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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↗
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↗
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↗
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↗
PubMed1996

ACE inhibition prevents and reverses L-NAME-exacerbated nephrosclerosis in spontaneously hypertensive rats.

Chronic nitric oxide inhibition exacerbates hypertension and nephrosclerosis in spontaneously hypertensive rats (SHRs). In this study, we determined whether angiotensin-converting enzyme (ACE) inhibition could prevent or reverse the systemic, renal, and glomerular hemodynamic alterations and the pathological changes of nephrosclerosis. Four groups of 20-week-old SHRs were studied: group 1, untreated controls; group 2, treated with N omega-nitro-L-arginine methyl ester (L-NAME, 50 mg/L for 3 weeks); group 3, L-NAME cotreated with quinapril (3 mg.kg-1.d-1 for 3 weeks); and group 4, L-NAME for 3 weeks followed by quinapril for 3 weeks (same doses). The results of this study demonstrated that both cotreatment (group 3) and posttreatment (group 4) with quinapril reduced mean arterial pressure (186 +/- 9 and 192 +/- 9 mm Hg, respectively, compared with group 2 SHRs, 221 +/- 5 mm Hg) and total peripheral resistance index associated with significant reductions in afferent and efferent arteriolar resistances; nephrosclerosis pathological scores; and urinary protein excretion (all at least P < .01). ACE inhibition also significantly increased stroke index, single-nephron glomerular filtration rate, and ultrafiltration coefficient compared with the L-NAME SHRs. Most notable were the findings that cotreatment with quinapril completely prevented the renal glomerular hemodynamic alterations with reduced glomerular capillary hydrostatic pressure and efferent arteriolar resistance compared with both the untreated and the L-NAME-treated SHRs (all at least P < .01). Posttreatment with quinapril also reversed the glomerular injury (subcapsular, -83%; juxtamedullary, -56%) and arteriolar (-87%) injury scores obtained from renal biopsy specimens (P < .005 and P < .0001, respectively). These changes were associated with decreased periarteriolar fibronectin and increased afferent arteriolar alpha-smooth muscle actin deposition (immunohistochemistry). These data, therefore, demonstrate that ACE inhibition not only prevents but also reverses L-NAME-exacerbated severe nephrosclerosis in SHRs, as indicated by improved systemic, renal, and glomerular hemodynamic changes, proteinuria, and histological alterations.

Analysis of Variance↗
PubMed1988

Blood pressure, nephrosclerosis, and age autopsy findings from the Honolulu Heart Program.

The aspect of nephrosclerosis reflected by fibrous intimal thickening of small arteries (arteriosclerosis) was measured by a newly introduced morphometric procedure in 154 autopsies of Japanese-American men in Honolulu. These men were subjects of the Honolulu Heart Program and had previously been assessed for blood pressure and other clinical characteristics in a prospective study. In periodic acid-Schiff (PAS)-stained sections of renal cortex, measurements were made of interlobular artery diameters and intimal thicknesses. Vessels of outer diameter 80 to 130 microns and 160 to 300 microns were examined separately and are called the "remote" and "close" levels of the interlobular arteries, respectively, defined in relation to the heart. Nephrosclerosis thus quantified, together with age, could be used to predict the levels of blood pressure (BP) to be found in retrospective review of past records. The mathematical function obtained in a former study to make these predictions was found to predict the observed levels of blood pressure to an acceptable degree in the groupings that involved 92% of the subjects. Verification of that formerly obtained predictive function is now claimed. Correlation coefficients relating BP to close and remote measures were about of equal magnitude (r = 0.34 and 0.40, respectively). Subjects with cardiovascular-renal causes of death differed in both nephrosclerosis and blood pressure from subjects whose cause of death was unrelated to cardiovascular-renal diseases; the two factors taken together each contributed significantly to the cause of death difference. Correlations between nephrosclerosis and aortic atherosclerosis were stronger than could be explained solely by a linkage to observed values of blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Proteinuria in benign nephrosclerosis.

