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Results for “ARTERIOLOSCLEROSIS”

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At least 199 records · Page 11Linked to original sources

PubMed1989

[De novo diabetic glomerulosclerosis in kidney transplants].

Report on 3 cases who had been non-diabetics at the time of cadaver kidney transplantation. After that within 1-5 years diabetes mellitus developed. The patients died 13-14 years after transplantation (9-12 years of diabetes duration). Autopsy revealed typical nodular glomerulosclerosis including diffuse mesangial widening, glomerular aneurysms, exudative lesions, capsular drops, arteriolosclerosis, and in 2 cases with hyalinosis of the vas efferens; moreover, chronic transplant glomerulopathy was found in all cases. Steroid therapy seemed to be responsible for the diabetic state, in 2 cases apparently in combination with disposition.

Diabetic Nephropathies↗

PubMed1989

[Case of multiple macroaneurysms of the retinal arteries].

A 74-year-old female with acquired macroaneurysms of the retinal arteries of the left eye is presented. During a follow-up period of three years of this rare case, six macroaneurysms developed one after another. Three of them were treated by argon laser photocoagulation because of severe complications such as retinal haemorrhage and exudation onto the macula. However, recovery of visual function of the final stage following treatment was unsatisfactory. Concerning the unusual clinical course of this case, we speculate that severe arteriolosclerosis of the retinal vessels played a fundamental role in this pathological condition.

Aged↗

PubMed1989

The woolly monkey (Lagothrix lagothricha): a possible model for human hypertension research.

The anatomical-pathological findings of 15 woolly monkeys were comparable with those described in man with essential benign or malignant hypertension. Kidneys revealed arterio- and arteriolosclerosis or an onion peel-like proliferation, in some cases necrotizing endarteritis. Obesity due to restricted physical activity, unnatural feeding, and psychical and physical stress could have contributed to the development of this condition. Further, high vulnerability of the genus woolly monkey is postulated. Thus, essential hypertension of woolly monkeys appears to be a multifactorial disease.

Animals↗

PubMedDate not supplied

[Angiographic and morphologic criteria of the manifestation of arteriolonephrosclerosis in vasorenal hypertension].

Parallel comparison of angiographic and morphologic indices of arterial nephrosclerosis levels was performed in 34 patients with vasorenal hypertension secondary to unilateral lesion of renal arteries. Coefficient of vascular picture absence zone in the kidney (30) presenting a percentage ratio of a vascular zone of kidney cortical layer and the total area of its section was employed. Amount of vascular index (ratio between the wall density of afferent glomerular arteriole and its lumen diameter) was used to assess arteriolosclerosis in morphologic examination of renal biopsy specimens. High level of reliable coefficient 30 in the evaluation of arteriolar nephrosclerosis degree was substantiated morphologically. Critical level of coefficient 30 was stated for the affected and contralateral kidneys, and its increase was suggestive of irreversible sclerosis of renal microvascular bed.

Adult↗

PubMed1989

[Relation of the effectiveness of surgical treatment of vasorenal hypertension and morphologic changes of the kidneys].

Renal puncture and incision biopsy specimens were investigated, using light and electron microscopic techniques, in 34 patients with vasorenal hypertension. The magnitude of the hypotensive effect of reconstructive surgery on renal arteries is shown to be largely dependent on the severity of arteriolosclerosis in the ischemized kidney rather than the contralateral one. Quantitative assessment of the severity of renal arteriolar sclerosis has established a critical vascular index (the ratio of arteriolar wall thickness to lumen diameter) above which the probability of reconstructive surgery producing a hypotensive effect becomes rather low.

Adult↗

PubMed1979

Cerebral vascular changes in systemic lupus erythematosus.

Cerebral vascular lesions of 26 cases in systemic lupus erythematosus during a period from 1963 to 1978 were examined histologically and the following conclusions were made: 1. The prominent vascular changes of the brain were thrombosis, fibrinoid degeneration, endothelial swelling and proliferation, arteriolosclerosis, and perivascular infiltration of inflammatory cells. 2. From clinico-pathological viewpoints, thrombosis seemed to play an important role in the development of neurological signs. In five cases, characteristic granular or homogeneous thrombi were observed in the small blood vessels including venule. Infarct without proved vascular obstruction but probably due to thrombosis was seen in four cases. The true character of the granular thrombi was not determined, either electronmicroscopically or immunohistochemically. These suggested the presence of a tendency for in situ formation of thrombus. 3. Fibrinoid degeneration seen in four cases mainly affected arterile of less than 50 micrometer in diameter in the cerebral cortex, basal ganglia, and brain stem. This change of arteriole did not play a significant role in neurological signs. 4. Endothelial swelling and proliferation of the small blood vessels were prominent in the cases with thrombosis and fibrinoid degeneration. 5. Perivascular infiltration of the inflammatory cells was observed in about one-half of the cases but its significance was not clear.

