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PubMed1992

Immunohistochemical detection of advanced glycosylation end products in diabetic tissues using monoclonal antibody to pyrraline.

Pyrraline is one of the major Maillard compounds resulting from the reaction of glucose with amino compounds at slightly acidic pH. For in vivo studies, monoclonal pyrraline antibodies were raised after immunization of Balb/c mice with keyhole limpet hemocyamin-caproyl pyrraline conjugate. Of 660 hybridoma clones from one donor, 260 produced an antibody to the free hapten, two of which named Pyr-A and Pyr-B also cross-reacted with L-lysyl pyrraline. Using Pyr-B antibody and an ELISA, a gradual increase in pyrraline immunoreactivity was observed in serum albumin incubated with glucose or 3-deoxyglucosone. Plasma pyrraline levels increased fourfold (P less than 0.001) in Sprague-Dawley rats upon induction of diabetes with streptozotocin and were twofold increased in randomly selected plasmas from diabetic humans. Highly specific pyrraline immunoreactivity was detected in sclerosed glomeruli from diabetic and old normal kidneys as well as in renal arteries with arteriolosclerosis and in perivascular and peritubular sclerosed extracellular matrix and basement membranes. The preferential localization of pyrraline immunoreactivity in the extracellular matrix strengthens the notion that the advanced glycosylation reaction may contribute to decreased turnover and thickening of the extracellular matrix in diabetes and aging.

Animals↗

PubMed2000

Primary hyperaldosteronism without suppressed renin due to secondary hypertensive kidney damage.

Primary hyperaldosteronism is characterized by high plasma and urinary aldosterone and suppressed PRA. Renin suppression is due to aldosterone-dependent sodium retention and mild extracellular volume expansion. We observed three patients with primary hyperaldosteronism, severe refractory hypertension, and normal to high normal PRA levels whose aldosterone/renin ratios were still elevated because of disproportionately high aldosterone levels. All available medical data on the patients as well as publications on the aldosterone/renin relationship in primary hyperaldosteronism were reviewed to explain the unusual findings. In one patient, histologically proven renal arteriolosclerosis was the probable cause of the escape of PRA from suppression by an aldosterone-producing adenoma. In the other two patients, hypertensive kidney damage due to primary hyperaldosteronism was the most likely explanation for the inappropriately high PRA, as in patient 1. All patients had high normal or slightly elevated serum creatinine levels and responded to 200 mg spironolactone/day with increased serum creatinine and hyperkalemia. Hyperkalemia was probably due to a decreased filtered load of sodium and a spironolactone-induced decrease in mineralocorticoid function. Two patients were cured of hyperaldosteronism by unilateral adrenalectomy but still need some antihypertensive therapy, whereas one patient has probable bilateral adrenal disease, with normal blood pressure on a low dose of spironolactone. In patients with severe hypertension due to primary hyperaldosteronism, PRA can escape suppression if hypertensive kidney damage supervenes. An increased aldosterone/PRA ratio is still useful in screening for primary hyperaldosteronism. These patients may respond to spironolactone therapy with a strong increase in serum creatinine and potassium. Early specific treatment of primary hyperaldosteronism is therefore indicated, and even a patient with advanced hypertension will profit from adrenalectomy or cautious spironolactone treatment.

Aldosterone↗

PubMed1993

Pathologic correlates of incidental MRI white matter signal hyperintensities.

We related the histopathologic changes associated with incidental white matter signal hyperintensities on MRIs from 11 elderly patients (age range, 52 to 82 years) to a descriptive classification for such abnormalities. Punctate, early confluent, and confluent white matter hyperintensities corresponded to increasing severity of ischemic tissue damage, ranging from mild perivascular alterations to large areas with variable loss of fibers, multiple small cavitations, and marked arteriolosclerosis. Microcystic infarcts and patchy rarefaction of myelin were also characteristic for irregular periventricular high signal intensity. Hyperintense periventricular caps and a smooth halo, however, were of nonischemic origin and constituted areas of demyelination associated with subependymal gliosis and discontinuity of the ependymal lining. Based on these findings, our classification appears to reflect both the different etiologies and severities of incidental MRI signal abnormalities, if it is modified to treat irregular periventricular and confluent deep white matter hyperintensities together.

Aged↗

PubMed1995

Histopathologic correlates of white matter changes on MRI in Alzheimer's disease and normal aging.