Benign nephrosclerosis seldom is associated with significant proteinuria or reduced renal function. This study demonstrated that, despite the finding of benign nephrosclerosis on a renal biopsy specimen, concomitant proteinuria is predictive of a poor prognosis. Twelve patients, ranging in age from 24 to 59 years, with hypertension, proteinuria (greater than 1 g/d), and findings of benign nephrosclerosis on renal biopsy specimens were studied retrospectively. In three of these patients, the hypertension and proteinuria were diagnosed during pregnancy. Follow-up was possible in 11 patients. Nine patients became nephrotic in the course of their disease. Two patients had endstage renal disease and required maintenance dialysis treatment. Seven patients had decreased renal function as shown by the increase in serum creatinine levels. Thus, the combination of hypertension, proteinuria (greater than 1 g/d), and benign nephrosclerosis may be indicative of a progressive condition with a high percentage of patients having renal failure.

Adult↗
PubMed1986

[Nosological characteristics of the morphogenesis of nephrosclerosis].

Morphology of nephrosclerosis at its early stage is characterized by nosologic specificity. Morphogenetic mechanisms of glomerulosclerosis vary greatly and depend on the specific feature of the disease pathogenesis, underlying nephrosclerosis. Stromal sclerosis of renal cortex stroma is associated with the increase in collagen-synthesizing function of interstitial fibroblasts. At the late stages of nephrosclerosis all renal tissue structures are equally affected with sclerosis, resulting in loss of nosologic specificity of the process. Arterial hypertension favours the progression of nephrosclerosis.

Adult↗
PubMed1985

[Morphological characteristics of nephrosclerosis of different etiologies].

Morphology of nephrosclerosis at the early stage of its development is characterized by its nosological specificity which is determined by qualitative alterations and by the degree of renal structural components involvement into the sclerotic process. Complex morphometric assessment allows one to reveal and make it objective the morphological differences between nosological variants of nephrosclerosis. All the structural renal components equally undergo sclerosis at the late stages of nephrosclerosis and this leads to the leveling off the nosological specificity in the majority of cases. Arterial hypertension in chronic glomerulonephritis and chronic pyelonephritis favours the progressing of the nephrosclerosis and leveling off its nosological differences.

Adult↗
PubMed1993

Clinical features of benign hypertensive nephrosclerosis at time of renal biopsy.

Although hypertension accounts for approximately 15-20% of end-stage renal disease and renal impairment occurs in 15% of patients with essential hypertension, there are few data available on the clinical features of patients with benign hypertensive nephrosclerosis, the histological consequence of hypertension on the kidney. To determine its prevalence on renal biopsy and its clinical features (including proteinuria and renal function), we used the U.K. MRC Glomerulonephritis Registry of 7339 biopsies from 20 centres to define all patients with benign hypertensive nephrosclerosis. In patients with no co-existing disease, 185 biopsies were classified solely as benign hypertensive nephrosclerosis (2.5%). Sixty-nine percent of patients were male and 72% aged over 50 years. Sixty-four percent had diastolic blood pressure above 90 mmHg and severe hypertension (diastolic > 120 mmHg) was present in 9%. Protein excretion of > 1.5 g/day was noted in 40%, with 22% excreting > 3 g/day. Eighteen percent had serum albumin values under 30 g/l. Eighty-one percent had serum creatinine > 120 mumol/l; in 51% this was > 250 mumol/l. There was significant correlation between serum creatinine and systolic blood pressure at time of biopsy (p = 0.01) and between serum creatinine and serum albumin (p = 0.001). Benign hypertensive nephrosclerosis accounts for 2.5% of all registered biopsies. Significant proteinuria is a common finding and proteinuria within the nephrotic range does occur. Systolic blood pressure appears to influence serum creatinine levels. Hypertensive nephropathy should be considered in all patients with heavy proteinuria and renal impairment.

Adult↗
PubMed1993

[Nephrosclerosis: current status].

Nephrosclerosis is the most typical and widespread renal manifestation of hypertension and can be judged as the pathological hallmark of essential hypertension. Nephrosclerosis is an important and frequent cause of progressive renal disease, however, information in the literature on the risk of developing renal failure in the course of essential hypertension is sparse. Traditionally, nephrosclerosis was thought to result from glomerular ischemia. Alternatively, glomerular sclerosis in hypertension may result from glomerular hyperperfusion or hypertension. Studies in experimental models of renal disease have identified a promising intervention with either Ca antagonists or angiotensin-converting enzyme inhibitors. Application of these therapies to patients with nephrosclerosis should await the results of careful clinical trials.

Angiotensin-Converting Enzyme Inhibitors↗