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

Analysis is carried out of the clinical, pathomorphological and immunological characteristic of lupus nephropathy in 62 patients, 56 females and 6 males. A series of new investigation methods were used for that purpose. An early tendency towards kidney involvement in the course of LED is established and in 22 of the patients (36%) the renal symptoms have been the first clinical manifestations of the basic illness. Lupus nephropathy progresses most often with a nephrosis syndrome (in 66.1% of the patients), rarely pure and not combined with hypertension and/or with renal insufficiency. The pathomorphological changes are rather multiform but in the majority of the cases almost all structural elements of glomerules and the rest of the renal tissue are affected. The clinical picture severity, histopathological changes and nephropathy evolution course were established to be distinctly dependent on the course acuteness of the basic morbid process. The importance of the detailed study of the clinico-morphological and immune characteristic of lupus nephropathy upon the timely diagnosis. Proper treatment and the prognosis assessment of the illness is stressed upon.
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PMID:[Clinical morphological and immunological characteristics of lupus nephropathy]. 7 Aug 87

This communication describes the electron microscopy (EM) study of the small arterial vessels in renal biopsies from 32 patients with a variety of glomerular and tubulointerstitial diseases. With the possible exception of lipoid nephrosis, all types of glomerular and tubulointerstitial diseases were associated with abnormal arterial vessels. The vascular abnormalities included variable thickening and irregularity of the basement membranes (sclerosis), excessive elastic tissue and collagen fibers, atrophic or necrotic smooth muscle cells, and electron-dense deposits. The EM of glomeruli and tubules from the same biopsy specimens often revealed similar features, i.e., sclerosis, necrotic changes and electron-dense deposits. The pathogenesis of the arteriolopathies, like that in many glomerular and tubulointerstitial diseases, remains unclear. Hypertension was considered a factor, but only 15 percent of the patients were hypertensive. Furthermore, vascular lesions in patients with hypertension were no worse than those without it. Whatever may be the pathogenesis of these arteriolopathies, the similarities between the renal arteriolar and glomerular abnormalities and between arteriolar and tubular lesions suggest a common mechanism of inducement of the lesions.
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PMID:Ultrastructural analysis of renal arteriolopathies in glomerular and tubulointerstitial diseases. 36 Sep 59

The wide utilization of renal biopsy and the introduction of electron microscopic and immunohistologic methods has allowed better definition of the clinico-pathological conditions associated with the nephrotic syndrome (NS). Two major categories of facts can be differentiated. In the first one, diffuse lesions of glomeruli, either secondary to specific diseases, or apparently primary diseases such as membranous or membrano-proliferative glomerulonephropathy (GN) are responsible for the increased permeability of the glomerular capillaries. In most of these, there is evidence that immunological mechanisms play a role in the injury of the glomerular capillary. Any of the following clinical symptoms are suggestive of this category of NS: an acute nephritic onset, a moderate NS, macroscopic hematuria, marked hypertension and/or renal insufficiency, poorly selective proteinuria and decreased plasma C3 levels. Patients affected with any of these glomerulopathies usually do not respond to steroids. In the second one, usually referred to as the idiopathic nephrotic syndrome (INS) the mechanism of glomerular capillary alteration is unknown and the nephrotic syndrome is more marked. Minimal change NS (MCNS) accounts for the great majority of INS and is characterized in most cases by a selective proteinuria, the absence of hematuria, a good response to steroids and a good prognosis. However, in some instances, renal biopsy reveals either diffuse mesangial proliferation (DMP) or focal glomerular sclerosis (which may be superimposed on MCNS or on DMP). In both instances, hematuria may be present and 50--75% of patients do not respond to steroids and have a poor prognosis. There is still considerable controversy about the exact relationship between these 3 patterns. We believe that they are not distinct entities but represent variants of the same disease. In addition to these 2 major categories of NS, there are, in infancy, 2 conditions associated with a NS of poor prognosis: congenital NS of Finnish type and infantile mesangial sclerosis. Since steroid-sensitive nephrosis is by far the commonest cause of NS especially in young children up to 8 years, a renal biopsy should be performed only in 2 instances: (a) when the clinical symptoms suggest diffuse glomerular lesions, and (b) when steroid resistance has been demonstrated.
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PMID:Clinicopathologic correlations in the nephrotic syndrome. 39 6

A 30 year old man developed renovascular hypertension and extreme elevation of plasma renin activity. Daily proteinuria ranged from 13 to 31 g. There were no criteria for the diagnosis of malignant hypertension. A primary glomerulopathy was excluded by a basically normal renal biopsy from the unprotected kidney. On electron microscopy the epithelial cell foot processes were not fused, thus ruling out simultaneous lipoid nephrosis. The source of renin was removed by means of a left nephrectomy. Following the procedure the patient became normotensive, the renin values normalized and the proteinuria disappeared. The results suggest that renin can cause significant proteinuria in man.
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PMID:Renin-induced massive proteinuria in man. 45 23

