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)

We evaluated clinical and morphological findings in 254 patients (138 men and 116 women), with idiopathic membranous glomerulonephritis (IMGN). The mean age was 44 years. At time of biopsy proteinuria was found in 98%, nephrotic syndrome (NS) in 45.2%, hypertension in 10%, elevated serum creatinine concentration of greater than or equal to 1.4 g/dl in 24%, and markedly decreased Ccr (less than or equal to 40 ml/min) in 12.5% of the patients. Of 254 patients, 51 (20%) were classified as Stage I, 131 (52%) as Stage II, 52 (20.5%) as Stage III, 9 (3.5%) as Stage IV and 11 (4.3%) as Stage V, which was a relapsing form. Both intraglomerular, peripheral electron dense deposit-size and mean thickness of the glomerular basement membrane (GBMt) were analyzed by ultrastructural morphometric methods. In patients with NS, both the mean deposit-size and the mean GBMt were largest when compared to all others (p less than 0.01). The largest subepithelial deposits (SED), in mean, were observed in Stages II and V, while the largest incorporated deposits (ICD) were measured in Stages II and IV. The mean GBMt was largest in Stage III. Furthermore, there were strong correlations between the degree of proteinuria and the deposit-size (r = 0.603, p less than 0.001), and GBMt (r = 0.456, p less than 0.001). The GBMt showed a correlation with serum creatinine concentration (r = 0.476, p less than 0.001) and Ccr (r = 0.471, p less than 0.001). We concluded that the size of the electron dense deposits and GBM thickness play an important role in the clinical manifestation of IMGN.
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PMID:Idiopathic membranous glomerulonephritis: a clinicopathologic and quantitative morphometric study. 149 64

Renal biopsy specimens of 29 Japanese non-insulin dependent diabetes mellitus (NIDDM) patients were examined by quantitative electron microscopic morphometry. In NIDDM the relative increase of percent total mesangium and mesangial capillary surface density (S/Vb) and the relative decrease of peripheral capillary surface density (S/Va) were compared with disease controls. However, mesangial-GBM-epithelial surface density (S/Vc) was not different between both groups. These results suggest that the increased mesangial matrix expands directly towards the capillary lumen as well as along the inner surface of GBM, and narrows the capillary lumen and filtration surface. The duration of diabetes mellitus (DM) did not correlate with all morphological parameters. The mesangial expansion correlated with urinary protein excretion and decreased creatinine clearance (CCr). GBM thickening correlated with proteinuria, but not with CCr. The degree of these morphological changes could be the indicators of hypertension of NIDDM patients. Areas of thin GBM were occasionally noticed in glomeruli which revealed thick GBM extensively, although the mechanism of GBM thinning is not known at the present time.
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PMID:An electron microscopic study of glomeruli in Japanese patients with non-insulin dependent diabetes mellitus. 151 97

In order to know the incidence and character of rapidly progressive glomerulonephritis (RPGN) in China, 20 patients with RPGN were analysed and 10 of them followed. Their diagnosis were confirmed by biopsy showing extensive crescent formation. Five patients were rebiopsied. RPGN was found in about 3% of the patients with glomerulonephritis in our center. Only one case was mediated by anti-GBM antibody, while the other 19 by immune complex. Prodromal infection was common (12/20). Hematuria, nephrotic syndrome and hypertension were found in 20, 15 and 12 patients respectively. Five patients without special treatment died of renal cause within 6 months. Intensive treatment (pulse methylprednisone or plasmapheresis) was effective in all of the four cases with cellular crescents. After the treatment, their renal function improved with decrease of proliferation and crescent formation as shown by rebiopsy. However, deterioration of renal function reappeared after 3 months to 3 years in three of the cases. It is shown that in China, RPGN was predominantly mediated by immune complex and is associated with a high incidence of prodromal infection. Clinically, nephrotic syndrome was more frequently seen here than in western countries. For improvement of the prognosis, it is necessary to pay attention not only to earlier diagnosis but also to protection of renal function after intensive therapy.
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PMID:[Diagnosis and treatment of rapidly progressive glomerulonephritis. An analysis of 20 cases]. 187 90

