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PubMed2001

[Clinical value of "zero-hour" biopsy in kidney transplantation].

We have performed 115 "zero-hour" biopsies of transplanted kidneys since 1994. Donor kidneys were divided into five groups, based on the morphological findings of "zero-hour" biopsies. No morphological abnormalities were found in 38.26% of the cases (group 1). Arteriolosclerosis was present in 22.61% of donor kidneys (group 2). Specific morphological alterations, i.e. acute tubular necrosis (24.35%), tubulointerstitial nephritis (5.22%) or glomerulonephritis (9.56%) were detectable in the remaining cases (groups 3-5). During an average of 644 days after transplantation clinical and histological follow-up were performed. According to our observations: 1. Higher creatinine was found in patients with grafts with arteriolosclerosis (group 2). 2. There were more non-viable grafts and longer periods of delayed graft function in patients with acute tubular necrosis (group 3). 3. Higher serum creatinine, more frequent rejections with the need of secondary hemodialysis were observed in patients who received a kidney with "zero-hour" biopsy of tubulointerstitial nephritis (group 4). 4. The only complication observed in patients with glomerulonephritis donor kidneys was delayed functioning of the graft (group 5). Biopsies did not cause complication in any of our patients. In conclusion, "zero-hour" biopsies can be useful and safe tools to predict early graft function. Besides, "zero-hour" biopsies help histological interpretation of consecutive graft re-biopsies.

Arteriosclerosis↗
PubMed2002

The renal pathology in children dying with hepatic cirrhosis.

The aim of this analysis was to observe the pathologic changes in the kidney in 23 children dying of cirrhosis, including five children with renal failure. Besides these pathologic changes, glomerular cellularity and arteriolar wall thickness of these patients were compared with 18 age matched autopsy controls dying of nonhepatic and nonrenal causes. Histologic examination of the kidneys in these cirrhotic children showed significant tubular changes in five patients, diffuse glomerulosclerosis in five, only one child had membranous glomerulopathy or glomerulonephritis and one cirrhotic with serum hepatitis B surface antigen positivity had polyarteritis nodosa. No statistically significant changes were observed in the glomerular cellularity and the arteriolar wall thickness in these cirrhotic children as compared to the controls. However, medial proliferation and hyaline arteriolosclerosis were observed in four cirrhotic children. Tubular bile casts and nephrocalcinosis were the sole lesions causing renal failure in two cases. A combination of glomerulosclerosis, cast formation and arteriolosclerosis was seen in the remaining three patients. Thus the kidney showed a spectrum of pathology in pediatric cirrhosis. The tubular lesions causing renal failure represent acute treatable lesions whereas glomerulosclerosis and arteriosclerosis stand for a more chronic and less reversible renal damage.

Child↗
PubMed2003

[Three-dimensional morphologic examination of normal and diseased renal arterioles].

INTRODUCTION: Earlier publications show the endothelial fenestration at the juxtaglomerular part of the afferent arteriole facing mesangial and granular cells and finger-like protrusions of urinary space into the region of the lacis in experimental animals such as the rat, the mouse, and Tupaia belangery. In human kidney both the endothelial fenestration in the wall of the afferent arteriole and protrusions with filtration slits of urinary space into the lacis, were observed with remarkable heterogeneity. There was found the fenestrated entdothelium facing the reningranulated cells of Amphiuma kidney too. Arteriolosclerosis frequently occurs in IgA nephritis, and is the hallmark of benign nephrosclerosis. The quantitative ultrastructure of juxtaglomerular arterioles is not known in these disorders. AIMS AND METHODS: The aim of both studies was to characterize the arteriolar parameters using stereology. In normal kidney was the permeability studied along the full length of afferent arteriole using ferritin particles as indicator of permeability/fenestration. In renal biopsies from patients with IgA nephritis and patients with benign nephrosclerosis the afferent and efferent arterioles were examined. Age-matched living renal transplant donors were used as controls. The thickness of the media (myomedial cells plus the mátrix) and the thickness of the medial matrix were estimated. From these estimates, the mátrix/myomedia ratio was calculated. RESULTS: In the normal kidney the density of ferritin particles was high close to the glomerulus and decreased continuously similarly to the profile of renin distribution. There was a correlation between the length of ferritin-positive and renin-positive portions. Based on these results, the afferent arteriole, according to its endothelial permeability, can be divided into two distinct portions i.e. the permeable and the non-permeable, the length and ratio of which may be related to the actual renin formation. In IgA nephritis with normotension or hypertension, the afferent media and its components did not exhibit significant thickening compared with the controls, whereas in benign nephrosclerosis the afferent media and its layers were markedly and significantly thickened. The efferent media in IgA nephritis and benign nephrosclerosis displayed mild and significant thickening, with normotension. CONCLUSION: The results indicate that the afferent arterioles are not the main sites of IgA nephritis-related arteriolosclerosis, and that benign nephrosclerosis represents different lesions. The stereological method was successfully used and provided essential information about the arterioles in both study.