Studies of 16 adults with nephrotic edema reveal a spectrum of disease, the extremes of which suggest two different pathophysiologic forms. Patients with the "classic" form--vasoconstriction or hypovolemic nephrosis--have high renin and aldosterone levels that are stimulated rather than suppressed by salt-loading but become lower before steroid diuresis. These patients have minimal lesion disease and, perhaps from diffuse capillary damage, tend to have hypovolemia with renin-induced vasoconstriction. Patients with the second, and heretofore undescribed, form--hypervolemic or overfilling nephrosis--have low renin and aldosterone values that rise normally after sodium depletion. Hypertension, mild renal insufficiency, hypervolemia, and steroid resistance with chronic glomerulonephritis are seen histologically. This form appears volume overloaded from impaired renal sodium excretion. In remission of either type, renin system deviations tend towards normal, but one form does not convert to the other. Renin-sodium profiling may help reveal the two forms and predict steroid responsiveness.
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PMID:Nephrotic syndrome: vasoconstriction and hypervolemic types indicated by renin-sodium profiling. 49 1

A patient with a single functioning kidney presented with the nephrotic syndrome. On the basis of highly selective proteinuria, a diagnosis was made of lipoid nephrosis. Steroid therapy over a 2-year period did not control the disease. The patient eventually developed end-stage renal failure and malignant hypertension. Nephrectomy was performed to control the hypertension. Histological examination showed congenital dysplasia in one kidney and sclerosing glomerulonephritis, malignant nephrosclerosis, as well as dysplastic changes in the other.
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PMID:Sclerosing glomerulonephritis and malignant hypertension in a patient with congenital renal dysplasia: A case report. 55 Apr 41

Seventeen children, 12 boys and 5 girls with histopathologic confirmation of focal sclerosing glomerulonephritis (FSG) presented with nephrosis (100%), hypertension (64.7%), intermittent hematuria (58.8%) and associated infection (82.3%). The coagulation-profile study in these patients revealed a hypercoagulable state characterized by significant elevation of fibrinogen and factor V concentrations and platelet count (P less than .002--.02). Increased blood viscosity (13.64 +/- 3.3 cp) was also noted in the patients (controls 10.8 +/- 0.9 cp). Determination of platelet half-life and fibrinogen half-life demonstrated that these were both shortened (P less than .001). Predominant shortening of platelet half-life was observed in 3 of the 4 patients during heparin therapy but this reverted to normal during therapy with the antiplatelet agent (Persantin). These findings signify the presence of a low-grade intravascular coagulation which perhaps occurs in the glomerular capillaries. Significant increments in creatinine clearance (CCr) and renal blood flow (RBF) were observed with treatment in the 9 anticoagulant-treated patients but not in the 8 control patients treated with prednisone and cyclophosphamide.
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PMID:Focal sclerosing glomerulonephritis: a kinetic evaluation of hemostasis and the effect of anticoagulant therapy: a controlled study. 72 13

We describe a method for determining those urinary total phenolic compounds that are tyrosine analogs or metabolites, such as thyroxine and catecholamines. The urine sample, 4-aminoantipyrine in carbonate-bicarbonate buffer, and potassium ferricyanide solution are mixed and the quinoneimine dye that forms is measured at 500 nm. Some cases of hyperthyroidism, diabetes mellitus, nephrosis, obesity, hypertension, or catecholamine-producing tumor showed above-normal values, so that this determination seems useful as a screening test for these disorders.
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PMID:Determination of urinary total phenolic compounds with use of 4-aminoantipyrine: suggested screening test for hyperthyroidism and for catecholamine-producing tumor. 91 84

To evaluate the contribution of systemic hypertension in the progression of nephropathies to glomerular sclerosis, a mild form of puromycin aminonucleoside (PAN) nephrosis was associated with Goldblatt hypertension and studied after 18 weeks. We studied four groups: Group I, controls; Group II, Goldblatt hypertension; Group III, PAN nephrosis; and Group IV, both conditions. Systolic blood pressure, 24-h proteinuria, serum cholesterol, triglycerides, glomerular hemodynamics, and histological studies were compared among the groups. Rats in groups II and IV developed systemic hypertension, but only group IV rats showed persistent proteinuria. No alterations in lipid metabolism were present in any of the groups. The most striking findings in the micropuncture studies were a significant increase of glomerular capillary pressure in group IV rats (63.15 +/- 1.34 mm Hg) as compared to controls (48.74 +/- 0.97 mm Hg) and to groups II and III (55.31 +/- 2.11 and 48.17 +/- 1.23 mm Hg, respectively), and a marked fall in Kf in groups III and IV. Only group IV showed significant histological alterations such as glomerular sclerosis, interstitial damage, and increased glomerular area. These results suggest that, in the presence of an underlying nephropathy, a greater fraction of systemic pressure is transmitted to the glomerular capillaries when systemic hypertension is present; the resulting elevation in glomerular pressure and proteinuria seems to be responsible for the progression to glomerular sclerosis.
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PMID:Mechanisms involved in the progression to glomerular sclerosis induced by systemic hypertension during mild puromycin aminonucleoside nephrosis. 141 51

Analysis and comparisons were made between the clinical and pathological data obtained from 42 cases of type I and 17 cases of type III membranoproliferative glomerulonephritis (MPGN). It was shown that type I MPGN differed from type III remarkably in following respects: (1) Nephrosis was a salient feature of type III while hypertension, impairment of renal function and hematuria were more common in type I. (2) Pathological glomerular sclerosis, tubular interstitial changes and crescents formation occurred frequently in type I but not in type III. (3) Long term prognosis for type III was much better than type I. It is concluded the type III MPGN is a distinct clinical entity which differs from the classical type I MPGN in many aspects.
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PMID:[Clinical and pathological features of type I and III membranoproliferative glomerulonephritis]. 147 29


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