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↗
PubMed1986

Decompensated benign nephrosclerosis and secondary malignant nephrosclerosis.

Using semiquantitative morphometric methods, the clinical picture of decompensated benign nephrosclerosis is distinguished from that of secondary malignant nephrosclerosis, designated as the consequence of high pressure. It is shown that hypertensive glomerulopathy triggered by high pressure and postglomerular interstitial fibrosis with tubular atrophy are in the foreground of pathologic changes in decompensated benign nephrosclerosis, whereas the preglomerular vessel network is most often affected in secondary malignant nephrosclerosis. The preglomerular vascular lesions in secondary malignant nephrosclerosis lead to such heavy stenosis of the afferent vessels that the clinical picture of hypertensive glomerulopathy is rarely observed, while that of ischemic glomerular capillary collapse is frequent. The preferred affliction of the glomeruli and the postglomerular vessel network leads in decompensated benign nephrosclerosis to severe interstitial fibrosis, which has a pyramidal form, decreasing from the base of the pyramid at the corticomedullary boundary to the outer renal cortex. In secondary malignant nephrosclerosis fibrosis of the renal cortical interstitium is homogeneous in all layers of the renal cortex. Clinically, decompensated benign nephrosclerosis and secondary malignant nephrosclerosis, which occur predominantly in young to middle-aged males, manifest malignant hypertension. They are also accompanied by progressive renal insufficiency.

Adult↗
PubMed1998

The long-term prognosis of benign nephrosclerosis accompanied by focal glomerulosclerosis and renal cortical interstitial fibrosis, designated so-called decompensated benign nephrosclerosis by Fahr, Bohle and Ratscheck.

The long-term prognosis of decompensated benign nephrosclerosis (DBN) was investigated by a retrospective analysis of the fate of 170 patients with this disease, which yielded the following results: 1) DBN carries a particularly poor prognosis. The renal survival rate (RSR) was 35.9% at 5 years and 23.6% at 10 years. The prognosis is therefore worse than that of any other primary glomerulopathy, with the exception of rapidly progressive glomerulonephritis. 2) DBN mainly affects males (sex ratio 5:1) and differs in this respect, among others, from focal sclerosing glomerulonephritis, in which the male:female ratio is 1.2:1. 3) The prognosis for females is no better than for males. 4) The severity of proteinuria at the time of biopsy has no influence on the prognosis. 5) The prognosis is particularly poor in cases in which the serum creatinine concentration is already elevated to more than 2.0 mg% at the time of biopsy. We conclude from these findings that not only the blood pressure, but also the serum creatinine concentration, should be assessed at regular intervals in all hypertensive individuals, so that DBN can be treated at an early stage, when it is still amenable to treatment.

Adult↗
PubMed1982

The compensated and the decompensated form of benign nephrosclerosis.

Decompensated benign nephrosclerosis, a disease which was briefly described by Theodor Fahr in 1925, defended by him in 1934, and then forgotten, is reported and differentiated from compensated benign nephrosclerosis. Decompensated benign nephrosclerosis can be differentiated from compensated benign nephrosclerosis by the frequent appearance of interstitial cortical fibrosis and glomerular alterations in the sense of hypertensive glomerulopathy. Hypertensive glomerulopathy results in ascending obliteration of the glomeruli, i.e., their transformation into PAS-positive hyaline globules. In compensated benign nephrosclerosis, interstitial fibrosis, if present at all, can usually be identified only in the subcapsular areas. In decompensated benign nephrosclerosis, however, a pyramid-like structure with its base at the corticomedullary border is formed. The severity of preglomerular vascular alterations does not differ in compensated and decompensated benign nephrosclerosis. Clinically, there is no significant difference between the degree of hypertension and the development of the disease. The nephritic symptoms are more pronounced in decompensated benign nephrosclerosis, which predominantly affects middle-aged men (male:female, 5.7:1), than in compensated benign nephrosclerosis. As a result, decompensated benign nephrosclerosis is frequently diagnosed and treated as chronic glomerulonephritis.

Chronic Disease↗
PubMed1995

The link between hypertension and nephrosclerosis.