We investigated the histopathologic correlates of white matter changes in Alzheimer's disease (AD) patients (n = 6) and controls (n = 9) using postmortem MRI. White matter changes were rated on a 0 to 3 scale in 51 regions. Histopathologically, we subjectively rated the loss of myelinated axons in the deep and periventricular white matter, denudation of the ventricular ependyma, gliosis, width of the perivascular spaces, and leptomeningeal congophilic angiopathy; we measured structural changes in the walls of the blood vessels in the white matter in micrometers. The AD brains displayed significantly more white matter hyperintensities on MRI than controls. Histopathologically, the denudation of the ventricular ependyma and the gliosis were significantly more severe in AD than in controls, and there was a trend toward more loss of myelinated axons in the deep white matter in the AD brains (p = 0.07). The MRI abnormalities correlated with the loss of myelinated axons in the deep white matter (r' = 0.37; p < 0.01) and with the denudation of the ventricular lining (r' = 0.54; p < 0.01). We could not find any evidence for arteriolosclerosis, but the mean thickness of the adventitia of the arteries of the deep white matter in AD almost doubled the value in control brains (p = 0.0009). We conclude that white matter abnormalities in AD patients and controls consist of loss of myelinated axons, probably caused by arterial changes and breakdown of the ventricular lining. Since imaging/histopathologic correlation was similar in AD patients and controls, these changes probably represent some form of accelerated aging.

Aged↗

PubMed1998

Leukoaraiosis and vascular dementia.

The emergence of sensitive techniques for brain imaging has drawn attention to the occurrence of diffuse or multifocal changes affecting the cerebral white matter. The white matter changes are usually termed periventricular leukoencephalopathy, or leukoaraiosis. Microscopic studies of affected areas in the deep white matter have shown mostly demyelination, reactive gliosis, and arteriolosclerosis, proportional to the degree of radiologic changes. Yet, many other disease conditions need to be ruled out. Risk factors for ischemic leukoaraiosis include arterial hypertension, a history of stroke, and age. In the hereditary disorder CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), severe white matter changes occur in the absence of hypertension. In "ordinary" cases of leukoaraiosis, genetic factors might similarly determine the effect of risk factors on the aging brain and might explain, for example, why not all patients with severe hypertension develop leukoaraiosis. Not surprisingly, diffuse demyelination affects cognitive function. Although reduced speed of mental processes is the most characteristic sign, attention, concentration, and verbal and visual memory are also affected. Most importantly, less severe forms of cognitive impairment represent a silent and perhaps largely preventable epidemic among aged or even middle-aged subjects. They live independently, but mentally they perform on a level well below their previous capacities. Although being "a bit odd" does not lead to hospital admissions, it seriously affects quality of life of a large part of the community. Moderate grades of leukoaraiosis constitute a major public health problem and deserve the attention of the scientific community.

Brain↗

PubMed2002

Higher lipoprotein (a) levels in atherothrombotic than lacunar ischemic cerebrovascular disease.

To investigate the role of plasma lipid abnormalities in ischemic cerebrovascular disease related to primary vessel disease, the authors assess lipid profiles in a hospital-based cohort of 202 consecutive patients with atherothrombotic or lacunar stroke subtypes. Lipoprotein (a) was the unique lipid parameter that differs between these two subtypes being its value twofold higher in patients with atherothrombotic than in lacunar stroke. This suggests that lipoprotein (a) promotes large vessel atheromatosis rather than small vessel arteriolosclerosis and favors thrombosis on atheromatous plaques by suppressing local fibrinolysis.

Adult↗

PubMed1999

Pathologic and electrocardiographic findings in sudden cardiac death in racehorses.

Five racehorses in apparently normal condition succumbed to sudden cardiac death (SCD) during or shortly after intensive training exercise. Cardiopathologic examination was performed. In 1 of the 5 horses, the use of an electrocardiogram (ECG) recording taken continuously for 440 sec enabled us to analyze some of the arrhythmias in the terminal event of SCD. The ECG tracing exhibited the R-on-T phenomenon following a pair of ventricular premature contractions (VPCs). The phenomenon rapidly degenerated into ventricular fibrillation, which led to cardiac arrest. In all 5 horses cardiopathologic examination revealed the following lesions: (i) foci of myocardial fibrosis in the right atrium located close to the sinoatrial (SA) node, (ii) fibrotic and/or fibroplastic changes in the upper portion of the interventricular septum, including the atrioventricular (AV) conduction system, and (iii) arterio- and arteriolosclerosis of the SA and AV node vessels. Pathogenetically, the process by which the focal lesions of myocardial ischemia secondary to vascular sclerosis progressed into fibrosis and/or fibroplasia could play a major role in the genesis of arrhythmias. Presumably the fibrotic and/or fibroplastic changes in the area of the AV bundle and its bundle branches are closely related to the onset of fatal ventricular arrhythmias such as VPCs, deteriorating into ventricular fibrillation. SCD in training and racing Thoroughbred horses appears to be due to arrhythmia.

