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 studied a group of 59 patients with renal amyloidosis. Mean age (45 male, 14 female) was 33.05+/-13.04 years. All of the cases had secondary amyloidosis. The causes of secondary amyloidosis were as follows: familial Mediterranean fever (FMF) 18 (30.5%), pulmonary tuberculosis 12 (20.33%), chronic oseomyelitis 8 (13.55%), bronchiectasia 9 (15.25%), rheumatic diseases 4 (6.4%), Castleman's disease 1 (1.6%), unknown aetiology 7 (11.86%). Hypertension was detected in 15.3% of the cases. In patients with less than 20 ml/min creatinine clearance (Ccr) hypertension was found in 20%. Hypotension was detected in 6 patients and all of these cases had severe hypoalbuminaemia (<2.1 g/dl). Nephrotic range proteinuria (>3.5 g/day) was found in 75% of cases. Daily proteinuria was correlated with serum levels of albumin, total lipid and cholesterol, haematocrit and duration of disease. The mean Ccr was 51.03+/-40.60 ml/min. Twenty-nine per cent of patients had Ccr less than 20 ml/min. Renal, subcutaneous fat and rectal biopsies demonstrated amyloid in 100%, 20% and 57.6%, respectively, of patients tested. Patients with secondary amyloidosis were treated with colchicine in addition to the therapy of primary disease (in 6 patients). Nine patients died, and end-stage renal disease developed in 12 patients during four years of follow-up. Proteinuria disappeared or decreased in patients with secondary amyloidosis except secondary to collagen tissue disease, without advanced renal failure. Colchicine did not affect amyloid deposition in 2 patients with normal renal function and negative proteinuria, who were rebiopsied. It can be questioned that "Colchicine may have effect(s) for decrement on proteinuria". At least colchicine can be of use in secondary amyloidosis.
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PMID:Report on 59 patients with renal amyloidosis. 1075 52

Amyloid-beta (A beta) deposition in cerebral vessels (cerebral amyloid angiopathy, CAA) is accompanied by degeneration of vascular cells, including pericytes and smooth muscle cells. Previous studies indicated that specific A beta protein isoforms are toxic for cultured human brain pericytes and smooth muscle cells. In particular, A beta 1-40 carrying the E22Q mutation, as in hereditary cerebral hemorrhage with amyloidosis of the Dutch type (HCHWA-D), is toxic. We investigated the effects of the A beta-binding protein apolipoprotein E (ApoE) on the toxicity of A beta for cultured human brain pericytes. We compared the toxicity of HCHWA-D A beta 1-40 for pericyte cultures with different ApoE genotypes, studied the accumulation of A beta and ApoE in these different cell cultures, and investigated the effects of exogenous ApoE. Pericyte cultures with an ApoE epsilon 2/epsilon 3 genotype were more resistant to HCHWA-D A beta 1-40 treatment than cultures with a epsilon 3/epsilon 3 or epsilon 3/epsilon 4 genotype. Cell death was highest in cultures homozygous for ApoE epsilon 4. The extent to which both A beta ApoE accumulated at the cell surface was parallel to the degree of toxicity. The addition of purified ApoE resulted in a decrease in cell death. These data suggest that ApoE4 may direct A beta more efficiently than other ApoE isoforms into a pathological interaction with the HBP cell surface. The results of this study are in line with the observations that inheritance of the ApoE epsilon 4 allele increases the risk of developing Alzheimer's disease, and that the ApoE epsilon 2 allele has a relatively protective effect.
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PMID:Amyloid-beta-induced degeneration of human brain pericytes is dependent on the apolipoprotein E genotype. 1081 7

