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 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

A newly recognized type of familial glomerulopathy observed in patients of both sexes in six families is reported. Proteinuria, often within the nephrotic range, microscopic hematuria, hypertension and a slowly decreasing renal function over several years were common. No underlying systemic diseases were identified. Generally, light microscopy showed enlarged glomeruli with minimal hypercellularity and with extensive deposits in the mesangium and subendothelial space. By electron microscopy, granular deposits with some admixture of fibrils were most common. In one family, the deposits were predominantly fibrillary. Immunoglobulins and complement factors were inconstant or lacking. A main finding was a strong immune reactivity to fibronectin, corresponding to the distribution of the deposits. In one patient, the deposits recurred in a renal transplant. There was no indication of systemic deposition. Abnormalities in the metabolism of circulating fibronectin may play a pathogenetic role in this disease of probably autosomal dominant inheritance.
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PMID:Glomerulopathy associated with predominant fibronectin deposits: a newly recognized hereditary disease. 756 73

Angiotensin II (Ang II) is the primary mediator of the renin-angiotensin system (RAS). Inappropriate control of the RAS is critically involved in the development and maintenance of hypertension and congestive heart failure. The actions of Ang II are thought to be mediated by specific surface receptors on the various target organs. At present, two receptors for Ang II have been firmly established in mammals, including man. According to current nomenclature, losartan represents the prototype antagonist of the Ang II type 1 (AT1) receptor and does not possess significant affinity for the so-called AT2 receptor. Losartan is the first of a new class of orally active, nonpeptide Ang II receptor antagonists able to very specifically and selectively inhibit the RAS while lacking the agonistic effects of the peptide receptor antagonists, e.g. sarlasin, or the bradykinin potentiating effects of the angiotensin converting enzyme (ACE) inhibitors. Virtually all of the known actions of Ang II, e.g. those defined by Ang II itself, saralasin, ACE or renin-inhibitors are blocked by losartan, emphasizing the major role of this distinct Ang II receptor subtype in mediating the responses of Ang II. The functional correlate of the AT2 receptor remains poorly understood. In several models of experimental and genetic hypertension, AT1 receptor antagonists are effective antihypertensive agents with similar efficacy to that of ACE and renin-inhibitors. In animal models of renal disease, AT1 receptor antagonists significantly decrease proteinuria, protect against diabetic glomerulopathy and increase survival in stroke-prone spontaneously hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A new class of therapeutic agents: the angiotensin II receptor antagonists. 763 3

Five patients with glomerulopathy and glomerular fibrillary protein deposits similar to those of amyloid but lacking the Congo red tinctorial affinity characterizing amyloid were studied. Clinically, these patients had severe proteinuria and microscopic hematuria, in addition, 2 patients had hypertension and renal function impairment. 5 renal biopsies were evaluated by light microscopy (LM), immunofluorescence (IF), immunoperoxidase (IP) and electron microscopy (EM). LM: mesangioproliferative, membranous (late stage) and membranoproliferative (late stage) patterns were seen in 2, 1 and 2 patients respectively. IF & IP: granular deposits, mainly of IgG, C3 and kappa, lambda light chains were found in all cases, either in mesangium and/or capillary walls. EM: randomly distributed fibrils with a diameter approximately 21nm (the diameter of amyloid fibrils is about 9.5nm) were found in glomerular basement membrane and/or mesangium. The pathologic findings suggested a new clinicopathological entity differentiated from amyloidosis. The relatively homogeneous nature of the immunoglobulin in the immune deposits is the basis for the fibril formation.
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PMID:[Observations on the ultrastructure of non-amyloidotic fibrillary glomerulopathy]. 765 79

We describe two patients with the primary antiphospholipid syndrome who presented with severe hypertension. Renal biopsy specimen provided histologic evidence of intra-renal vascular disease with intravascular microthrombosis and nephrosclerosis, without feature of proliferative glomerulopathy. Accelerated hypertension and nephroangiosclerosis might indeed be one of the complications associated with anticardiolipin antibodies. The mechanism responsible might be the interaction of anticardiolipin antibodies, platelets and endothelial cell leading to microthrombi formation and increased local mitogenic activity that attract and stimulate neighbouring smooth muscle cell and fibroblast proliferation.
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PMID:Accelerated hypertension and nephroangiosclerosis associated with antiphospholipid syndrome. Report of two cases and review of the literature. 769 70

