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PubMed1987

Morphometrical and functional correlations in benign nephrosclerosis.

To ascertain whether or not vascular lesions lead to renoparenchymal damage through ischemia and to a deterioration of renal function in patients with essential hypertension, correlations among morphometrical findings and renal function were examined in 36 renal biopsies from Japanese patients with a benign nephrosclerosis. The following histological parameters were investigated; glomerular sclerotic index (GS), interstitial volume (IV), measured by the point-counting method, index of arteriolar hyaline change (HC) and intimal thickening (IT), determined by morphometry. Arteries were divided into two groups; those with less than 3 layers of medial smooth muscle cells (SMC less than 3) and those with more than 3 cell layers (SMC greater than or equal to 3). The mean of IT in each size was calculated. IT (SMC less than 3) showed a significant correlation with GS and IV. IT (SMC less than 3), GS and IV significantly correlated with Ccr. On the other hand, IT (SMC greater than or equal to 3) and HC showed no correlation with GS nor Ccr. IT (SMC less than 3) and HC correlated with both blood pressure and the duration of hypertension, and here, IT (SMC greater than or equal to 3) showed no correlation. These data suggest that hyaline change and intimal thickening of small arteries and arterioles (SMC less than 3) are closely related to high blood pressure and that intimal thickening of small arteries rather than hyaline change causes renoparenchymal damage through ischemia and leads to a deterioration of renal function, in those with a benign nephrosclerosis.

Adolescent↗
PubMed1987

Malignant arterial hypertension. Relationship between blood pressure control and renal function during long-term observation of patients with malignant nephrosclerosis.

Eleven patients with malignant arterial hypertension and malignant nephrosclerosis, verified by percutaneous renal biopsy, were examined during an observation period of 47 months (median). All patients received antihypertensive therapy. Patients were divided into three groups with regard to development of renal function during the observation period. In two patients (group I), the integrated average blood pressure (IA-BP) was 134/95 mmHg (median) and the calculated creatinine clearance (Ccr) increased from 19 to 56 ml/min (medians). In four patients (group II), IA-BP was 154/102 mmHg and Ccr remained stable-at approximately 60 ml/min. In five patients, (group III), IA-BP was 189/114 mmHg, owing to lack of patient compliance and absence from regular control, and Ccr was reduced from 26 ml/min to less than 5 ml/min. During the first 2 months of antihypertensive therapy, renal function was temporarily reduced in 7 of the 11 patients. It is concluded that effective blood pressure control in patients with malignant arterial hypertension and malignant nephrosclerosis can be accompanied by a considerable improvement, or at least a preservation of renal function.

Adult↗
PubMed1967

Hypertension and nephrosclerosis: a reappraisal and a new theory of renal ischemia.

An observation in human autopsy material showing a statistically close relationship between complicated atherosclerosis of the aorta, at or above the renal artery take-off, and nephrosclerosis of usual type (i.e. the "granular kidney" of essential hypertension) led to a study of platelet aggregates as a cause of renal lesions. The renal cortical surface is peculiarly sensitive to ischemic damage. When an embolic source, which sheds repeatedly, was placed in the thoracic aorta of rabbits, they became hypertensive. The hypertension persisted for six months, at which time the kidneys showed nephrosclerosis characterized by surface cortical lesions consisting of shrunken glomeruli and atrophical tubules, subtended by arterioles whose intimas showed fibrous thickening. It is suggested that the renal component of the hypertension so induced is transitory, serving as a trigger mechanism for sustained hypertension.

Animals↗
PubMed1980

Hyaline arteriolar nephrosclerosis. Immunofluorescence findings in the vascular lesions.

Of 536 renal specimens examined by direct immunofluorescence in the past 2 years, 153 contained vascular deposits of C3 without associated immunoglobulin or fibrin deposition. Excluding vasculitides, renal transplants, and outside cases with inadequate clinical data, 110 were selected for further study. Light microscopy showed periodic acid-Schiff-positive hyaline vascular deposits in 83 cases, and large electron-dense deposits were identified by electron microscopy in 47 cases. Fifty-one patients had immunologic glomerular disease in addition to hyaline arteriolar nephrosclerosis. Albumin, transferrin, and alpha-2 macroglobulin were not detected in the vessel walls of several selected cases so tested, indicating that passive diffusion probably does not explain C3 deposition. However, properdin was present in 11 of 14, and C4 in two of 11. The mechanism for this association between C3 and properdin deposition and hyaline arteriolar nephrosclerosis is not clear at present, but our findings suggest possible involvement of the alternative pathway of the complement system.