Animals↗
PubMed1991

[Age-related changes in the kidney of patients with mild mesangial proliferative glomerulonephritis].

In order to clarify age-related changes in kidneys, the renal function and histological changes were evaluated in 962 patients with mild mesangial proliferative glomerulonephritis (Mes PGN) whose ages ranged from 7 to 82 years. The glomerular filtration rate (GFR) (Ccr), renal plasma flow (RPF) (CPAH) and PSP excretion rate were significantly lower in nephritic patients than in normal subjects. Age-related decreases of GFR, RPF, PSP excretion rate and maximal urine specific gravity in Fishberg concentration test were found in both groups. Serum levels of creatinine, urea nitrogen and uric acid were significantly higher in nephritic patients than in the normal population. Age-related increases of those parameters were found in both groups. The incidence of sclerotic glomeruli was almost same as that of the normal population estimated by Kaplan et al. The incidence of arterio- and arteriolosclerosis was also higher than that of normal subjects estimated by Bell. Thus, arterio- and arteriolosclerosis seems to be more age-dependent than glomerulosclerosis in patients with mild Mes PGN. In conclusion, renal functions decrease and renal arteriolar lesions increase gradually in proportion to aging. Mes PGN, even mild, can accelerate the physiological age-related decrease of renal function.

Aging↗
PubMed1983

[Some pathologico-anatomic substrates of hypertensive lesions].

After some introductory remarks on the definition of the various forms of hypertension, a short description of the changes in arterial vessels associated with hypertension is given. Hypertension is by no means a prerequisite for atherosclerosis and arteriolosclerosis, but hypertension enhances such vascular changes. In malignant hypertension, typical fibrinoid arteriolonecroses occur. Hypertension leads to hypertrophy of the left ventricle through enlargement of individual muscle fibres, but numeric hyperplasia also occurs. At the same time, coronary atherosclerosis may be aggravated by systemic hypertension. Hypertrophy together with coronary sclerosis may result in various forms of ischemic heart disease among which myocardial infarction and its complications are the most important ones. There are intimate mutual interactions between hypertension and ischemic renal damages, the most important of which are briefly discussed. Again, many of these changes do not necessarily require hypertension as a prerequisite. Massive haemorrhage into the substance of the brain is usually associated with systemic arterial hypertension, but requires predisposing atherosclerosis and arteriolosclerosis: Walls of healthy arteries do not give way, however high the blood pressure may be.

Arteries↗
PubMed1994

[Osteophyte formation in the knee joint: a radiological study].

Reported here are the results of a study on the significance of osteophyte formation in the osteoarthritic knee joint. The osteophyte formation was examined in a total of 795 cases involving 1040 joints. Of these, 415 cases (660 joints) had no symptoms of osteoarthritis of the knee joint (Group A); while the other 380 (380 joints) had primary osteoarthritis of the knee joint (Group B). The osteophyte location and osteophyte length were determined in all cases of Group A and Group B. The rate of annual increase in osteophyte length was determined in 224 cases (369 joints) of Group A (average study period: 7.1 years) and in 122 cases (122 joints) of Group B (average study period: 7.5 years). A special measuring unit called the "spur index" was devised for the present study to determine a corrected measurement of the osteophyte length; 1 spur index unit corresponded to 1/100 of the width of the proximal tibial articular surface. By using this spur index, measurements could be corrected for the magnifying effect of X-ray photography and for variations in the size of knee joints. On the assumption that age, obesity, arteriolosclerosis and femorotibial angle were factors that promoted the progression of osteoarthritis in the knee joint, the correlation between the osteophyte length and each of these factors was investigated. A significant difference in osteophyte length, and in the annual increase in osteophyte length, was found between Group A and Group B, but no difference between them with regard to osteophyte location. A significant correlation was found between the osteophyte formation and each of the above-mentioned factors. The correlation was strongest with the femorotibial angle followed by age, arteriolosclerosis and obesity, in that order.