The histopathological characteristics of the kidney using light microscopy and immunofluorescence studies in samples obtained by renal percutaneous biopsy in 19 women and 7 men with non-insulin dependent diabetes mellitus (NIDDM) (mean of age: 55.07 +/- 9.04 yr and mean of "known" diabetes duration: 7.50 +/- 6.87 yr) were studied. The relationship with age, blood pressure, diabetic retinopathy and other complementary diagnostic methods such as serum creatinine (Cr), creatinine clearance (CrC), renal plasma flow (RPF), proteinuria and filtration fraction (FF) were also determined. Light microscopy studies detected 92.3% of patients with renal lesions of different degrees of severity. The presence and severity of glomerulopathy and arteriolopathy were related to diabetes duration (r: 0.764) and they were related to each other (rs: 0.773). In 2 patients, lesions were not observed and in 11 out of 14 patients with less than 5 yr of diabetes duration, mild lesions were detected. However, the histological changes became worse after that period. The glomerulopathy was also statistically correlated with Cr, CrC, RPF, proteinuria and FF. By immunofluorescence, fibrinogen, IgA and C3 were the most frequent and intense precipitates observed. They increased with diabetes duration and were located predominantly in the wall and the periphery of the glomerules and in renal tubules, suggesting that they originated by trapping. There were no precipitates in the mesenchyma, they were scarce in the interstice, Bowman's capsule and arterioles. Statistical correlation between diabetic histopathological renal changes and retinopathy was found. These results confirm that lesions in the kidney and retina in non-insulin dependent diabetic patients generally appear and evolve in a similar manner. Hypertension was diagnosed in 80.76% of patients, without statistical correlation between blood pressure and renal lesions. This suggests that at the onset, in non-insulin dependent diabetic patients hypertension and nephro-pathy are caused by different and independent pathogenic mechanisms. However, at an end stage, it seems that both situations can influence each other in a way that their evolution becomes more severe. Nephropathy in non-insulin dependent diabetes mellitus displayed scarce clinical signs and poor laboratory evidence except when the renal lesions become too severe. The lack of correlation between renal lesions and patients' age and blood pressure suggests the participation of diabetes at the onset of kidney structural impairment.
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PMID:[Histopathological and functional study of the kidney in non-insulin dependent diabetes mellitus]. 771 26

The magnitude of type II diabetic nephropathy dilemma is observable in the growing number of diabetic patients with end-stage renal lesion receiving various modalities of treatment. Progressive glomerulopathy associated with proteinuria and hypertension is strongly causative of renal failure and mortality in diabetic patients. Besides hypertension, diabetes exceeds all other glomerulopathies in causing end-stage renal failure. Alterations in glomerular structure and function observed in diabetic patients are implicated in the development and progression of renal derangement. Diabetic glomerulosclerosis, an aggregate of structural and functional perturbations of the kidney, is indicated by alterations in the accumulation of extracellular matrix components, The pathology, epidemiology, risk factors, and other dependent variables may throw some light in the pathogenetic mechanisms and the prevention, treatment, and management modalities of type II diabetic nephropathy.
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PMID:Type II diabetic nephropathy in perspective. 773 45

A 51-yr-old man presented with renal failure, proteinuria, hematuria, and hypertension. The serum contained two monoclonal protein spikes, an IgG4 lambda and free lambda light chains. Free gamma heavy chains were absent from serum. A bone marrow biopsy did not show evidence of a plasmalymphocytic dyscrasia. Renal biopsy showed a nodular glomerulopathy with linear deposits of gamma 4 heavy chains alone along glomerular, tubular, and vascular basement membranes and in mesangial regions. No light chains were detected in the kidney despite staining with antisera directed against both free and bound light chains and the F(ab')2 fragment of IgG. The term heavy-chain deposition disease is appropriate in view of the above features.
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PMID:IgG heavy-chain deposition disease. 783 42

Formation of diabetic glomerulosclerosis was followed by the electron microscopy of 21 puncture renal biopsy and 12 incisive pancreatic biopsies from patients with insulin-dependent diabetes mellitus. The influence of the B-cell destruction and the decrease or absence of their activity (the presence of serum C-peptide) on the degree of renal damage and clinical symptoms of the diabetic nephropathy (proteinuria, hypertension) is noted. Dynamics of the diabetic glomerulosclerosis formation is as follows: 1st group--thickening of capillary basal membrane in the glomeruli, mesangial ectopy, formation of nodules at the periphery of loops; 2nd group--increase of the mesangial matrix, doubling of the glomerular capillary basal membrane, hyalin droplets in the capsule membrane. 4 stages in the development of diabetic glomerulopathy are distinguished: diabetic segmentary mesangioproliferative glomerulonephritis, mesangiolysis, two stages of glomerulosclerosis progression. Duration of the disease more than 15 years predetermines the development of diabetic glomerulosclerosis.
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PMID:[Diabetic glomerulosclerosis--a prolonged stage of diabetic glomerulopathy]. 784 6

Idiopathic focal segmental glomerulosclerosis (FSGS) is an infrequent renal biopsy diagnosis in the elderly. In our single-centre referral registry there were only 17 cases seen in 822 biopsies performed in patients aged 60 or over giving an incidence of 2%. These seventeen patients ranged from age 61 to 78 at the time of biopsy and were followed a median period of 29.5 months. The incidence of nephrotic syndrome at baseline was similar to younger adults (70.5%), but both hypertension (71%) and renal insufficiency (53%) were higher. Fifty-three percent (9/17) of the patients were treated with either steroids or a combination of steroids and cytotoxic therapy. A complete remission in proteinuria was observed in 44% of the treated patients versus none in the untreated patients. No relapses were seen in those that had a complete remission. As well, none of the patients with a complete remission, versus 9/14 (63%) of the untreated or non-responsive patients progressed to renal failure during the observation period. One patient who was treated with cytotoxic therapy and steroids subsequently died of a pancreatic carcinoma. Idiopathic FSGS is an infrequent glomerulopathy in the elderly but it is important given its malignant natural history. Alternate day prednisone for up to 6 months may be a reasonable approach since a complete remission in proteinuria was seen in 44% of our treated patients and this response was closely linked to a good long-term prognosis. The risks of therapy however must be carefully weighed against the potential benefit in each case because of the advanced age of these patients.
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PMID:Steroid therapy and prognosis of focal segmental glomerulosclerosis in the elderly. 792 61


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