Nephrotic syndrome represents a constellation of symptoms including hyperalbuminuria, hypoalbuminemia, edema formation, hypercholesterolemia, hypertension, hypercoagulopathy, and increased infection risk. The hallmark of this syndrome is proteinuria greater than 3.5 grams per 24 hours, and the clinical features are secondary manifestations of an underlying primary glomerular or systemic disease. The objectives of treatment are threefold: correcting the primary disease, decreasing the symptoms and secondary effects associated with this syndrome, and preventing complications. This article presents a case report of a man diagnosed with nephrotic syndrome secondary to amyloidosis. The clinical aspects of the disease processes, the diagnostic evaluation, the treatment course, and disease management are discussed.
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PMID:Nephrotic syndrome secondary to amyloidosis. 1088 98

In the present work, 199 patients with leprosy who underwent autopsy between 1970 and 1986 were retrospectively studied to determine the prevalence, types, clinical characteristics, and etiologic factors of renal lesions (RLs) in leprosy. Patients were divided into two groups: 144 patients with RLs (RL+) and 55 patients without RLs (RL-). RLs observed in 72% of the autopsied patients were amyloidosis (AMY) in 61 patients (31%), glomerulonephritis (GN) in 29 patients (14%), nephrosclerosis (NPS) in 22 patients (11%), tubulointerstitial nephritis (TIN) in 18 patients (9%), granuloma in 2 patients (1%), and other lesions in 12 patients (6%). AMY occurred most frequently in patients with lepromatous leprosy (36%; nonlepromatous leprosy, 5%; P < 0.01), recurrent erythema nodosum leprosum (33%; P < 0.02), and trophic ulcers (27%; 0.05 < P < 0.10). Ninety-seven percent of AMY was found in patients with lepromatous leprosy, 88% showed recurrent trophic ulcers, and 76% presented with erythema nodosum leprosum. NPS was found in older patients with arterial hypertension, neoplastic diseases, infectious diseases, and vasculitis associated with GN. Most patients with AMY presented with proteinuria (95%) and renal failure (88%). The most frequent causes of death were renal failure in patients with AMY (57%), infectious diseases in patients with GN (41%) and TIN (45%), and cardiovascular diseases in patients with NPS (41%). No difference in survival rates was observed among RL- patients and those with AMY, GN, NPS, or TIN.
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PMID:Renal lesions in leprosy: a retrospective study of 199 autopsies. 1143 Nov 77

The aim of this study was to examine the incidence of different renal lesions in rheumatoid arthritis (RA) and to determine their relationships with the type of previous drug therapy and with the specific features of immune disorders. Ninety four patients, 84 (89.9%) females and 10 (10.6%) males) with RA whose mean age was 45.2 +/- 11.9 years and duration of the disease 7.5 +/- 6.5 years were examined. Most of them had degrees 2 and 3 PA (62.7 and 24.4%, respectively). Systemic manifestations were encountered in 60 (63.8%) patients. Eighty one patients took nonsteroidal antiinflammatory drugs (NSAID) continuously: 18 patients for a year, 32 for 5 years, 14 for 6 to 10 years, and 17 for over 10 years. All the patients underwent clinical, laboratory, and instrumental study of partial functions of the kidney. Immunological study involved solid-phase immunoassay of IgA and IgM rheumatoid factor, von Willebrand factor antigens (WF:Ag), C-reactive protein. The serum concentrations were measured by the Mancini method. Changes in urinalysis and/or signs of decreased glomerular and tubular functions were found in 69 (73.%) patients, 25 (26.6%) had arterial hypertension. Tubular dysfunctions were more common [31 (32.9%) patients]. Signs of early renal failure were detected in 20 (21.2%) patients. There were no cases of acute renal failure. Amyloidosis, glomerulonephritis, pyelonephritis were diagnosed in 5 (5.3%), 16 (17%), and 13 (13.8%) patients, respectively. The above renal lesions were concurrent in some patients. Renal lesion correlated with the progression and severity of RA, the presence of systemic manifestations, and age. There was no relationship of both 5- and 10-year use of NSAID to the symptoms of renal disease. The use of these drugs for over 10 years was concurrent with the signs of chronic renal failure and arterial hypertension. Analyzing immunological disorders showed an association of increased erythrocytic sedimentation rates and WF:Ag with amyloidosis, that of higher IgA concentrations with proteinuria and tubular dysfunctions. It is concluded that renal lesion is common in RA, there is a predominance of tubular interstitial changes. In rare cases nephropathy is characterized by a benign course and fails to result in uremia. The symptoms of renal diseases are largely associated with RA progression and severity and the patients' age. Prolonged continuous use of NSAID may contribute to the development of renal failure. Different immune mechanisms are involved in the pathogenesis of glomerular and tubular nephropathy in RA.
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PMID:[Clinico-immunological aspects of renal lesions in rheumatoid arthritis]. 1152 52