The renal selectivity properties towards albumin were evaluated in ten diabetic patients with arterial hypertension before and after the pharmacological normalisation of blood pressure, and were compared to 12 subjects with essential hypertension. While all patients of the control group were normoalbuminuric during hypertension, six of the diabetic group were microalbuminuric when hypertensive and became almost normoalbuminuric after blood pressure pharmacological control. All microalbuminuric diabetic patients presented altered properties of renal selectivity as epitomised by a non-preferential urinary excretion of glycosyl albumin (GA) (urinary GA/serum GA less than or equal to 1). At variance the selectivity properties were normal in normoalbuminuric diabetic patients and in essential hypertension. It was concluded that in diabetes mellitus arterial hypertension is associated with microalbuminuria when the renal properties of selectivity are altered, but does not implicate any proteinuric effect in those cases where the GBM function is preserved.
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PMID:Hypertension and renal selectivity properties in diabetic microalbuminuria. 212 64

The present study was made to clarify the mechanisms of the antinephritic action of SA-446, an angiotensin I converting enzyme inhibitor, on crescentic-type anti-GBM nephritis in rats as compared to the actions of spironolactone (an antialdosterone agent), kallidinogenase (a kallikrein agent) and saralasin (an angiotensin II antagonist). SA-446 (25 mg/kg/day, p.o.) had a tendency to reduce the urinary protein excretion and plasma urea nitrogen content. In addition, this drug remarkably inhibited not only glomerular histopathological changes (i.e., crescent formation, the adhesion of capillary walls to Bowman's capsule and fibrinoid necrosis) but also the elevation of blood pressure. Spironolactone (25 mg/kg/day, p.o.) and kallidinogenase (25 KU/day, i.m.) also showed beneficial effects on glomerular histopathological changes and hypertension, although both drugs were not as effective as SA-446. However, saralasin (72 micrograms/day, s.c.) caused a marked aggravating action on this nephritis. This nephritic model showed a marked low activity of plasma renin all through the 40 day experimental period. In this model, the urinary aldosterone excretion was increased, in spite of the decrease in plasma renin activity. SA-446 and kallidinogenase significantly inhibited the decrease in plasma renin activity and the increase in urinary aldosterone excretion. Spironolactone inhibited only the increase in the aldosterone excretion. However, saralasin decreased the plasma renin activity under the control level and strongly increased the urinary aldosterone excretion (about 1.8 times the control level on the 20th day). These results suggest that the antinephritic effect of SA-446 may be related to the antihypertensive action and the increase in renal blood flow through activation of the kallikrein-kinin and prostaglandins systems.
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PMID:Studies on mechanisms of antinephritic action of SA-446 an angiotensin I converting enzyme inhibitor (1). A comparison with actions of spironolactone, kallidinogenase and saralasin. 302 37

The authors report two cases of contralateral intratumoral hemorrhage after tumor biopsy in patients with bilateral glioblastoma multiforme. There was no evidence of systemic hypertension during either procedure. The occurrence of hemorrhage distant to the site of biopsy may be related to some aspect of the surgical procedure and should be recognized as a possible complication of brain tumor biopsy procedures.
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PMID:Contralateral intracerebral hemorrhage as a complication of tumor biopsy. 302 82

Functional and morphologic glomerular alterations induced by antiglomerular basement membrane (anti-GBM) nephritis were investigated in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto controls (WKY) for assessment of the role of systemic hypertension in immunologically mediated renal injury. Over a 6-week period serial measurements of systolic blood pressure (BP), serum creatinine (SCreat), creatinine clearance (CCreat), and urinary albumin excretion (UAlbV) were obtained with inulin clearances (CInulin) at the end of the study. Renal tissue was examined by light microscopy (LM), electron microscopy, immunofluorescence, flash 3H-thymidine autoradiography (AR), and staining for nonspecific esterase (NSE). Immunologic humoral response was evaluated by measurement of rat anti-rabbit IgG antibody production. At all time periods studied, SHR and WKY rats with anti-GBM nephritis demonstrated comparable elevations in SCreat and UAlb V as well as diminution of CCreat and CInulin as compared with non-nephritic control rats of each strain. In nephritic WKY rats mild hypertension developed, whereas in nephritic and control SHR rats marked elevations in BP developed. Morphologic injury as assessed by percent glomerular crescents and hypercellularity on LM, numbers of monocyte macrophages by NSE staining, immunofluorescence for IgG, C3, fibrinogen and Ia positivity, and numbers of glomerular 3H-thymidine-labeled cells by AR was notably comparable in both nephritic strains. Humoral antibody responses were also shown to be similar in all rats studied. These results demonstrate that the 5-week course of experimental anti-GBM nephritis is not exacerbated by systemic hypertension. Glomerular autoregulatory capacity may be important in determining the extent of immune-mediated renal injury.
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PMID:No aggravation of the course of experimental glomerulonephritis in spontaneously hypertensive rats. 351 2

