except for CSF leak (5% in the BCNU wafer-treated group vs. 0.8% in the placebo-treated group) and intracranial hypertension (9.1% in the BCNU wafer-treated group vs. 1.7% in the placebo group). This study confirms that local chemotherapy with BCNU wafers is well tolerated and offers a survival benefit to patients with newly diagnosed malignant glioma.
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PMID:A phase 3 trial of local chemotherapy with biodegradable carmustine (BCNU) wafers (Gliadel wafers) in patients with primary malignant glioma. 1267 79

A 5-year randomized, double blind, placebo-controlled study was carried out to determine the effect of the angiotensin-converting enzyme (ACE) inhibitor enalapril (E) on the progress of renal function and histology in subjects with type 1 diabetes and microalbuminuria. Seventy three type 1 diabetic patients with BP <140/90 and with persistent albuminuria (AER 20-200 microg/min) and normal renal function were randomly assigned to receive E (n=37) or placebo (n=36). A percutaneous renal biopsy was successfully performed in 69 patients and repeated in 59 patients after 5 years. The mean glomerular volume (MGV), mesangial volume (Vv mes) and glomerular basement membrane thickness (GBMT) were measured histomorphometrically. Before treatment, both groups had similar clinical characteristics, blood pressure, HbA(1c), albumin excretion rate (AER), glomerular filtration rate (GFR), serum creatinine and renal structural damage. Blood pressure was well controlled in both groups. In the patients treated with E, albuminuria decreased significantly (P<0.05) and only 8.1% (3/37) of subjects progressed to clinical albuminuria (AER >300 mg/24 h) compared with 30.5% (11/36) in the placebo group. The E treatment resulted in absolute risk reduction of 22.4 percentage points for the development of clinical albuminuria over a 5-year period (P<0.01). After 5 years of treatment, GBM thickness showed a consistent, though statistically insignificant, increase in the placebo group, whereas it remained stable in the E group. A significant increase in MGV and Vv mes was also observed in the placebo group on completion of the study. The present study indicates that long term therapy with E may decrease or delay the progression of structural glomerular damage in microalbuminuric diabetic subjects without marked hypertension (BP <140/90).
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PMID:Effect of 5-year enalapril therapy on progression of microalbuminuria and glomerular structural changes in type 1 diabetic subjects. 1270 22

The study reports on plasma total homocysteine (tHcy) levels in Tunisian patients with chronic renal failure (CRF) and those treated with hemodialysis (HD) and renal transplant (RT). The aims of the study were to identify the determinants of tHcy concentration and to test the association between hyperhomocysteinemia and atherothrombotic disease in end-stage renal disease (ESRD). A total of 35 CRF patients on conservative treatment, 50 HD patients, and 30 RT recipients, and 31 age- and sex-matched healthy subjects were included. Plasma tHcy was assessed by a fluorescent-polarizing immunoassay method. Multivariate analysis was applied to identify the main determinants of tHcy concentration and to assess the relationship between hyperhomocysteinemia and cardiovascular disease. Plasma mean tHcy concentration was significantly increased (p < 0.001) in CRF patients (mean +/- SD) (28.9 +/- 9.8 micromol/l), in HD patients (29.4 +/- 11.1 micromol/l), and in RT (19.3 +/- 6.3 micromol/l) patients compared to controls (11.9 +/- 4.1 micromol/l). Multivariate analysis using GLM ANOVA modeling demonstrated that tHcy was significantly higher in males (p = 0.02), and was related to age (p = 0.008), albumin (p = 0.005), vitamin B12 (p = 0.002), folate (p = 0.00001), and creatinine clearance (p = 0.0008). However, tHcy was not associated with C-reactive protein and did not significantly differ between CRF, HD, or RT patients. The upper quartile of tHcy concentration was significantly associated with atherothrombotic cardiovascular disease (unadjusted odds ratio (OR) = 3.09; 95% CI, 1.11-8.61; p = 0.01). This association remained significant after adjusting for sex, age, hypertension, and smoking (multi-adjusted OR = 4.78; 95% CI, 1.92-11.9; p = 0.0008). The mean tHcy concentration was 2 to 3 times higher in ESRD patients than in subjects with normal renal function. This increase could be related to glomerular filtration rate reduction and functional B vitamins deficiency, but was not associated with inflammation. The upper quartile of tHcy concentrations confers 4.78-fold increased independent risk for atherothrombotic events in ESRD patients.
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PMID:Hyperhomocysteinemia and end-stage renal disease: determinants and association with cardiovascular disease in Tunisian patients. 1281 66