Adolescent↗

PubMedDate not supplied

[Is the kidney lesion caused by hypertension really ischemic?].

Renal damage is systemic hypertension has traditionally been related to an ischemic glomerular injury secondary to arteriosclerosis and arteriolosclerosis of preglomerular vessels. The use of micropuncture techniques with histopathologic studies have suggested non ischemic mechanisms of renal damage in systemic hypertension. Indeed in experimental models of hypertension which include DOCA-Salt, Goldblatt hypertension or genetic hypertension, the development of glomerular damage is associated with hyperfiltration secondary to increases in flow and pressure to the glomerular capillary. Hyperfiltration as a mechanism of renal damage in human systemic hypertension has not been established. Recent studies from our group have demonstrated lack of renal functional reserve in patients with systemic hypertension, reserve which is reestablished after 3 days of antihypertensive treatment. These data suggest therefore the presence of hyperfiltration as a possible mechanism of renal damage in patients with essential hypertension.

Animals↗

PubMed1987

Cardiopathology of sudden cardiac death in the race horse.

Twenty thoroughbred race horses were selected for postmortem cardiopathological study of sudden cardiac death; ten of the twenty horses died suddenly. In order to define accurately the morphological changes observed in these ten hearts, ten other thoroughbred race horses considered to have normal hearts were selected as a control group and studied by postmortem coronary angiography. Of the ten horses that died suddenly, eight were witnessed to have died either during or shortly after training or racing. The death was instantaneous except in one horse, which showed ventricular tachycardia and died 4.5 h after a race. The other two died unexpectedly in the stable at night. Pathologically, the horses that died suddenly generally showed multifocal myocardial lesions that were ischemic and fibrotic. These lesions were found in the atrial tissue close to the sinoatrial (SA) node and in the atrioventricular (AV) junction, including the upper portion of the interventricular septum. Such myocardial lesions were often associated with vascular changes including arterio- and/or arteriolosclerosis. Angiographically, the SA node appeared to be perfused by atrial branches of the left and right coronary arteries. One branch originating from the left coronary artery gave off a few branches into the AV junction. These pathological findings, mainly consisting of both atrial lesions and lesions in the AV junction, were similar to those observed in horses with either atrial fibrillation, SA block, or paroxysmal ventricular tachycardia. A finding of particular interest was the angiographic demonstration that the blood supply to the AV junction partly came from the SA node artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Spontaneous hypertension in the fawn-hooded rat: a cardiovascular disease model.

The fawn-hooded (FH) rat develops hypertension spontaneously. Systolic blood pressure is already elevated at 5 weeks of age, increases with age, and the final range is 180-240 mmHg at the age of 1 year. Concomitantly with the rise in blood pressure proteinuria occurs and increases with age. Fawn-hooded rats reaching the accelerated phase of the hypertension are characterized by blood pressure values exceeding 220 mmHg, heavy proteinuria and increased heart, kidney, liver, adrenal and spleen weights. Those prone to malignant hypertensive disease show a period of increased water turnover for several weeks after weaning; during this period, they do not show the pronounced decrease in water intake upon fasting for 24 h as observed in FH rats of the same age prone to a milder form of hypertension, i.e. diuresis and drinking continue even when no food is consumed. The major cause of death for FH rats is malignant nephrosclerosis with the nephrotic syndrome and/or cardiac failure with chronic pulmonary congestion. Some animals die of bleeding from mesenteric vessels with periarteritis nodosa. In FH rats with malignant hypertension, heart, kidney, liver and spleen weights are significantly increased compared with FH rats of the same age with mild hypertension. Histopathology shows myocardial fibrosis and myocardial infarctions. Generalized arteriolosclerosis is common, sometimes accompanied with local fibrinoid degeneration and (peri)arteritis. Some major arteries show intimal proliferation. It is concluded that the FH rat provides an interesting model for the study of hypertension and its consequences.