Atrial fibrillation (AF) is a common clinical problem, particularly in the elderly, and in patients with organic heart disease. A small percentage of patients, have a potentially reversible cause. Atrial fibrillation is in most patients (approximately 70%) associated with chronic organic heart disease including valvular heart disease, coronary artery disease, hypertension, particularly if left ventricular hypertrophy is present, hypertrophic cardiomyopathy, dilated cardiomyopathy and congenital heart disease and most commonly in adults, atrial septal defect. As in many chronic conditions, determining whether AF is the result or is unrelated to the underlying heart disease, remains unclear. The list of possible etiologies also include cardiac amyloidosis, hemochromatosis and endomyocardial fibrosis. Other heart diseases, such as mitral valve prolapse (with or without mitral regurgitation), calcification of the mitral annulus, atrial myxoma, pheochomocytoma and idiopathic dilated right atrium, present a higher incidence of AF. The relationship between these findings and the arrhythmia are still unclear. Atrial fibrillation may occur in the absence of detectable organic heart disease, the so-called "lone AF", in about 30% of cases. The term "lone AF" or "idiopathic AF" implies the absence of any detectable etiology including hyperthyroidism, chronic obstructive lung disease, overt sinus node dysfunction, and overt or concealed preexcitation (Wolf-Parkinson-White syndrome), only to mention a few of other rare causes of AF. In every instance of recently discovered AF, thyrotoxicosis should be ruled out. The autonomous nervous system may contribute to the occurrence of AF in some patients. Atrial fibrillation occurs commonly in patients with valvular heart disease, particularly when it involves the mitral valve. The occurrence of AF is unrelated to the severity of mitral stenosis but is more common in patients with enlarged left atrium and congestive heart failure. In patients with coronary artery disease, Af occurs predominantly in older patients, males and patients with left ventricular dysfunction. Important predictive factors of AF include hypertension, left ventricular hypertrophy and diabetes. However, the relation between AF and hypertension remains unclear. The risk of the development of AF, in an individual patient, is often difficult to assess but increasing age, presence of valvular heart disease and congestive heart failure, increase the risk of AF.
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PMID:Atrial fibrillation, the arrhythmia of the elderly, causes and associated conditions. 1210 96

Many studies have been devoted to investigating new techniques and new dialysis strategies aimed at achieving adequate removal of "uremic toxins". Conversely, few studies focus on the effect of different dialysis techniques on long-term outcome, including large series and with adequate follow-up. Dialysis dose, membrane biocompatibility and permeability, convective techniques, and the number and duration of dialysis sessions have all been considered as potentially related to patient outcome. The available data from the literature clearly show a significant relationship between the urea kinetic model based dialysis delivered and long-term patient outcome. A significant positive correlation between survival and Kt/V up to 1.3 per session in patients treated three times a week with standard low flux cellulosic dialyzers has been shown. Many studies have shown an effect of high flux membranes on the appearance of symptoms related to dialysis amyloidosis. It is likely that such an effect is further enhanced by convective or mixed techniques. The role of these techniques in patient survival is suggested by some studies, but should be confirmed in larger series. The use of techniques suitable for ultra-pure dialysis fluids are mandatory whenever high permeability membranes are used. Treatment schedules which include long dialysis sessions or an increased number of sessions such as daily dialysis, seem to be beneficial for the control of hypertension or hyperphosphatemia. However, their role on patient survival has not yet been clearly assessed. Together with the choice of the best strategy, great attention should be paid to other factors known to be related to patient outcome, such as early patient referral, and the type and efficiency of vascular access.
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PMID:[New dialysis therapy modalities: what role do they play in the hemodialysis patient's outcome?]. 1216 42

