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)

A 22-year-old woman with systemic lupus erythematosus complicated by mild renal insufficiency and severe systemic hypertension inadvertently received an excessive amount of clonidine hydrochloride. In association with a presumed toxic level of clonidine in the serum, the patient developed abnormalities of cardiac conduction, including 2:1 atrioventricular block, complete heart block, 3:2 Wenckebach block, and first-degree atrioventricular block. The transient nature of these abnormalities, with the return of normal conduction upon the cessation of therapy with clonidine, implicates this drug as being capable of producing high-grade atrioventricular block at toxic levels.
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PMID:Cardiac toxicity of clonidine. 92 17

Analgesic-induced renal disease occurs more commonly than is recognized; unless specific inquiry is made, it is seldom diagnosed. Patients with chronic pain, especially those with hypertension, urinary tract infection, or renal insufficiency, should be suspect. The condition is preventable and even in the late stages is manageable if recognized. Analgesic abuse may result in end-stage renal disease; it accounts for a significant percentage of patients entering chronic hemodialysis or renal transplant programs.
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PMID:Analgesic nephropathy--a continuing problem. 99 79

The present study discusses the light, electron and immunofluorescence microscopy as well as some clinicopathologic correlations of rejection change in human renal allograft glomeruli. It is based on examination of 126 tissue specimens from 54 grafts obtained from 50 patients (1966-1973). The most frequent and characteristic lesion was membranous transplant glomerulopathy (MG) with irregular fibrillar thickening of capillary walls but without conspicuous hypercellularity. This thickening was caused by subendothelial depositsdifferent from classical fibrinoid lesions. During further progression, widening and peripheral extension of mesangium with degenerative changes became apparent. Advanced MG was encountered most frequently in the 2nd year after transplantation (TPL) at moderate to medium proteinuria and hypertension. It was accompanied by endarteristic rejection changes, and renal insufficiency set on usually in the course of the 3rd year. Nevertheless, the course, symptoms, and graft survival exhibited considerable variations. - The morphology and manifestations of destructive segmental transplant glomerulopathy (SG) depended on the time of its development. In the early stage (within about 3 months after TPL), the lesion was characterized by areas of fibrinoid insudation and necro(bio)sis associated with severe vascular changes, most frequently obliterative arterio(lo)pathy (OA). The ultrastructure was characterized by endothelial defects with host's polynuclear reaction and focal intravascular coagulation. The grafts thus affected failed soon, their function usually subsiding within the first trimester at a moderate, but gradually increasing proteinuria and severe persistent hypertension. The late from of destructive SG presenting as fibrohyaline obliteration of the loops with foam cells always accompanied advanced MG with severe arterial lesions. - Fluorescence microscopy revealed both linear and focal fixation of antisera, which, however had no apparent correlation with the microscopical and clinical presentations.
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PMID:Glomerulopathies in human renal allografts. 109 48

In a retrospective clinicopathological study, 48 kidney biopsy specimens from 16 children (mean age, 7 years) and 17 adults (mean age, 33 years) with histological evidence of focal glomerular sclerosis (FGS) were examined using light, immunofluorescence and electron microscopy. The histopathological findings were related to the clinical course of each patient. At the clinical onset of the disease, the nephrotic syndrome was seen more commonly in children (12/16) than adults (7/17), while the incidence of both hypertension (children 1/16 versus adults, 9/17) and renal insufficiency (children, 0/16 versus adults, 7/17) was greater in adults. Despite a shorter average follow-up, (adults 3 10/12 years versus children, 7 years), the incidence of hypertension (adults, 13/17 versus children, 7/16) and renal functional impairment (adults, 13/17 versus children, 3/16) remained greater in the adult patients. One child and three adults died in renal failure while two adults underwent transplantation and on requires regular dialysis therapy. Nine of 15 pediatric patients treated with corticosteroids experienced partial or complete remission in either their nephrotic syndrome or level of urine protein excretion, while just 3 of 6 adult patients treated with corticosteroids experienced a partial remission, but never became protein-free. There was an excellent correlation in all patients between the degree of functional renal impairment and the extent of glomerular and nonglomerular histopathological damage in the kidney. It is concluded that in the adults, FGS represents a more severe and progressive disease process and is less responsive to therapy.
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PMID:Focal glomerular sclerosis: contrasting clinical patterns in children and adults. 110 46

Calcium oxalate crystals were demonstrated in the retinal pigment epithelium (RPE) of a 66-year old white man with changes in the fundus oculi consistent with the flecked retina ayndrome. The patient had a history of rheumatoid arthritis, mild hypertension, and mild renal insufficiency presumed due to his hypertension. He underwent prolonged abdominal surgery under methoxyflurane anesthesia, following which he developed acute irreversible renal failure. Calcium oxalate crystals were demonstrated postoperatively in a kidney biopsy specimen. He subsequently was maintained on renal dialysis with decreasing renal function. Several weeks before his death fundus examination revealed a picture suggestive of a flecked retina syndrome. At autopsy, widespread oxalosis was found including crystals in the RPE and in some areas in the neural retina and cillary epithelium.
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PMID:Flecked retina. Appearance secondary to oxalate crystals from methoxyflurane anesthesia. 111 83