Adult↗
PubMed1993

Nature of progressive glomerulosclerosis in human membranous nephropathy.

In membranous nephropathy (MN) the mechanism of progression is not well defined. We studied the lesions of focal segmental glomerulosclerosis (FSGS) in 95 patients with idiopathic MN in relation to other morphologic and clinical data. Forty-one patients (43%) showed FSGS, frequently accompanied by synechiae and hyalinosis. The patients with FSGS had a significantly greater degree of mesangial expansion, glomerular basement membrane (GBM) thickening, interstitial fibrosis, and arteriolosclerosis, as well as an increased level of serum creatinine, when compared to the patients without. Relative interstitial volume, in particular, significantly correlated to the serum creatinine level, thickness of GBM and % of glomeruli with FSGS. Glomerular size was not different in patients with or without FSGS. When clinical and morphological data of these patients were analyzed according to a staging technique of Ehrenreich and Churg [1968], the occurrence of FSGS was more frequently present in advanced stage. Intraglomerular fat deposition was only noted in advanced stage. No other morphologic or clinical parameters were related to the staging. Thickness of GBM or index of electron density of deposits, though well related to the morphological staging, did not show any relationship to clinical or laboratory data. Sixty-four patients were followed for more than a year (mean 3 years). Patients with FSGS had more frequent progression compared with those without. Patients with advanced stage and FSGS did not do worse than patients with stage I-II+II and FSGS. From these observations, we believe that the mesangial expansion, advanced GBM thickening, interstitial fibrosis and arteriolosclerosis are important morphological parameters, which may play a role in the genesis of FSGS or progression in MN. In addition, the occurrence of FSGS, but not the morphological staging, can predict the course of individual patients in MN.

Adult↗
PubMed1994

Premature atherosclerosis with photomyoclonic epilepsy, deafness, diabetes mellitus, nephropathy, and neurodegenerative disorder in two brothers: a new syndrome?

We describe two brothers with sensorineural deafness, diabetes mellitus, progressive neurological deterioration with photomyoclonic epilepsy, and progressive deterioration in renal function, resulting in death in the third decade of life. Autopsy showed diffuse atherosclerosis and arteriolosclerosis of the systemic vasculature. There was no evidence of these abnormalities in the patients' 2 sisters or either parent. Mitochondrial enzyme analysis documented partial deficiencies of Complex III and IV of the respiratory chain. This deficiency was expressed in skin fibroblasts, kidney and liver but not in muscle. This suggests that the disease-causing mutation is either in the mitochondrial or nuclear DNA. Various modes of inheritance are considered, including maternal, autosomal recessive, or X-linked recessive. We suggest this is a new genetic syndrome characterized by an underlying metabolic disease and premature atherosclerosis, possibly of mitochondrial origin.

Adult↗
PubMed1994

Bundles of amyloid precursor protein-immunoreactive axons in human cerebrovascular white matter lesions.

Cerebral white matter lesions commonly observed in Binswanger's disease, multi-infarct encephalopathy and elderly people are neuropathologically characterized by diffuse incomplete demyelination and considered to be ischemic in nature. Arteriolosclerosis in the white matter is a common feature in these white matter lesions. To investigate a possible alteration of the distribution of amyloid precursor protein (APP), chromogranin A (CgA) and synaptophysin (Syn) in such white matter lesions, we examined 15 cases with white matter lesions and 5 without white matter lesions. Many bundles of axons with APP-like immunoreactivity (LI) were observed particularly in mild white matter lesions. Such bundles of axons showed similar but less intense CgA-LI and Syn-LI. They appeared to occur in areas with many ameboid or ramified microglia labeled with anti-leukocyte common antigen and few astrocytes labeled with anti-glial fibrillary acidic protein. In the center of moderate of severe white matter lesions bundles of axons with APP-LI were never observed. Since APP, CgA and Syn undergo fast axonal transport, and since following ischemic insults to central nervous system microglial reaction occurs earlier than astroglial changes, our results suggest that axonal damage, which induces disturbance of fast axonal transport, can occur even in the early stage of white matter lesions.