Adolescent↗
PubMed1997

[Circadian hydroxyprolinuria in the early diagnosis of nephrosclerosis in patients with chronic pyelonephritis].

The time course of daily urinary excretion of hydroxyproline (HOP) was followed up in patients with chronic pyelonephritis. Manifest hyperhydroxyprolinuria was observed in these patients at the earliest stages of nephrosclerosis, and it augmented with development of renal insufficiency. Measurements of HOP in the urine of patients with chronic pyelonephritis is proposed as an indicator reflecting the metabolic status of renal connective tissue at the early stages of nephrosclerosis. It can be used to assess the activity of the sclerotic process in the kidneys of patients with chronic pyelonephritis, predict the disease course and outcome, and, probably, to develop methods of adequate pathogenetic therapy with biochemical monitoring. The method is not invasive, sufficiently informative, and available for clinical diagnostic laboratories.

Chronic Disease↗
PubMedDate not supplied

[Hormonal disorders in patients with chronic pyelonephritis with nephrosclerosis and kidney failure].

Blood plasma content was studied of hydrocortisone, parathyroid hormone (PTH) and calcitonin in patients with chronic pyelonephritis (ChP) using methods of radioimmunologic and immunoenzymatic analyses. ChP patients had marked alterations of blood plasma levels of hydrocortisone, PTH and calcytonin, with the reduced levels of hydrocortisone and hypercalcitoninamia being noted during the early stages of nephrosclerosis. It is suggested that hydrocortisone and calcitonin content in blood of ChP patients might be used as indicators of state of the endocrine mechanisms controlling the renal connective tissue metabolism during the early stages of nephrosclerosis. The above measure will also be helpful in the assessment of activity of the sclerotic process in the kidneys, prognosis of the outcome of the medical condition, and development of treatment options of adequate pathogenetic therapy.

Adult↗
PubMed1996

Quantitative ultrastructural study of afferent and efferent arterioles in IgA glomerulonephritis and benign nephrosclerosis.

Arteriolosclerosis frequently occurs in IgA nephritis (IgAN), and it is the hallmark of benign nephrosclerosis (BNS). The quantitative ultrastructure of juxtaglomerular arterioles is not known in these disorders. We examined afferent and efferent arterioles in renal biopsies from 25 adult patients with IgAN (hypertension at biopsy: 14 patients) and 9 patients with BNS. Six age-matched living renal transplant donors acted as controls. A systematic independent sample of profiles was obtained in thin sections taken at predetermined levels. The thickness of the media (myomedial cells plus the matrix) and the thickness of the medial matrix were estimated stereologically. From these estimates, the matrix/myomedia ratio was calculated. In IgAN with normotension or hypertension, the afferent media and its compartments did not exhibit significant thickening compared with the controls, whereas in BNS the afferent media and its layers were markedly and significantly thickened. The efferent media in IgAN and BNS displayed mild and significant thickening, with significant thickening of the matrix in BNS and IgAN with normotension. The matrix/myomedia ratio was not altered significantly in any group. The results indicate that the afferent arterioles are not the main sites of IgAN-related arteriolosclerosis, that arteriolosclerosis in IgAN and arteriolosclerosis in BNS are different lesions, and that increased efferent arteriolar thickness, demonstrated here for the first time in IgAN and BNS, might be a manifestation of angiotensin II-mediated autoregulatory efferent vasoconstriction exerted to maintain the glomerular filtration pressure.

Adolescent↗
PubMed1993

The diagnostic dilemma of hypertensive nephrosclerosis: the nephrologist's view.