It is now firmly established that a variety of immune mechanisms are responsible for most glomerulonephritides, and that they act largely through the activation of complement, recruitment of leukocytes and macrophages, stimulation of clotting, and liberation of vasoactive kinins. The etiological factors which originate the process can be either infectious agents, endogenous antigens (DNA, tumoral antigens), or exogenous toxins. The activation of the immune system may take different forms, including: the production of anti-GBM antibodies which may at times cross-react with other tissues or organs; the formation of antigen-antibody complexes of specific solubility, molecular size, permeability, which will variously tend to localize in the mesangium, in subepithelial, or subendothelial deposits; the development of antibodies which specifically react with native antigens present in the GBM in a discontinuous manner; the trapping of antigens within the GBM, which then act as "planted" antigens. The morphologic type of glomerulonephritis and its clinical course will probably depend upon the predominant type of antigen produced, its persistence, its mode of action, and the concurrent degree of activation of complement, recruitment of PMNs and macrophages, stimulation of the clotting system, as well as upon the development of hypertension and the functional response of the kidney to reduced renal mass. Whether or not it will be possible, in the future, to relate directly each type of glomerulonephritis to specific etiologic agents, to the type of immune response, and to genetic predisposition is unclear, but this will determine whether it will be possible to devise specific treatment strategies for each condition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunopathologic mechanism of glomerular injury--an overview of current concepts. 406 38

A 14-year-old girl with neurofibromatosis presented with severe hypertension. She was subsequently found to have a cerebellar glioblastoma multiforme and vascular lesions producing coarctation of the abdominal aorta and 50% and 95% stenosis of the left and right renal arteries respectively. No evidence of pheochromocytoma was found. After removal of the cerebellar tumor, marked amelioration of the hypertension suggested that the tumor had a major role in the pronounced elevation of her blood pressure. Patients who have both neurofibromatosis and hypertension should be carefully evaluated for these several potential lesions.
Hypertension
PMID:Hypertension and neurofibromatosis. Case report. 629 87

To clarify the clinical and pathological significance of thin glomerular basement membranes (Thin-GBM) appearing in evident diabetics, we examined the renal biopsies from 179 diabetes mellitus (DM) patients with urinary abnormalities in which the number of non insulin dependent diabetes mellitus cases was 140 cases while the remaining 39 cases had insulin dependent diabetes mellitus. In addition, 17 of these cases were found to have either segmental or diffuse Thin-GBM by electron microscopy. The clinical and morphological parameters between the diabetics with Thin-GBM (DM-Thin-GBM) and the diabetics without Thin-GBM (the controls) were significantly different regarding DM duration (DM-Thin-GBM vs control: 5.3 +/- 5.5 vs 9.8 +/- 6.5 years, p < 0.01), Ccr (67.0 +/- 25.5 ml/min vs 45.6 +/- 24.4 ml/min, p < 0.01), the incidence of hematuria (52.9% vs 24.5%, p < 0.05) and hypertension (13.3% vs 51.3%, p < 0.05). The severity of glomerular damage was mild in the DM-Thin-GBM group as compared to the control. The renal survival rate from the onset of urinary abnormalities was higher in the DM-Thin-GBM group than in the control (p < 0.01). In the case of DM-Thin-GBM, the grade of proteinuria correlated with the mean width of the thickened GBM (p < 0.01) and the spread of the thickened GBM which was more than 500 nm in width (p < 0.001). The severity of microscopic hematuria correlated with the spread of the Thin-GBM (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thin glomerular basement membrane in diabetic patients with urinary abnormalities. 852 10


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