Nephrosclerosis is literally defined as hardening of the kidneys (Greek derivation: nephros, kidney; sklerosis, hardening). It is the result of scarring or replacement of the normal renal parenchyma by dense collagenous tissue. In practice, nephrosclerosis refers to diseases with predominant pathologic changes occurring in the preglomerular microvasculature and secondarily involving the glomeruli and interstitium. The relationship between mild to moderate hypertension and either nephrosclerosis or end-stage renal disease (ESRD) remains circumstantial, although these syndromes have long been associated in the medical literature. Nephrologists credit hypertension as the etiology of nephrosclerosis in 25% of patients initiating Medicare-supported renal replacement therapy, even though other processes may cause similar renal pathologic findings. Strikingly, serum creatinine values infrequently increase in patients with long-standing mild to moderate hypertension. Patients classified as having hypertensive ESRD typically present with advanced disease, making the processes that initiated the renal disease difficult to detect. Nephrologists are twice as likely to label an African-American patient as having hypertensive nephrosclerosis, compared with a white patient, when presented with identical clinical histories. This review proposes that many patients classified as having hypertensive nephrosclerosis actually have intrinsic renal parenchymal diseases, renal artery stenosis, unrecognized episodes of accelerated hypertension, or a primary renal microvascular disease. The familial clustering of ESRD attributed to hypertension in African-Americans and the identification of genes associated with renal injury in animals support the concept that inherited factors may predispose to renal failure. African-American families often have members with ESRD from disparate etiologies, including hypertensive ESRD. This suggests that common mechanisms, be they inherited or environmental, underlie the development of progressive renal failure in diverse forms of nephropathy. Identification of the mechanisms producing susceptibility to progressive renal disease would support the concept that mild to moderate elevations in blood pressure per se are uncommon causes of nephrosclerosis.

Animals↗
PubMed2003

Stent angioplasty of severe atherosclerotic ostial renal artery stenosis in patients with diabetes mellitus and nephrosclerosis.

Atherosclerotic renal artery stenosis (ARAS) may lead to deterioration of renal function or hypertension. The clinical outcome after stent angioplasty of ARAS on renal function and blood pressure control in patients with diabetes and nephrosclerosis is the subject of some controversy. We have analyzed the results of our single-center experience with stent angioplasty for severe (>/= 70%) ostial ARAS and present here the results of a subgroup analysis of those patients who had diabetes mellitus and nephrosclerosis. From 1996 to 2001, 241 patients underwent stent angioplasty for the treatment of ARAS at our center. Of these, 99 patients had diabetes mellitus (41%) and 176 patients (73%) had nephrosclerosis defined as intrarenal resistance index (RI) >/= 0.7 diagnosed by duplex ultrasound. All lesions (n = 355) were treated successfully. Mean blood pressure at baseline was comparable and significantly improved immediately after the intervention in all groups (nondiabetics: 102 +/- 12 to 93 +/- 10 mm Hg; diabetics: 102 +/- 14 to 93 +/- 11 mm Hg; RI < 0.7: 105 +/- 13 to 95 +/- 10 mm Hg; RI = 0.7-0.8: 100 +/- 12 to 92 +/- 10 mm Hg; RI > 0.8: 102 +/- 15 to 92 +/- 11 mm Hg; P < 0.0001 each). Baseline serum creatinine was not significantly lower in nondiabetics compared to diabetics (1.46 +/- 0.9 vs. 1.62 +/- 1.2 mg %; P < 0.05) and increased in patients with nephrosclerosis (RI < 0.7: 1.18 +/- 0.6 mg %; RI = 0.7-0.8: 1.57 +/- 1.1 mg %; RI > 0.8: 1.96 +/- 1.6 mg %). Except for patients without nephrosclerosis who had a normal baseline creatinine, serum creatinine decreased significantly in all subgroups during follow-up. Stent angioplasty of ARAS offers favorable acute and long-term clinical results for the preservation of the renal function and for blood pressure control in patients with diabetes mellitus and nephrosclerosis.

Adult↗
PubMed1993

Hyperfiltration and conservation of renal function in hypertensive nephrosclerosis patients.