A common problem among elderly people, orthostatic hypotension is associated with significant morbidity and mortality, which may be caused by medications, the cumulative effects of age- and hypertension-related alterations in blood pressure regulation, or age-associated diseases that impair autonomic function. Evaluation requires multiple blood pressure measurements taken at different times of the day and after meals or medications. Central and peripheral nervous system disorders should be sought, and the laboratory evaluation should concentrate on ruling out diabetes mellitus, amyloidosis, occult malignancy, and vitamin deficiencies. If orthostatic hypotension is detected, it should be considered a risk factor for adverse outcomes and treated first with nonpharmacologic interventions, including the withdrawal of potentially hypotensive medications. In patients with hypertension and orthostatic hypotension, the judicious treatment of hypertension may be helpful. For persistent, symptomatic orthostatic hypotension caused by autonomic failure, pharmacologic interventions include fludrocortisone, midodrine, and a variety of other agents. The careful evaluation and management of orthostatic hypotension will hopefully result in a significant reduction in falls, syncope, and fractures, and an attenuation of functional decline in elderly patients.
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PMID:Orthostatic hypotension. 1218 Feb 46

DMSO is an amphipathic molecule with a highly polar domain and two apolar methyl groups, making it soluble in both aqueous and organic media. It is one of the most common solvents for the in vivo administration of several water-insoluble substances. Despite being frequently used as a solvent in biological studies and as a vehicle for drug therapy, the side-effects of DMSO (undesirable for these purposes) are apparent from its utilization in the laboratory (both in vivo and in vitro) and in clinical settings. DMSO is a hydrogen-bound disrupter, cell-differentiating agent, hydroxyl radical scavenger, intercellular electrical uncoupler, intracellular low-density lipoprotein-derived cholesterol mobilizing agent, cryoprotectant, solubilizing agent used in sample preparation for electron microscopy, antidote to the extravasation of vesicant anticancer agents, and topical analgesic. Additionally, it is used in the treatment of brain edema, amyloidosis, interstitial cystitis, and schizophrenia. Several systemic side-effects from the use of DMSO have been reported, namely nausea, vomiting, diarrhea, hemolysis, rashes, renal failure, hypertension, bradycardia, heart block, pulmonary edema, cardiac arrest, and bronchospasm. Looking at the multitude of effects of DMSO brought to light by these studies, it is easily understood how many researchers working with DMSO (or studying one of its specific effects) might not be fully aware of the experiences of other groups who are working with it but in a different context.
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PMID:Multidisciplinary utilization of dimethyl sulfoxide: pharmacological, cellular, and molecular aspects. 1266 39

The extrarenal manifestations of hypernephroma in 34 medical patients are described, and the literature on this subject is reviewed. One case presented with hematuria and 11 other cases with metastases. Presentation was not obviously related to metastases in 22 patients. Eight were first seen because of fever or general weakness. Vascular disturbances in six included hypertension, thrombophlebitis, inferior vena caval obstruction and varicocele. Four patients had gastrointestinal complaints; one had hypercalcemia and another musculoskeletal symptoms. Two cases had neurological syndromes, one of which proved to be due to metastases. The overall incidence of systemic features was greater and included anemia, eosinophilia, a leukemoid reaction and thrombocytosis. Polycythemia, amyloidosis and hyponatremia were not encountered. Urographic procedures were performed in half of the patients, most of whom had an abdominal mass. Calcium was visible radiologically in the tumour in five cases. The diagnosis was not made in 19 and was an unexpected finding at autopsy in 10. Appreciation of the extrarenal manifestations of hypernephroma might lead to earlier diagnosis.
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PMID:The extrarenal manifestations of hypernephroma. 1394 85


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