Aged↗
PubMed1992

Does methylmercury intoxication induce arteriosclerosis in humans? A pathological investigation of 22 autopsy cases in Niigata, Japan.

In order to clarify whether or not arterio- and/or arteriolosclerosis is induced or exacerbated in patients with methylmercury (Me-Hg) intoxication, the pathological features of arteries and arterioles in specific areas in 22 patients and 36 control subjects were examined qualitatively and quantitatively. Vessels investigated were: (1) small arteries and arterioles in the subarachnoid space and cortex of the postcentral gyrus, transverse temporal gyrus, first visual area and cerebellar vermis, as well as the myocardium and renal cortex; (2) the lateral striate artery; (3) the internal carotid, anterior, middle and posterior cerebral, basilar and vertebral arteries, as well as the coronary and renal arteries; and (4) the aorta. The arteriosclerotic changes observed in the patients with Me-Hg intoxication were indistinguishable both qualitatively and quantitatively from those of controls. The results indicate that Me-Hg intoxication does not induce or exacerbate sclerotic changes in arteries and arterioles. Thus, the peculiar neurological symptoms and neuropathological features of Me-Hg intoxication are thought to be induced not by ischemia but by selective primary degeneration of the neurons in specific regions.

Adult↗
PubMed1975

Vascular changes in the surrounding of osteoid osteomas.

Authors observed in 11 instances of osteoid osteoma out of 20 revised cases the characteristic features of arteriolosclerosis in the small arteries supplying the nidus. With these, earlier hypothesis of Jaffe about an increased intravascular pressure in the nidus and supplying vessels in supported.

Arteries↗
PubMed1975

[The left ventricle in chronic cor plumonale (author's transl)].

The volume of both ventricles was estimated in 25 hearts with chronic cor pulmonale. Also, the weight of the left ventricle, including the whole septum and the free part of the right ventricle, was determined to be 100 g. Distinct hypertrophy of the right ventricular part of the septum could be demonstrated in all cases. A weight increase of the left ventricle, including the whole septum, is frequently caused by the hypertrophic ventricular part of the septum. Th relative weight of the right ventricular portion )calculated according to Muller's method) was subtracted from the weight of the left ventricle plus the whole septum. After this weight correction, a hypertropyh of the left ventricle could only be demonstrated in cases with hypertension or renal arterio= and arteriolosclerosis. In one case of left ventricular hypertrophy, hypertension could not be ruled out. In most of the cases a distinct dilation of the left ventricle could be found. The highest degrees of dilation were found in patients with brohchiectases of the lungs. Our results indicate that the structural dialation of the left ventricle may be due to an increased shunt-volume by bronchopulmonary anastomoses.

Adult↗
PubMed1992

Binswanger's disease in the absence of chronic arterial hypertension. A case report with clinical, radiological and immunohistochemical observations on intracerebral blood vessels.

The cerebral changes are described in a woman of 54 who suffered from Binswanger's encephalopathy: there were no signs or symptoms of chronic arterial hypertension. The disease presented as dementia of about 3 years duration. Computed tomography of the brain 2.5 years before her death showed bilateral widespread hypodense lesions in the cerebral white matter. She died of an asthmatic attack. Autopsy disclosed extensive bilateral degeneration of the central white matter, lacunes and gliosis. Severe obliterative arteriolosclerosis occurred in the meningeal vessels and those supplying the affected parts of the brain. Light microscopy showed that the most severe lesions occurred in the arterioles. Immunohistochemistry demonstrated profound extravasation of plasma proteins chiefly albumin, indicating dysfunction of the blood-brain barrier. Thus, the lesions characteristic of Binswanger's encephalopathy may develop in the absence of chronic arterial hypertension. Additional pathogenic factors, possibly genetic predisposition to vascular injury may play a role in the development of this condition.

Blood Proteins↗
PubMed1989

Cutaneous telangiectasia, sparse hair and membranoproliferative glomerulonephritis. A new case of a newly recognized entity.