Renal glomerular hyperfiltration has been proposed as an important contributing factor to the progression of hypertensive nephrosclerosis in rats with reduced renal mass. However, no clinical studies have assessed the role of glomerular hyperfiltration in the pathogenesis of hypertensive nephrosclerosis in humans. In a prospective, randomized, long-term blood pressure control study with up to 3 years follow-up, we showed that good blood pressure control with a mean diastolic blood pressure < or = 95 mm Hg preceded by a 2- to 4-month period of diastolic blood pressure < or = 80 mm Hg improved renal function in hypertensive nephrosclerosis patients. Patients treated with minoxidil, an angiotensin-converting enzyme inhibitor (enalapril), or a calcium entry blocker (nifedipine) had improvement in renal function, as indicated by a positive slope of the reciprocal serum-creatine concentration versus time and an increment in glomerular filtration rate. These results suggested that improvement in renal function occurred with these major types of antihypertensive drug treatment. To assess the renal hemodynamics of minoxidil, enalapril, and nifedipine, eight patients with hypertensive nephrosclerosis were admitted to the General Clinical Research Center for renal clearance studies on each drug while ingesting a fixed-calorie, 12% protein, 40% fat, and 100 mEq Na/d diet. Mean blood pressure, effective renal plasma flow, and renal vascular resistance did not change during the three phases of treatment. However, minoxidil treatment increased the glomerular filtration rate by 48% versus enalapril and by 79% versus nifedipine. Since minoxidil treatment improves renal function while causing a relative hyperfiltration, glomerular hyperfiltration per se is an unlikely mechanism for the progression of hypertensive nephrosclerosis in humans.

Adult↗
PubMed1994

Renal biopsy findings in presumed hypertensive nephrosclerosis.

The 'classic' descriptions of renal histologic abnormalities in patients with hypertensive nephrosclerosis were based upon specimens obtained at autopsy or sympathectomy and were evaluated by light microscopy, without the aid of immunofluorescence or electron microscopy. Patients with renal insufficiency accompanied by elevated blood pressure, hypertensive target organ damage (retinal disease and left-ventricular hypertrophy) and mild proteinuria are typically labelled as having hypertensive nephrosclerosis in the absence of renal biopsy material. Herein, we report the clinical summaries and renal pathology from 2 patients initially diagnosed with hypertensive nephrosclerosis. Glomeruli exhibiting focal and segmental sclerosis and interstitial scarring were present in both cases. The presence of primary renal disease in patients felt to have hypertensive nephrosclerosis is likely more common than currently appreciated. This may result from the lack of renal histologic material and the late presentation of these patients to nephrologists. Misclassification of hypertensive nephrosclerosis would impact greatly on the epidemiology of end-stage renal disease and the evaluation and treatment of patients with chronic renal insufficiency.

Biopsy↗
PubMedDate not supplied

Immunohistochemical analysis of type III and IV collagens in tubulointerstitial damage in human benign nephrosclerosis.

Prolonged hypertension causes structural changes including glomerulosclerosis and tubulointerstitial damage of the kidney, termed benign nephrosclerosis. It is generally accepted that, in benign nephrosclerosis, increased accumulation of extracellular matrix in the glomeruli results in glomerulosclerosis. Little is known, however, about the possible role of the extracellular matrix in the tubulointerstitial damage in benign nephrosclerosis. In this study, the possible roles of type IV basement-membrane collagen and type III interstitial collagen in tubulointerstitial damage caused by hypertension were explored. Immunohistochemical techniques were used to investigate the distribution of type III and type IV collagens in the kidney sections of 15 patients with benign nephrosclerosis with tubulointerstitial damage and in 10 controls. In the control renal sections strong immunostaining for type III collagen was found in the interstitium and immunostaining for type IV collagen was present in the tubular basement membrane and weakly in the interstitium. In the patients with tubulointerstitial damage there was increased immunostaining for both type III and type IV collagens in the expanded interstitium and damaged tubules than was found in the control kidney sections. These findings indicate that increased accumulation of both type III and type IV collagens might play a significant role in the tubulointerstitial damage in benign nephrosclerosis.

Atrophy↗
PubMed1996

Possible relationship between hyperinsulinemia and glomerular hypertrophy in nephrosclerosis.