The authors study "pearl necklace" arteries (PNA) in vascular nephropathies with acute renal insufficiency. Seventeen patients underwent aortography complemented by selective angiography of the renal, superior mesenteric and coeliac arteries to seek renal and extra-renal lesions. PNA were discovered remarkably often (mesenteric branches and renal arteries above all). Three types of PNA are described. PNA do not occur in acute angitis (3 cases, 2 PAN). They almost invariably occur in ATN (7 cases) and may be seen in ASMN (7 cases), which eliminates any diagnostic value in the distinction of these two types of acute anuric vascular nephropathy. The functional nature of PNA is open to discussion, but it appears that in the long term histological changes and functional modifications in the involved areas may occur. The role of hypertension and vaso-active substances in the aetiology of PNA is discussed.
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PMID:["Pearl necklace" arteries in vascular nephropathy with acute renal insufficiency (author's transl)]. 115 21

A 28 year old woman, with diabetes since age 18, had the nephrotic syndrome, hypertension and renal insufficiency. The initial renal biopsy specimen revealed diffuse glomerulosclerosis with early nodular changes. After an initial decline in renal function, her creatinine clearance progressively improved and has remained normal. Within 2 years she had a spontaneous remission of the nephrotic syndrome despite the presence of more pronounced nodular glomerular lesions. Although the renal hemodynamic functions were normal, certain tubular functions were impaired. Since we found no etiology for the nephrotic syndrome other than diabetic glomerulopathy, the complete remission of the nephrotic syndrome and improvement in renal function were very unusual events.
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PMID:Spontaneous remission of the nephrotic syndrome in diabetic nephropathy. 116 52

Primary hyperparathyroidism during pregnancy has been reported in 36 women; 1 new case is reported here. Screening by determining serum calcium levels is a valuable method of diagnosing the disease. Radioimmunoassay of serum parathyroid hormone (PTH) greatly aids in the diagnosis. Amniotic fluid PTH values are discussed. Hyperparathyroidism has a high association with progressive renal insufficiency, renal calculi, hypertension, and bone disease. During pregnancy, there is an increased incidence of stillborns, premature labor, and neonatal tetany. Acute hyperparathyroid crisis may result in maternal death. This is the first reported case surgically treated during the third trimester of pregnancy. Surgery should be considered when the diagnosis is made late in pregnancy, as this may protect the infant from neonatal tetany.
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PMID:Primary hyperparathyroidism during the third trimester of pregnancy. 116 24

8 patients suffering from acute renal failure (shock kidney) with anuria extending over 3 to 5 days, were treated with L-thyroxine for 5 to 9 days (5-6 mug per kg body weight per day orally). Diuresis was restored within 34 to 46 hrs. Plasma levels of urea and creatinine decreased earlier and much more rapidly to normal than was to be expected from the natural history of the disease, indicating the prompt and extensive increase of glomerular filtration rate. Polyuria seemed less pronounced and also shortened as compared with the ordinary course of that form of sudden renal insufficiency. Obviously, the well-known diuretic response in the normal individual to high doses of thyroid hormones in not a factor in the induction of diuresis in acute renal failure. The tendency with L-thyroxine treatment to dilate the preglomerular arterial vessel is considered a consequence of the stimulation of sodium reabsorption in the upper nephron. High values of RPF and GFR, regularly observed in hyperthyroidism or after L-thyroxine administration, do not depend on any augmentation of cardiac output or on arterial hypertension, since such symptoms were missed in our patients and, in our view, such an interpretation is excluded by the very existence of the so-called autoregulation of the kidney which leaves RPF (and therefore GFR) independent of systemic blood pressure. The same intrarenal feed-back mechanism, normally adapting the glomerular blood supply to the resorptive capacity of the proximal-tubular epithelium (mediation via the juxta-glomerular apparatus), is responsible for the GFR- and RPF-raising effect of exogenous L-thyroxine in the intact kidney as well as in acute renal failure: both sodium reabsorption and sodium filtration are accelerated.--The special conditions under which L-thyroxine interferes with the pathogenetic process of acute renal failure, the latter being characterised by the critical insufficiency of tubular sodium reabsorption and therefore by preglomerular arterial constriction, is discussed on the basis of a new hypothesis concerning the thyrogenic nephrotropic effects in general.
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PMID:[Thyroxine treatment in acute renal failure (author's transl)]. 119 15

In a series of 1,000 consecutive percutaneous renal biopsies, adequate tissue for diagnosis was obtained in 94.9%. The rate of complications was 8.1% and was directly related to 1. age of the patient, 2. presence of renal insufficiency, and 3. arterial hypertension. The use of fluoroscopic control for localization of the kidney did not affect the rate of complications, nor did it improve the success rate in obtaining adequate tissue.
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PMID:Complications of percutaneous renal biopsy: an analysis of 1,000 consecutive biopsies. 120 61


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