A boy with sparse red hair, absent eyebrows and eyelashes, cutaneous telangiectasia, poorly developed subcutaneous fat and normocomplementaemic membranoproliferative glomerulonephritis is described. Additional findings were an old-looking, peculiar face, mild developmental delay, calcified choroid plexus and renal arteriolosclerosis. It is believed that this is a new case of a newly recognized entity.

Biopsy↗
PubMed1990

Variations in renal arteriolar diameter in deoxycorticosterone acetate-salt hypertensive rats. A microvascular cast study.

The relation between hypertensive glomerular damage and arteriolar diameter was examined in a microvascular cast study in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The blood pressure and urinary protein excretion increased progressively in the DOCA rats. In controls afferent arteriolar diameters increased during the course of the experiment, and efferent arteriolar diameters remained unchanged. In the DOCA rats, however, afferent arteriolar diameters did not change significantly, while efferent arteriolar diameters increased. Histological studies showed severe arteriolosclerosis and glomerulosclerosis in the DOCA rats. The results show that these arteriolar changes might contribute to the reduction of glomerular capillary pressure in the development of DOCA-salt hypertension. However, they are not sufficient to protect glomeruli from hypertensive damage.

Animals↗
PubMed2006

A comparison of pathomolecular markers of fibrosis and morphology in kidney from autopsies of African Americans and whites.

African Americans have an increased incidence of chronic kidney disease (CKD) due to hypertension and arteriosclerosis and increased death due to coronary artery disease, compared with whites. The pathogenesis of CKD involves the increased presence and activation of myofibroblasts and macrophages, promotion of tubulointerstitial fibrosis, and effects of tubulointerstitial cell mitosis and apoptosis. We hypothesized that increased risk of hypertensive vascular disease may be identified by renal pathomolecular markers that are associated with progressive CKD. Renal sections were available from 50 autopsies of 33 African Americans (55% males) and 17 whites (76% males) undergoing forensic autopsy for unexpected death. Sclerotic glomeruli, severity of cortical fibrosis, and renal arteriolosclerosis, total glomerular number (N (glom)), average glomerular volume (V (glom)), birth weights, and blood pressure were known. Presence and locality of markers for myofibroblasts (alpha-SMA), macrophages (CD68), collagen, pro-fibrotic transforming growth factor-beta1 were scored in renal autopsies, and tubulointerstitial apoptosis was recorded. The results demonstrated a strong positive correlation between age, cortical fibrosis and alpha-SMA (p<0.05), and between CD68 and hypertension and coronary artery disease (p<0.05). The findings confirm the role of myofibroblasts and macrophages in pathogenesis of human CKD. However, the markers showed no significant relationships to V (glom), N (glom), birth weight, or race.

Actins↗
PubMed1995

Cardiac conduction system involvement in sudden death of obese young people.

Involvement of the conduction system in the sudden death of obese young people has not been documented in the literature. We therefore studied the conduction system by serial section examination in 7 subjects, 5 obese and 2 mild to moderately obese, who died suddenly at ages 6, 11, 14, 16, 20, 30, and 32 years of age (5 males, 4 black and 1 white; two females, 1 black and 1 white). Three had a history of sleep apnea. The heart was hypertrophied and enlarged in 6; all 6 had a distinct ventricular septal bulge and epicardial coronary arteries were normal. All had focal mononuclear cells in and around the sinoatrial node and/or its approaches, with marked fat throughout the conduction system in 3, fibrosis of the atrioventricular (AV) bundle and/or the left bundle branch in 5, and the branching bundle sandwiched between the bulbar muscle and the summit of the ventricular septum in 5 (2 with left-sided bundle, 1 with loop formation, and 1 with a markedly fragmented bundle). The AV node was partly within the central fibrous body and/or the atrial septum in 6 patients; focal mononuclear cells were present to a varying degree, with focal fibrosis of the ventricular septum in 6 patients, arteriolosclerosis in 4, and myocardial disarray in 3. The mild to moderately obese patients demonstrated lesser amounts of fat with more fibrosis when compared with the markedly obese. In summary, there are significant pathologic findings in the conduction system in the sudden death of obese young people.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