Hyperinsulinemia is potentially associated with the development of vascular sclerosis. On the other hand, the relationship between hyperinsulinemia and nephrosclerosis has not been elucidated. In this investigation clinicopathological studies were performed in 40 patients with nephrosclerosis, with special attention to the relationship between hyperinsulinemia and glomerular hypertrophy. Forty patients with biopsy-proven nephrosclerosis were divided into two groups by the 75-g oral glucose tolerance test (OGTT): group A, 2-hr plasma glucose concentration > 140 mg/dL (n = 25); group B, 140 < or = 2-hr plasma glucose < 200 mg/dL (n = 15). Patients with diabetes mellitus or diabetic nephropathy were not included. Morphometric analysis of the glomeruli revealed a significantly larger mean glomerular volume in subjects with nephrosclerosis in both subgroups. In addition, the mean glomerular volume was significantly correlated with the fasting insulin level, while no significant correlation was observed between the mean glomerular volume and creatinine clearance or degree of global sclerosis. These results indicate that hyperinsulinemia may be intimately related to glomerular hypertrophy in patients with nephrosclerosis.

Biopsy, Needle↗
PubMed1986

[Morpho- and pathogenesis of nephrosclerosis: a clinico-morphological analysis].

The authors have defined 2 phases in morphogenesis of nephrosclerosis: "nosological" and "syndrome". In the first phase the development of nephrosclerosis is determined by the peculiarities of pathogenesis of the main disease and associated with a certain structural element of the kidney (arterioles, glomerula, stroma). The second phase occurs after the formation of block of the renal blood flow at one or another structural level (arteriolar, glomerular, capillary-parenchymatous) including the hypoxic factor which determines subsequent progression of nephrosclerosis. The nosological signs of nephrosclerosis in this phase are leveled down, replaced by the signs of the syndrome of chronic renal failure. Arterial hypertension is a factor contributing to the progression of nephrosclerosis irrespective of nosological entity.

Amyloidosis↗
PubMed1971

New patterns of immunoglobulin deposition in the lesions of malignant nephrosclerosis, with special reference to IgE.

Localization of immunoglobulins (including IgE), complement and fibrinogen and the morphologic alterations in the kidneys of 10 patients with malignant nephrosclerosis were investigated. Thirteen kidneys with benign nephrosclerosis and 5 normal ones were also studied. In contrast to a previous series of patients with malignant nephrosclerosis, the number of necrotic arterioles and the deposition of IgG and complement in the renal arterioles, were reduced in a parallel fashion. These differences seem to reflect modern treatment and support the hypothesis that IgG and complement play a role in the pathogenesis of the arteriolar necrosis in the disease. IgE was deposited massively in many renal arterioles of 9 patients with malignant nephrosclerosis. The role of reaginic antibody in the pathogenesis of the disease is not clear since IgE was also focally present in some arterioles of 4 normal kidneys and of 8 kidneys with benign nephrosclerosis.

Adolescent↗
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↗
PubMed1997

Nephrosclerosis and hypertension.

In patients with benign nephrosclerosis, the histologic changes are characterized by hyaline degeneration of afferent arterioles with reduced kidney size. Although the glomeruli are nearly intact in patients with adult essential hypertension, the greatest numbers of sclerotic glomeruli are seen in nephrosclerosis with the aging process. Aging undoubtedly plays a role. In the authors' experience, the kidney of an elderly subject, although with normotensive pressure and normal level of cholesterol, shows an increased mesangial matrix and hypertrophic vascular medial smooth muscle cells. Kidneys of elderly subjects also are associated with a large number of sclerotic glomeruli. Experimental evidence supports the notion that the pathogenesis of glomerulosclerosis with nephrosclerosis has been demonstrated as important factors: (1) the elevation of PG (glomerular hypertension); (2) mesangial dysfunction, such as mesangiolysis and increased mesangial matrix; and (3) genetic abnormalities (apoptosis) in mesangial cells with glomerular hypertension. Malignant nephrosclerosis is characterized histologically by vascular endothelial damage and fibrinoid necrosis of afferent and interlobular arteries. In an afferent arteriole or a glomerulus, NOS or endothelin produced in endothelial cells may play a role in the reduction or the maintenance of vascular tone. The frequency of malignant hypertension has decreased because of the effective treatment of essential hypertension with new antihypertensive agents: calcium antagonists, ACE inhibitors, and angiotensin II receptor antagonists. Therefore, the importance of the prevention of essential hypertension with these antihypertensive agents, by slowing and stopping the increase in blood pressure from mild hypertension, has received widespread recognition in the prevention of organ damage, such as cases of cardiovascular disease and ESRD. Thus, prevention of renal injuries is an important goal of antihypertensive therapy.

