Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Nephrosclerosis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1978

Renal insufficiency in nephrosclerosis (benign nephrosclerosis resp. transition from benign to secondary malignant nephrosclerosis) correlations between morphological and functional parameters.

62 tissue specimens with the only diagnosis benign nephrosclerosis (or benign nephrosclerosis with transition to secondary malignant nephrosclerosis) were investigated attempting to correlate morphological findings (relative interstitial volume of the renal cortex, types of hyalinisation and kinds of periglomerular changes, vessel index) with each other and with the serum creatinine concentration as a parameter of renal function. There are significant correlations in form of exponential and parabolic functions between relative interstitial volume of the renal cortex and the serum creatinine concentration at the time of biopsy. Furthermore 5 types of glomerular and periglomerular changes, which could be discriminated, seem to influence renal function in a different way and at different stages of the disease. An additional factor are the arteriolar changes. There are positive rank correlations between vessel index and serum creatinine concentration as well as between vessel index and relative interstitial volume. In cases with a higher percentage of hyalinized glomeruli more pronounced arteriolar lesions (partly alterations which can be found in secondary malignant nephrosclerosis) were observed. No connections seem to exist between mean blood pressure and the mentioned morphological and functional parameters. The reduction of renal function seems to be caused by tubular and interstitial factors: the often observed atrophy of tubules in fibrotic areas possibly impairs resorptional capacity. The mechanisms of the glomerular-tubular-balance may lead to a diminished glomerular filtration. On the other hand alterations of the capillaries may induce perivascular edema, which, if not reabsorbed, leads to interstitial fibrosis. The produced collagen fibres may reduce the cross sectional area of the postglomerular vessel network. This may lead to a slowing of the renal cortical and glomerular blood flow, thus inducing an increase of the serum creatinine concentration. Weighing all factors, the interstitial fibrosis seems to be the most important.

Arterioles↗
PubMed1976

Malignant nephrosclerosis during pregnancy and in the postpartum period (the uremic hemolytic syndrome).

Histologic, immunohistologic, and ultrastructural features are presented of two cases with malignant nephrosclerosis during pregnancy. Primary malignant nephrosclerosis emerges as a clinical entity which can be distinguished from toxemia of pregnancy in the midtrimester and post partum. The first description of malignant nephrosclerosis dates from 40 years ago, but only a few cases were reported associated with pregnancy. Although disseminated intravascular coagulation seems involved, the morphology is different from that of toxemia. Malignant nephrosclerosis reveals a close similarity to the hemolytic uremic syndrome. Early diagnosis by renal biopsy and proper treatment may prevent a lethal outcome due to progressive failure.

Adult↗
PubMed1975

The glomerular mesangium in hypertension: a morphometrical comparison of nephrosclerosis with mesangioproliferative glomerulonephritis on renal biopsies.

Glomerular changes were morphometrically studied in renal biopsies of 27 cases of nephrosclerosis showing clinically benign or malignant hypertension and of 15 cases of mild mesangioproliferative glomerulonephritis with hypertension. In nephrosclerosis, there was a mild increase in mesangial matrix without cell proliferation. The degree of the mesangial changes varied little despite a large variation in blood pressure and showed no significant difference between benign and malignant hypertension. In mild mesangioproliferative nephritis with hypertension, mesangial matrix, as well as the number of mesangial cells, showed an increase of varying degree. A quantitative assessment of the mesangium was proved effective in differentiating the glomerular changes in nephrosclerosis from those in mesangioproliferative nephritis with hypertension.

Adult↗
PubMed1976

Primary malignant nephrosclerosis.

1. As proposed by Schürmann & MacMahon (1933), we suggest that two types of malignant nephrosclerosis exist. 2. In the type called primary malignant nephrosclerosis, renal vascular lesions precede hypertension. 3. In the second type, called secondary malignant nephrosclerosis, renal vascular lesions are considered to be the consequence of malignant hypertension.

Basement Membrane↗
PubMed1976

Nephrosclerosis postpartum and in women taking oral contraceptives.

The condition of a patient with postpartum nephrosclerosis improved during heparin therapy. Review of the literature disclosed 29 other patients with the same histopathologic characteristics, eight of whom also recovered substantial renal function after anticoagulation therapy. Also reported is a patient in whom renal failure occurred while she was taking oral anovulatory agents. Renal biopsy specimen showed the same histopathologic features, which raises the question of similar factors mediating the expression of this disease. We suggest a uniform terminology for this syndrome, either postpartum nephrosclerosis or nephrosclerosis in women taking oral contraceptives.

Adult↗
PubMed1992

Nephrosclerosis and aortic atherosclerosis from age 6 to 70 years in the United States and Mexico.