We report an anti-GBM antibody-positive crescentic glomerulonephritis patient who benefitted from maintenance hemodialysis 4 months after the initial treatment, which included steroid pulse therapy and plasma exchange. A-29-year-old male was referred to our hospital because of high fever, abnormal urinary findings (leukocytes 3+, protein 2+, occult blood 3+) and a moderate degree of azotemia(S-Cr 2.9 mg/dl). C-reactive protein (CRP) was 18.9 mg/dl and antibiotics were administered intravenously for 7 days under the diagnosis of pyelonephritis. High fever persisted, however, and S-Cr increased to 9.2 mg/dl even though a sufficient volume of urine was maintained. Blood and urine cultures were negative for bacteria. A kidney biopsy was performed and cellular crescents were observed around the glomeruli. No abnormal finding was observed in the lung and the nasopharyngeal region. To treat the crescentic glomerulonephritis, steroid and cyclophosphamide were administered while hemodialysis was carried out simultaneously. Although P-ANCA and C-ANCA were negative, anti-GBM antibody was proven to be positive thereafter (169 U) and six sessions of plasmapheresis were additionally performed to remove the antibody. Two months after the last plasmapheresis, the reduced urine volume (300 ml/day) gradually returned to normal. Hemodialysis was terminated because the S-Cr concentration reached a plateau at 4 mg/dl. Repeated biopsy revealed marked glomerulosclerosis, hence hypertension treatment and a low protein diet were ordered. In conclusion, residual renal function might improve even after 4 months of hemodialysis in cases of intensively treated anti-GBM-positive crescentic glomerulonephritis, though consecutive renoprotective therapy is required.
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PMID:[A case of anti-GBM-antibody positive rapidly progressive glomerulonephritis who was weaned from hemodialysis after combination therapy with steroid and plasmapheresis]. 1640 34

With the aim to investigate microvascular endothelial function in chronic kidney disease (CKD) patients on conservative treatment, skin blood flowmotion (SBF) was explored by spectral Fourier analysis of skin forearm laser Doppler tracing, registered before and following forearm ischemia in 32 III to V stage CKD patients (23 males, mean age: 52+/-12 years), without diabetes or cardiovascular disease, and in 32 age and sex matched healthy subjects. The power spectral density (PSD) of the 0.009-1.6 Hz total spectrum SBF, as well as of five sub-intervals, each of them related to endothelial (0.009-0.02 Hz), sympathetic (0.02-0.06 Hz), myogenic (0.06-0.2 Hz), respiratory (0.2-0.6 Hz) or cardiac (0.6-1.6 Hz) activity, was measured in PU(2)/Hz (PU=perfusion unit; 1 PU=10 mV). Under basal conditions CKD patients and controls did not differ in skin perfusion or in PSD of total spectrum SBF, as well as of each of the five subintervals considered. No substantial difference was also observed in skin post-ischemic hyperemia between patients and controls. A significant post-ischemic increase in the normalized value of endothelial sub-interval was observed in controls (p<0.05, GLM ANOVA analysis of variance), but not in CKD patients. A lower per cent increase in absolute PSD value of endothelial sub-interval was also observed in CKD patients compared to controls (185+/-98 % vs 279+/-243 %, p<0.05). The post-ischemic per cent increase in absolute PSD of endothelial sub-interval was negatively related to the systolic blood pressure (r=-0.45, p<0.01), to the mean arterial blood pressure (r=-0.40, p<0.05) and to the PTH serum levels (r=-0.38, p<0.05) in CKD patients. The blunted post-ischemic increase of the endothelial SBF sub-interval can be considered an early sign of microvascular endothelial dysfunction in the CKD studied patients. Arterial hypertension seems to be the main factor related to this SBF abnormality, together with the hormonal CKD related abnormalities.
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PMID:Blunted post-ischemic increase of the endothelial skin blood flowmotion component as early sign of endothelial dysfunction in chronic kidney disease patients. 1793 69

Pleomorphic xanthoastrocytoma (PXA) is a rare primary astrocytic tumour of the nervous system usually involving the superficial temporal cortex of children and young adults. Although the tumour may exhibit histological features of pleomorphism or cellular atypia, the overall prognosis is good compared with other glial tumours, with only 30% of PXA recurring and 20% undergoing anaplastic transformation. Increased mitotic activity, high MIB-1 and proliferating cell nuclear antigen labelling indices and necrosis are poor prognostic factors, whereas abundant lymphocytic infiltration is associated with more benign biological behaviour. Rarely, in older patients, PXA may have a poor prognosis as these patients tend to have intracranial hypertension and focal deficits, as well as histological features of mitosis, increased cellularity and necrosis. We report the case of a 76-year-old woman who presented with dysphasia and right hemiparesis. A left fronto-temporal lobe PXA was misdiagnosed as glioblastoma multiforme. Although a rare and benign tumour type, PXA in the elderly tend to be more malignant, may have the radiological appearance of a malignant tumour and have poor prognosis.
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PMID:Pleomorphic xanthoastrocytoma in elderly patients may portend a poor prognosis. 1825 94


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