Animals↗

PubMed1987

Malignant or accelerated hypertension in IgA nephropathy.

A retrospective analysis of 66 adult patients diagnosed as having IgA nephropathy by renal biopsy revealed that 24 (36%) were hypertensive when first seen. Of these hypertensive patients, 10 (15%) had malignant or accelerated hypertension. All patients but one were male and had no knowledge of their renal disease and sought medical advice for symptoms due to hypertension. Five patients had no history of gross hematuria. Histological vascular findings showed, in three proliferative endarteritis and fibrinoid necrosis, in five arteriolosclerosis and in two vascular hypertrophy. In spite of good blood pressure control, six patients reached terminal uremia within a maximum of 14 months. In summary, the incidence of malignant hypertension in adults with IgA nephropathy is higher than previously reported, and its true incidence can only be known if more histopathologic studies of patients with malignant hypertension are performed. Patients with this association reach end stage renal failure in a short period of time.

Adult↗

PubMed1979

Postpartum hemolytic uremic syndrome: a study of three cases with a review of the literature.

Three cases of postpartum hemolytic uremic syndrome (HUS) are presented. Symptoms of acute renal failure, hypertension and microangiopathic hemolytic anemia with thrombocytopenia occurred 10, 17 and 24 days after delivery. Despite early heparin therapy in all cases, one patient went into terminal renal failure needing chronic hemodialysis, with persistent hypertension which became uncontrollable requiring bilateral nephrectomy 6 months later. The second patient had diuresis one month after starting hemodialysis, but 3 months later developed malignant hypertension. Slight improvement in renal function with persistent hypertension occurred after hemodialysis for 20 months. The third patient showed complete clinical recovery after 2 months. Pathological examination of renal tissue showed the typical lesions of thrombotic microangiopathy (TMA). However, striking differences were observed in the lesion seen in early and late specimens. Early lesions could be differenciated from infancy TMA because the medium-dize arteries were more severely involved. Late lesions were variable, ranging from minor changes in glomeruli and blood vessels, via ischemic and sclerotic lesions in glomeruli with arteriolosclerosis, to the vascular and glomerular lesions seen in malignant nephrosclerosis. There was a good correlation between the renal pathology and the clinical outcome of the patients. HUS with renal TMA as a cuase of postpartum renal failure has been reported in 49 patients with a fatal outcome in 61%. The pathogenesis of the syndrome probably involves a primary endothelial damage. This causes local renal intravascular coagulation in the presence of the usual postpartum hypercoagulable state. This is shown by the presence of fibrin-fibrinogen in glomeruli and vessels, increased plasma fibrin degradation products, thrombocytopenia and lowered levels of coagulation factors. There is little hematological or pathological evidence fo disseminated intravascular coagulation or an immune-complex disease. Hypocomplementemia seen frequently is probably due to local C3 activation via the alternative pathway.

Adult↗

PubMed1977

[Morphology of diabetic nephropathy (author's transl)].

Renal complications occur frequently in diabetics. Glomerular lesions exist in basal membrane thickening, diffuse and nodular glomerulosclerosis, exudative lesions and glomerular aneurysms. Tubular and interstitial changes are characterized by Armanni-Ebstein cells, by pyelonephritis and papillary necroses. Vascular changes occur in the form of arteriosclerosis and arteriolosclerosis. Nodular glomerulosclerosis is characteristic of diabetic renal damage, all other changes only occur more frequently in diabetics. Recently, studies deserve attention which suggest a regression of glomerular lesions if the diabetic metabolism is normalized.

Aneurysm↗

PubMed1979

[The problem of hypertension and ovulation inhibitors].

It is reported on a 46-year-old woman who died of a haemorrhage of the cerebral matter in renally fixed hypertension and severe arteriosclerosis of the arteries of the basis of the brain. The possible connection between hypertension, arteriolosclerosis of the kidneys and arterioclerosis of the arteries of the brain basis and an intake of ovulation inhibitors lasting 10 years is critically discussed.

Cerebral Hemorrhage↗

PubMed1979

[Diabetic angiopathy. Proteinuria as an initial symptom].

Follow up studies in 19 diabetic patients with manifestation in the youth. Proteinurie within few years; later on nephropathy: 7 cases with glomerulosclerosis, 8 with arteriolosclerosis, 3 with pyelonephritis and 1 with chronic glomerulonephritis. In all cases retinopathy, very often coronarsclerosis, seldom peripheral and cerebral sclerosis. 14 patients died, mostly in young age in consequence of nephropathy. Proteinurie is a malignant symptom of diabetic angiopathy; in contrast to the retinopathy.