With increasing age, the thoracic aorta shows progressive fibroplastic intimal thickening, which is thought to be pre-atheromatous. A similar progressive intimal thickening in the renal cortical arteries is the distinguishing feature of the nephrosclerosis which underlies essential hypertension. Therefore, the earliest detectable youthful precursors of atherosclerosis and hypertension show strong morphological resemblances to each other. In this study, close statistical associations have been shown between the two types of arterial intimal fibroplasia. Both conditions show similar sigmoid growth curves from ages 6 to 70 years, thereby generating correlations across age groups of r = 0.99 in New Orleans and r = 0.95 in Mexico City. Specimens gathered in New Orleans were found to have about 1.4 times greater arterial intimal thickening than specimens from Mexico City, and this excess was seen at all ages in both the aortas and the renal cortical arteries. It seems likely that intimal fibroplasia of arteries is reflecting similar biological principles at all levels of the vascular tree. Whatever etiological factors vary between New Orleans and Mexico City, those factors appear to act directly at a tissue level to promote the early precursors of atherosclerosis and of the nephrosclerosis that underlies hypertension.

Adolescent↗
PubMed1978

[Are clotting disorders a pathogenetic factor in nephrosclerosis and hypertension? (author's transl)].

The clinical course of the haemolytic-uraemic syndrome in four patients suggests that hypertension may result from it. The morphological changes in the kidney are those of primary malignant nephrosclerosis. Hypercoagulability is thought to be an important pathogenetic factor in the development of the disease. But irreversible renal failure is not, contrary to typical primary malignant nephrosclerosis, an inevitable sequel. Abortive forms with predominant involvement of glomerular vessels have a more favourable prognosis than those forms with additional preglomerular vascular changes, in which a more or less marked impairment of renal function and hypertension persists. These forms are of particular interest because they indicate a renal pathogenetic mechanism of chronic hypertension. The described observations--taken together with those on the pathogenesis of hypertension caused by oral contraceptives--provide a pointer to the importance of clotting disorders in the initiation and development of some forms of hypertension.

Adult↗
PubMed1975

[Primary malignant nephrosclerosis (author's transl)].

Primary malignant nephrosclerosis shows a haemolytic-uraemic symptomatology and can be differentiated from secondary malignant nephrosclerosis on clinical and histological grounds. The disease was observed in 4 patients: a 25-year-old man and 3 women aged 19, 28 and 49 years. The disease is characterized by a fulminating course, malignant hypertension with progressive retinopathy, and development of progressive renal failure with subsequent irreversible anuria. In addition haemolytic anaemia or posthaemolytic states as well as consumption coagulopathy occur. In 2 cases schizozytes and in particular helmet-shaped forms could be demonstrated. On histology an obliterating necrotizing vascular change is seen which is limited to the kidneys as was demonstrated in one case by angiography. Therapeutic attempts included antibiotics, steroids, heparin, streptokinase, antihypertensive drugs, and haemodialysis. The 3 female patients died, the man survived after bilateral nephrectomy.

Acute Disease↗
PubMed1978

An accelerated hypertension with neither malignant nephrosclerosis nor elevation of plasma renin activity.

A case of accelerated hypertension, which was unique in a resistance to an angiotensin antagonist, and a lack of the elevation of plasma renin activity (PRA) is reported. Non-elevated PRA was coincided with non-malignant nephrosclerosis in renal histology. The acceleration was attributed to the neurological cause i.e., cerebral hemorrhage in the right hypothalamus which extended to the ventricle and subarachnoid space. The case therefore clinically seemed malignant-like, but it was not malignant hypertension in the sense of Volhard's classical definition. This does not conflict with the usefulness of the determination of PRA in the diagnosis of malignant hypertension with nephrosclerosis.

Aged↗
PubMed1978

Pathology of malignant nephrosclerosis with special reference to the difference between histologic manifestations of pure and exacerbated forms.

Fourteen autopsied cases of malignant nephrosclerosis were classified into 6 of pure form in which syndrome of malignant hypertension developed from the beginning of the disease, and 8 of exacerbated form with appearance of the syndrome in the course of essential hypertension. Pathohistological study of these cases elucidated the differences in histologic manifestations between pure and exacerbated forms of malignant nephrosclerosis as to which little had been known as yet. In the pure form arterioles and small arteries characteristically demonstrated acute or recent lesions such as fibrinoid necrosis and hemorrhage into intima, and intimal cellular hyperplasia of somewhat longer duration, whereas in the exacerbated form coexistence of vascular lesions of various intensities and durations, acute (fibrinoid necrosis and hemorrhage), intermediate (intimal cellular hyperplasia) to chronic (sclerosis and lamellar elastosis), and superposition of more recent vascular lesions on more advanced or older ones were noted. Superposition of vascular alterations was interpreted to be not necessarily specific for exacerbated form but histologic manifestation of recurrence which is liable to be the case more frequently in exacerbated form than in pure form in the longer course of essential hypertension or of malignant hypertension. Some other related problems were also considered and discussed.

Adult↗
PubMed1975

Low-renin hypertension: nephrosclerosis?

A substantial group of patients with essential hypertension have abnormally low renin levels which respond poorly to stimulation. Important differences in response to therapy and in prognosis have been described between these and other hypertensive patients. It is suggested that the vascular changes of nephrosclerosis, which may be seen in both hypertensive and normal subjects, result in a reduction of afferent arteriolar distensibility, with impairment of basal renin secretion and responsiveness. This hypothesis accords with both of the known clinical characteristics of low-renin hypertension and with the known effect of arterial changes upon the activity of other baroreceptors.