The appearance of progressive renal disease in elderly patients with essential hypertension, sometimes irrespective of blood pressure control, is frequently related to the association of hypertension and atheromatous renal disease. This disease may lead to renal failure through a renal artery stenosis and/or chronic microembolization into the kidney. Nonsevere uncomplicated essential hypertension is constantly associated with renal vascular changes that are qualitatively indistinguishable from those related to aging. Notwithstanding the fairly constant presence of so-called benign hypertensive nephrosclerosis in patients with established hypertension, only a subset of these patients show progressive renal damage. Three mechanisms of progression may be at play: (1) a combination of ischemic and hypertensive glomerular mechanisms in some susceptible humans; (2) nonhemodynamic factors such as local immune mechanisms; or (3) the involvement of metabolic abnormalities which favor glomerulosclerosis.

Aged↗
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↗
PubMed1994

Glomerular expression of type III and type IV collagens in benign nephrosclerosis: immunohistochemical and in situ hybridization study.

The development of glomerular sclerosis in benign nephrosclerosis (BNS) was studied. We investigated the intraglomerular expression of type III and IV collagens and their mRNAs by immunohistochemistry and by the in situ hybridization method. Formalin-fixed paraffin sections from 28 patients with BNS and 10 control cases were stained by the avidin-biotin complex (ABC) method using monoclonal antibodies for human type III and IV collagens. In the course of the sclerotic process of the glomerulus in BNS, the glomerular staining intensity of type IV collagen increased. The strongest staining was observed in the glomerulus at the early sclerotic stage, and intensity decreased slightly at the later stages. Although type III collagen was absent in normal and nonsclerotic glomeruli, peripheral regions of the sclerotic glomeruli were positive at the early sclerotic stage. Later, type III collagen was diffusely observed in the completely hyalinized glomeruli. The expression of type III and type IV collagen mRNAs was detected in the glomeruli of BNS by the non-radioactive in situ hybridization method using thymine-thymine (T-T) dimerized synthetic oligonucleotides. The number of mRNA positive cells for type III and type IV collagens increased at the presclerotic and early sclerotic stages. But these cells gradually decreased in number as glomerular sclerosis developed. We concluded that type III collagen was presumably synthesized by the intraglomerular cells and may contribute to the development of glomerular sclerosis in BNS along with type IV collagen.

Adult↗
PubMed1982

The glomerular lesions in endotheliotropic hemolytic nephroangiopathy (hemolytic uremic syndrome, malignant nephrosclerosis, post partum renal insufficiency).

The term "Endotheliotropic Hemolytic Nephroangiopathy" (EHN) comprises various clinically or pathomorphologically defined disease states with severe renal lesions (e.g. hemolytic uremic syndrome, malignant nephrosclerosis, post partum renal insufficiency) which, to date, have been considered as different entities. We attempted to assign accompanying glomerular changes based upon light and electron microscopy to the above mentioned clinical pictures and their various stages. The accordingly classified glomerular lesions (G1--G3 and Ga) are of critical importance in pathohistological differential diagnosis. Since it is assumed that fibrin is a causing event in the pathogenesis of the vascular lesions, quantitative evaluation of glomerular fibrin deposits was done. The results, when viewed with respect to time, lead to the conclusion that the microthrombotic component represents a secondary phenomenon. Thus, the primary and hence pathogenetically most important finding is a severe damage to the endothelium of the terminal renal vasculature. This endothelial damage although being expressed with variable intensity has to be regarded as the common denominator inherent to all types of glomerular lesions in EHN.

Acute Kidney Injury↗
PubMed1995

"Strict" blood pressure control and progression of renal disease in hypertensive nephrosclerosis.

Hypertensive nephrosclerosis is a progressive renal disease and the leading cause of end-stage renal disease (ESRD) in blacks in the United States. It is generally believed that hypertensive renal injury is responsible for progressive renal failure; however, it is not known whether pharmacologic lowering of blood pressure to any level prevents progression of renal disease. Accordingly, we performed a long-term prospective randomized trial to determine whether "strict" [diastolic blood pressure (DBP) 65 to 80 mm Hg] versus "conventional" (DBP 85 to 95 mm Hg) blood pressure control is associated with a slower rate of decline in glomerular filtration rate. Eighty-seven non-diabetic patients (age 25 to 73; 68 black, 58 male) with long-standing hypertension (DBP > or = 95 mm Hg), chronic renal insufficiency (GFR < or = 70 m/min/1.73 m2) and a normal urine sediment were studied. DBP was pharmacologically lowered to < or = 80 mm Hg (3 of 4 consecutive measurements at 1 to 4 weeks intervals) after which patients were randomized. DBP and GFR (renal clearance of 125I-iothalamate) were measured at baseline, at three months and every six months post-randomization. The rate of decline in GFR (GFR slope, in ml/min/1.73 m2/year), estimated by the method of maximum likelihood in a mixed effects model, was the primary outcome variable. In a secondary analysis, 50% reduction in GFR (or a doubling of serum creatinine) from baseline, ESRD and death were combined.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Effect of 2,3-dimercaptosuccinic acid on nephrosclerosis in the Dahl rat. I. Role of reactive oxygen species.