Animals↗
PubMed1998

Antihypertensive agents prevent nephrosclerosis and left ventricular hypertrophy induced in rats by prolonged inhibition of nitric oxide synthesis.

We investigated the ability of the angiotensin converting enzyme (ACE) inhibitor imidapril hydrochloride, and of the calcium channel blocker amlodipine besilate, to prevent nephrosclerosis and left ventricular hypertrophy (LVH) in rats with hypertension induced by chronic inhibition of nitric oxide (NO). Male Wistar rats were given distilled water (control), NG-nitro-L-arginine methyl ester (L-NAME) 500 mg/L, L-NAME plus imidapril 10 mg/L or 100 mg/L, or L-NAME plus amlodipine 50 mg/L or 100 mg/L in the drinking water (n = 10-12). We then collected 24-h urine samples at 2, 4, and 6 weeks, obtained blood samples at 6 weeks, and histologically examined the kidney and heart. L-NAME markedly reduced the levels of NO metabolites in serum and urine while increasing the tail-cuff blood pressure, the urinary albumin level (1.90 +/- 0.65 v 0.05 +/- 0.02 mg/day/100 g in control), and the area of the left ventricular wall (83.3 +/- 3.0 v 69.8 +/- 1.8 mm2 in control). Nephrosclerosis and myocardial interstitial fibrosis were documented histologically. The plasma renin activity was significantly higher in rats treated with L-NAME than in the control rats. The concomitant administration of imidapril (10 mg/L) with L-NAME completely normalized the tail-cuff pressure, the LVH (70.8 +/- 1.8 mm2), the albuminuria (0.05 +/- 0.01 mg/day/100 g), and the histologic changes. Amlodipine (50 mg/L) also ameliorated the L-NAME-induced effects, but to a lesser extent. Thus, the chronic inhibition of NO synthesis in rats produced nephrosclerosis and LVH that were effectively prevented by giving imidapril at a dose lower than that of amlodipine. We conclude that ACE inhibitors can prevent nephrosclerosis and LVH even in the presence of a reduction in NO production, implying that in rats the inhibition of the renin-angiotensin system is more effective than the blockade of calcium channels in preventing hypertensive tissue injury.

Amlodipine↗
PubMed1996

Renal vascular lesions in the elderly: nephrosclerosis or atheromatous renal disease?

In white Europeans, renal size and function decline with age. This phenomenon has long been attributed to nephrosclerosis, i.e. primary vascular lesions associated with glomerular obsolescence, tubulointerstitial lesions and fibrosis. The part played by ageing and by pre-existing hypertension is still a matter of debate. Nephrosclerosis is a diagnosis of exclusion when no renal histology is available. As renal biopsy is rarely carried out in an elderly patient with atrophic kidneys, a long history of hypertension and only microalbuminuria or no proteinuria, the diagnosis of nephrosclerosis is generally overestimated. Even when renal histology is available, only subtle differences in vascular lesions have been claimed to distinguish those due to ageing from those due to hypertension. At any rate, meticulous control of blood pressure is certainly the most efficient means of protecting the renal vessels from further deterioration. Atheromatous renal disease has more recently been recognized as a major cause of progressive renal failure in the elderly. Renal artery stenoses due to atheromatous plaques might well be the cause of 10-15% of end-stage renal failure in whites aged > 50 and be the fourth cause of uraemia in this age group. Such stenoses are usually bilateral and developing. Present imaging methods, such as duplex ultrasound scanning and renal scintigraphy, are valuable means of diagnosis. Renal angioplasty can halt the the pace of renal insufficiency, or even durably improve it in nearly half of the cases. Finally, aorto-renal atheroma is a common and underestimated cause of cholesterol embolism. Minor, spontaneous forms thereof are indistinguishable from nephrosclerosis. Massive embolism entails a dismal prognosis, in terms of both renal function and patient survival. In conclusion, renal vascular lesions in the elderly remain a major concern. Improving non-invasive diagnostic procedures and applying preventative as well as curative measures should significantly reduce the incidence of end-stage renal disease is such patients.

Arteriosclerosis↗