Age Factors↗
PubMed1976

[Oral contraceptives, hypertension and nephrosclerosis (author's transl)].

Five personal cases and many reports in the literature demonstrate the not rare development of hypertension after oral contraceptives or an increase of an existing hypertension. In addition, the drug may also cause vascular changes in the kidneys with development of benign or malignant nephrosclerosis, similar to the increased risk of thrombo-embolic complications of the venous-arterial system. It is, therefore, necessary to check the blood pressure of women on oral contraceptive and, if hypertension exists or develops, discontinue these drugs.

Adult↗
PubMed1977

[Renal transplantation in malignant nephrosclerosis (author's transl)].

Renal transplantation was performed 3 to 64 months after the onset of dialysis in 6 patients with histologically ascertained malignant nephrosclersosis and malignant hypertension, as well as terminal renal failure. Three patients were nephrectomized on both sides before and one after the transplantation. 24 to 105 months after the transplantation all patients were normotensive. Only one patient required low-dosage antihypertensive medication. There was evidence for marked improvement of cardiovascular complications, and no evidence for recurrence of malignant nephrosclerosis in the transplanted kidney.

Adult↗
PubMed1978

Glomerular injury in malignant nephrosclerosis.

Electron microscopic analysis of subendothelial and mesangial alterations in the glomeruli was performed in 15 cases of malignant nephrosclerosis (MNS). 8 cases showed segmental or diffuse subendothelial accumulation of proteinaceous 'fibrinoid' material associated with thickening of glomerular basement membranes. 2 of these cases also showed similar deposits in the mesangium. When severe, this mesangial insudation resulted in almost complete replacement and destruction of the mesangial matrix. Endothelial injury with alteration of glomerular microcirculation and secondary intravascular coagulation is believed to play a role in the development of the glomerular lesions in MNS.

Basement Membrane↗
PubMed1978

Arteriolar nephrosclerosis in the Syrian hamster.

Syrian hamsters developed spontaneous renal lesions that resembled those of arteriolar nephrosclerosis in man, and differed from other spontaneously occurring or virus-induced renal diseases in other rodent species. Morphologic changes were mainly degenerative with little cellular exudation and were associated with histologic changes in the intrarenal vasculature. The renal lesions were progressive, often fatal and sometimes were complicated by glomerular amyloidosis with the nephrotic syndrome and uremia. Endstage kidneys often had fibrinoid necrosis of intrarenal arterioles and thus resembled lesions characteristic of the malignant phase of human essential hypertension. Fibrinoid necrosis of small arterioles was common in the uterus, ovaries or testes of affected animals; it was less frequent in mesenteric or coronary vessels. Cardiac thrombosis, often involving the left atrium or left atrioventricular valves, also was common. Changes occurred earlier and often were more severe in females than in males. This disease was a major cause of morbidity and mortality and hampered life-span studies.

Animals↗
PubMed1978

[Oral contraceptives, hypertension and nephrosclerosis].

Oral contraceptives are of pathogenetic importance in hypertension of women aged 26 to 35 years. The hypertensive reaction occurs predominantly in those women who have hereditary predisposition to hypertension or diabetes mellitus, who suffer themselves from diabetes or who showed toxemia in previous pregnancies. Our findings are not in agreement with the suggestion that oral contraceptive hypertension in women is always reversible. Simultaneous administration of estrogen and progestogen accelerates Goldblatt-type hypertension in rats. Neither estrogen nor progestogen alone alters arterial blood pressure. In the hormonal combination the hypertensive effect of estrogen can be replaced by epsilon-aminocapronic acid. Estrogen is the only substance increasing plasma renin activity. There is no correlation between the increase of blood pressure and the plasma renin activity in the various groups of experimental animals receiving the different pharmacological substances. Estrogen and the synthetic progestogen cause sodium retention. Because of this, oral contraceptive hypertension may be supposed not to result from a stimulation of the renin-angiotensin-system. Oral contraceptive hypertension may result from a combination of endothelial lesions due to the estrogen's effect on blood coagulation leading to nephrosclerosis, and sodium retention produced predominantly by the synthetic progestogen.

Adult↗
PubMed1978

Late follow-up in women with nephrosclerosis diagnosed at pregnancy.

Thirteen nephrosclerotic women were followed for 2 to 7 years from the time a diagnosis was made following a pregnancy complicated by hypertension. Ten patients developed sustained hypertension. Twelve women who were examined responded with a hypertensive pattern to acute salt load. Of the 10 patients who were examined, seven had a reduced renal plasma flow (RPF) demonstrated by the phenolsulfonphthalein (PSP) excretion test. The present observations support the view that the vascular lesion in the kidneys precedes and persists independently of pregnancy. The pregnant state brings the hypertensive disease to clinical expression.

Adult↗