2,3-Dimercaptosuccinic acid (DMSA), a sulfhydryl-containing chelator, has previously been shown to reduce mean blood pressure in lead-treated rats. In the present study we have demonstrated that DMSA (0.5% for 5 days every 2 weeks) also reduces mean blood pressure in the Dahl salt-sensitive (SS) rat. Six-week-old Dahl SS and salt resistant (SR) rats were placed on a 0.3% NaCl diet for two weeks, followed by an 8% NaCl diet for four weeks. Eight SS and 8 SR rats remained untreated while 8 SS and 8 SR rats were treated with DMSA. DMSA treatment ameliorated the mean blood pressure rise in the Dahl SS rats (141 +/- 5 vs. 120 +/- 4 mm Hg at 6 weeks, P < 0.001). Nephrosclerosis was severe in untreated SS rats but absent in treated SS rats as well as in both treated and untreated SR rats. Reactive oxygen species formation, as assessed by kidney cortex content of malondialdehyde (MDA) and immunohistochemical demonstration of nitrotyrosine (a byproduct of peroxynitrite) in interlobular arteries, was increased in Dahl SS rats, but abolished by DMSA (MDA 9.65 +/- 0.33 nmol/g wet wt, untreated SS, vs. 6.46 +/- 0.51, treated SS, P < 0.001). The anti-nephrosclerotic action of DMSA was clearly disproportionate to the reduction in blood pressure. We conclude that the effect of DMSA was related instead to the reactive oxygen species scavenging properties of the thiol groups.

Animals↗
PubMed1997

Accuracy of the diagnosis of hypertensive nephrosclerosis in African Americans: a report from the African American Study of Kidney Disease (AASK) Trial. AASK Pilot Study Investigators.

African Americans have excess hypertension and end-stage renal disease presumed due to hypertension compared to Caucasians. The AASK was designed to examine the impact of antihypertensive therapies and two levels of blood pressure control on the rate of decline of GFR in African Americans with presumed hypertensive renal disease. During the pilot phase of the trial, eligible participants were requested to undergo renal biopsy to assess the underlying lesions in this population. Eighty-eight hypertensive (diastolic BP > 95 mm Hg) non-diabetic African American patients between the ages of 18 to 70 years, with GFR between 25 to 70 ml/min/1.73 m2 and without marked proteinuria were assessed for possible renal biopsy. Forty-three patients did not undergo renal biopsy due to refusal or contraindications. Adequate renal biopsies were obtained in 39 of the remaining 46 patients. Biopsy findings were analyzed and then compared to clinical parameters. The 39 patients studied, 29 men and 10 women, were on average 53.0 +/- 11.0 years old, and had a MAP of 109 +/- 15 mm Hg and GFR 51.7 +/- 13.6 ml/min/1.73 m2 (not significantly different from nonbiopsied patients). Thirty-eight of these 39 biopsies showed arteriosclerosis and/or arteriolosclerosis, severity on average 1.5 +/- 0.9 and 1.5 +/- 0.8, respectively on a 0 to 3+ scale. Interstitial fibrosis was moderate, 1.3 +/- 0.9 (0 to 3+ scale). Segmental glomerulosclerosis was present in five biopsies, and in one patient, biopsy and clinical findings were consistent with idiopathic focal segmental glomerulosclerosis. Additional lesions included mesangiopathic glomerulonephritis in one patient, basement membrane thickening suggestive of diabetic nephropathy in one, and cholesterol emboli in two cases. Arteriolar and arterial sclerosis were tightly linked, and correlated with interstitial fibrosis and the reciprocal of serum creatinine. Global glomerulosclerosis was extensive, involving on average 43 +/- 26% of glomeruli. The extent of this lesion did not correlate with degree of arteriolar or arterial thickening, but did correlate with systolic blood pressure (P = 0.0174), the reciprocal of serum creatinine (P = 0.0009), serum cholesterol (P = 0.0129) and interstitial fibrosis (P < 0.0001). These data underscore that renal biopsies in non-diabetic hypertensive African-Americans with mild to moderate renal insufficiency in the absence of marked proteinuria are overwhelmingly likely to show renal vascular lesions consistent with the clinical diagnosis of hypertensive nephrosclerosis.

