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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necrotizing vasculitis is not usually considered in the differential diagnosis of hypertensive crisis. Three cases are presented in which hypertensive crisis with encephalopathy was the principal initially seen manifestation of systemic necrotizing vasculitis. The correct diagnosis was suspected because of the patients' young age, elevated ESRs, and evidence of previous exposure to hepatitis B virus and was confirmed by renal angiography. All three patients had metabolic alkalosis, and two of the three patients had hyponatremia and hypokalemia. The literature presents a picture of hypertension in necrotizing vasculitis as insidious, relentless, and progressive. Our cases illustrate that it can be a dramatic, life-threatening initial manifestation. A renal angiogram can be justified in similar patients, since effective therapy for necrotizing vasculitis exists. In these patients control of BP ultimately depends on successful treatment of the underlying vasculitis.
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PMID:Systemic necrotizing vasculitis seen initially as hypertensive crisis. 397 86

Infarct kidney hypertension was induced in congenital athymic nude rats and in their haired normal littermates. In both groups a significant and similar elevation of blood pressure was observed. The mesenteric vessels were studied histologically five, 12 and 20 days after operation. Necrotizing vasculitis with and without perivascular inflammatory reactions was found in mesenteric arteries and arterioles in six out of six athymic and in six out of 11 control rats. In sham operated athymic rats and in haired littermates neither hypertension nor vasculitis was observed. These observations indicate that the thymus play no role in the pathogenesis of acute hypertensive vascular disease.
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PMID:Necrotizing vasculitis in athymic rats with infarct kidney hypertension. 668 Oct 44

The renal biopsy technique has made it possible to classify lupus nephritis into its varied forms. Utilizing light histology, immunofluorescence microscopy, and ultrastructural techniques, the following renal morphological manifestations of systemic lupus erythematosus can be identified: mesangial abnormalities; focal proliferative, diffuse proliferative and membranous glomerulonephritis; glomerular sclerosis; interstitial nephritis; vascular sclerosis and necrotizing renal vasculitis. Each of the morphological forms is associated with distinctive clinical features and prognosis. Mesangial and focal proliferative lupus nephritis may occur in the absence of clinical abnormalities, and in general have a favorable prognosis. Diffuse proliferative lupus nephritis often is manifested by the nephrotic syndrome and renal functional impairment which proves to be irreversible and progressive. Transition from the milder forms to diffuse proliferation occurs in about one-sixth of patients. Membranous lupus nephritis is characterized by the nephrotic syndrome, which often is persistent, but renal functional impairment develops slowly and is rarely severe. Necrotizing vasculitis, which supervenes on occasion during the course of diffuse proliferative lupus nephritis, produces the clinical picture of malignant hypertension and progresses rapidly to uremia. Interstitial nephritis usually occurs in combination with one of the glomerular forms, but at times may be the predominant renal lesion both morphologically and clinically. Glomerular sclerosis, often associated with hypertension and vascular sclerosis, commonly develops in the course of lupus nephritis, especially in the more severe forms, and may progress even though active disease has remitted. An awareness of clinico-pathologic correlations in lupus nephritis provides a basis for intelligent management and critical assessment of therapy.
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PMID:Clinical usefulness of the morphological classification of lupus nephritis. 710 64

Rapidly progressive glomerulonephritis (RPGN) is rarely associated with macroscopic polyarteritis nodosa (PAN), as seen in this series of 7 out of 235 patients. The clinical symptoms of PAN were as follows: myalgias 6; fever 1; arthralgias and mononeuropathy multiplex 5; cutaneous vasculitis 3; arterial hypertension 4, 3 of which were malignant. The mean proteinuria was 2.7 g/24 h; creatininemia 458 microM/l; microscopic hematuria was present in 4 of the 7 patients; only 1 patient was anuric. Markers of hepatitis B virus were absent in all cases. Arteriography revealed microaneurysms and renal infarcts in 6 patients and distal arterial stenosis in one. Renal biopsies from all 7 patients demonstrated extracapillary glomerulonephritis, which was associated with tubulointerstitial fibrosis in one. Necrotizing vasculitis lesions were associated in 5 cases. Immunofluorescence was positive in 5 cases. The association of RPGN and PAN exists and may be underestimated due to the lack of systematic angiographic examinations during RPGN and renal biopsies in PAN patients with renal involvement.
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PMID:[Rapidly progressive glomerulonephritis in macroscopic periarteritis nodosa. 7 cases]. 790 9