Adolescent↗

PubMed1983

[Clinical aspects and differential diagnosis of primary and secondary microangiopathies].

Diseases of the terminal vascular system are of particular diagnostic and differential-diagnostic importance in clinical angiology. While in the functional microangiopathies of the skin as a rule disturbances of the vasomotor function without an essential value of the disease are concerned, secondary organic changes of the wall of the vessel not infrequently determine the course and the prognosis of the basic disease (rheumatoid arthritis, collagenoses, hypertension and diabetes). Vasomotor trophic disturbances are observed also post-traumatically, post-operatively, after exposition to cold, in a lesion of the central nervous system and vertebra nerve irritations. For the allergic hyperergic vasculitides, which show an extraordinary polymorphism in the clinical picture in characteristic histological findings, an auto-immune pathogenesis is to be supposed. The chronic arterial hypertension leads to arteriolosclerosis and necrosis with adequate organic symptoms. In the diabetic microangiopathy we may demarcate functional pre-stages from irreversible structural changes of the vessels, in which case apart from the peripheral microangiopathy of the skin the retinopathy and nephropathy are to be classified as particularly important clinical manifestations.

Cyanosis↗

PubMed1983

Morphologic aspects of low-potassium and low-sodium nephropathy.

Renal biopsies from 40 patients with hypokalemia and hyponatremia of an average of 10 years' duration due to abuse of laxatives or diuretics, anorexia nervosa, or chronic vomiting were examined with morphometric methods. Light microscopy revealed the following alterations in the renal cortex as compared with 36 normal kidney: JGC were sometimes slightly and sometimes enormously enlarged (mean, 217%). Smaller glomeruli were found with reduction in the area of the glomerular capillaries and of Bowman's capsule (+/- 7%) but an increase in the area of the mesangial matrix by 25%. The proximal and distal tubules contained nonspecific vacuoles in only 8 of 40 biopsy specimens. Only minor, age-dependent arteriolosclerosis was demonstrable. In 75% of the cases, the interstitial surface area was increased (by 107%) with predominantly focal lymphocytic cellular infiltration. Interstitial fibrosis was more pronounced in emaciated patients. The morphologic-functional correlation between the increase of interstitial surface area and the rise in serum creatinine concentration was highly significant. Typical kaliopenic nephropathy is therefore detectable by light microscopy. GFR impairment correlates with the extent of interstitial fibrosis.

Adult↗

PubMed1982

Cellular arteriolar nodules. Their presence in heart, pancreas, and kidneys of patients with malignant nephrosclerosis.

Angioblastic-appearing nodules of small arteries of heart, pancreas, and kidneys were found during microscopic study of autopsy specimens form subjects with hypertension that had responded poorly to treatment. These vascular lesions were noted in three of 15 subjects studied; they were associated with a proliferative arteriolosclerosis that was most severe in the kidney and the pancreas, but was occasionally found in the arterioles of the heart. Two of these three subjects had received treatment with dialysis; one had not. The nodules originated concentrically along a segment of small artery and consisted of a mass of mesenchymal cells and capillary-sized blood channels. There were fragmentation and focal loss of the internal elastic lamina at their points of origin, and vessel-wall necrosis in an occasional lesion. Many of these nodules appeared identical to plexiform lesions of the lung and to cellular types of Charcot-Bouchard aneurysms of the CNS.

Adult↗

PubMed1982

[Postmortem diagnosis of hypertension].

The postmortem diagnosis of hypertension is of importance both for the determination of basic disease or terminal cause of death and for statistical investigations based on autopsy material or for comparisons between clinical and epidemiological data as well. The analysis of our autopsy records revealed: 1. The most important macroscopical findings are an increased weight of the heart, an arteriosclerosis of the peripheral extracerebral arteries of the brain, and an adenomatous hyperplasia or adenomas of the suprarenal cortex, they should be looked for at autopsy. 2. A microscopical finding of a hypertension is in the first place the arteriolosclerosis of kidneys followed by that of the pancreas, myocardium, liver, and brain. In practice, a specimen of kidney and pancreas should be investigated histologically in each case of a possible hypertension.

Adenoma↗