Adult↗
PubMed1980

Asymptomatic mild hyperuricaemia: an indicator of nephrosclerosis in essential hypertension.

1. Glomerular filtration rate, renal and systemic haemodynamics and intravascular volume were measured in 20 established essential hypertensive patients classified according to serum uric acid level into two groups (below 0.36 mmol/l, and above 0.54 mmol/l). 2. Although glomerular filtration rate was comparable between the two groups, renal blood flow was lower and renal vascular and total peripheral resistances were higher in the patients with the highest uric acid levels (P < 0.02). 3. Cardiac output, heart rate and splanchnic blood flow were similar in both patient groups but arterial pressure tended to be higher in patients with high uric acid levels. 4. These data suggest that unexplained hyperuricaemia in patients with essential hypertension most likely reflects early renal vascular involvement, i.e. nephrosclerosis.

Adult↗
PubMed2003

Pathological changes in the cerebral medullary arteries of five autopsy cases of malignant nephrosclerosis: observation by morphometry and reconstruction of serial sections.

Hypertension (HT) is a serious risk factor of not only cerebral infarction and bleeding, but also Binswanger's encephalopathy (BE). In BE especially, severe stiffening of the cerebral medullary arteries because of hypertensive changes with loss of medial smooth muscle cells (SMC) occurs, which induces diffuse atrophy of the cerebral white matter. But, it is not yet ascertained whether HT is particularly severe in BE. Therefore, a spectrum of the pathological changes of the cerebral arteries were investigated by reconstruction of serial sections and morphometry of the medial thickness in five autopsied patients with malignant nephrosclerosis (MN) of exacerbated form. Each presented clinically acute progression of long-standing HT at the terminal stage and pathologically typical renal changes. The heartweight was 380-900 g. Morphometry of the medial thickness of the arachnoid arteries presented significant medial hypertrophy in four cases of MN, but in the medullary arteries it presented in only two cases with marked cardiomegaly of 700 g and 900 g. In four cases of MN, only a few medullary arteries showed slight pathological changes. However, in another case with cardiomegaly of 900 g, all 10 medullary arteries showed multiple segments of atheroma, medial SMC loss, and prominent dilatation; edematous concentric intimal fibrosis with luminal obstruction and atrophy of the white matter were absent. In conclusion, only one case of MN showing marked cardiomegaly of 900 g presented severe pathological changes of the cerebral medullary arteries comparable with those of BE, although other MN-cases showing severe cardiac hypertrophy presented only trivial arterial changes. Therefore, the cerebral medullary artery seems to be protected from HT, yet it is involved in a case of severe and long-standing HT inducing an extreme cardiomegaly.

Adult↗
PubMed1998

Progression of renal failure and hypertensive nephrosclerosis.

Data provided by end-stage renal disease (ESRD) registries document a progressive and striking increase in the incidence of hypertension-related ESRD over the years, and its prevalence supports the classic statement that the kidney may be a victim of hypertension. Two clinical conditions should be considered separately when the role of hypertension in progressive renal disease is discussed: (a) hypertension and primary renal disease and (b) progressive renal disease in essential hypertension. The appearance of systemic hypertension is one of the major risk factors for the progressive deterioration of primary renal disease both in experimental models and in humans. Strict blood pressure control is able to significantly reduce the disease progression to renal failure. Angiotensin-converting enzyme inhibitors probably show a better nephroprotective action than other antihypertensive agents. Long-lasting hypertension may induce ESRD in some patients through hypertensive nephrosclerosis. In many cases of progressive renal disease associated with essential hypertension, particularly in elderly Caucasians, atheromatous renovascular disease via renal artery stenosis and/or cholesterol microembolization represent the main cause of ESRD.

Disease Progression↗