Animals↗

PubMed1992

The conduction system in transplanted hearts.

This is a serial section examination of the conduction system (CS) in six patients who died seven months, 11 months, two years four months, four years two months, 11 years, and 16 years eight months following cardiac transplantation. The heart was hypertrophied and enlarged in all. There was myocarditis of varying degree in all cases with arteriosclerosis and arteriolosclerosis. These findings were more dominant in the atria than in the ventricles. In the CS, myocarditis with fibrosis was found in all in the approaches to the sinoatrial (SA) node, the SA node, the atria, the atrioventricular (AV) node, and the bundle and bundle branches, to a varying degree. When compared with the endomyocardial biopsy findings, the autopsied cases revealed more myocarditis and fibrosis than those estimated to be present in the biopsy specimen. In summary, this study demonstrates that there are fibrotic changes in the CS with the persistence of inflammatory phenomena of the myocardium and the CS to a varying degree in transplanted hearts. This is accompanied by the ubiquitous coronary artery disease affecting not only the large coronaries but also the small vessels. The pathologic changes in and around the CS may be responsible for arrhythmias and sudden death in some cases of cardiac transplantation.

Adolescent↗

PubMed1988

Conduction system in a trained jogger with sudden death.

A 47-year-old extremely active, entirely asymptomatic trained jogger was found dead in bed. He was known to have had sinus bradycardia with first-degree atrioventricular block for eight years and a type 1 second-degree block five years prior to death. A permanent pacemaker had been inserted, and apparently the patient was then in good health and maintained his jogging program until he died suddenly. The conduction system revealed an atrioventricular node situated more to the left of the atrial septum than usual, which made tenuous connection with the surrounding atria due to marked fatty infiltration. The atrioventricular node as it joined the left-sided His bundle revealed fatty metamorphosis, fibrosis, disarray of myocardial fibers, and mononuclear cell infiltration. The right bundle branch was intramyocardial and fibrosed throughout. Increased aging changes of the left side of the septum with arteriolosclerosis and patchy fibrosis were present. This is the first case in which the atrioventricular node was more to the left side of the atrial septum with fatty separation of the node from the surrounding atrial musculature, with myocardial disarray of the nodal-His bundle junction. Although congenital abnormality of the conduction system may remain silent without symptoms for a long time, it should be kept in mind that sudden death may occur sooner or later in some susceptible individuals.

Atrioventricular Node↗

PubMed1989

Conduction system in children with acquired immunodeficiency syndrome.

Six children died of acquired immunodeficiency syndrome (AIDS), four of them females, ages 7 months, 13 months, 2 years 8 months, and 4 years; and two of them males, aged 2 1/2 and 7 years. They were born to IV drug-addicted parents. The conduction system (CS) and the entire heart were studied by serial section. In all cases the heart was hypertrophied and enlarged; one had total thrombotic occlusion of the right coronary artery with extensive infarction of the ventricular septum. Vascular changes also were found in all hearts, involving small arteries, arterioles, and venules. In the arteries, they involved the intima, media, and adventitia, and perivascular areas in a degenerative and inflammatory process. The elastic tissue was especially affected. A nonspecific myocarditis was present in four cases and epicarditis in all. Changes in the summit of the ventricular septum were present in four cases, consisting of increased fibrosis and arteriolosclerosis. The CS changes varied in location, showing either vasculitis, myocarditis, or fragmentation of the bundle with lobulation and fibrosis. The changes in the conduction system were not as severe as the changes in the surrounding myocardium. In one case the ECG was abnormal, showing left hemiblock. This corresponded to the finding of fibrosis, vacuolization of cells, and space formation in the left bundle branch.

Acquired Immunodeficiency Syndrome↗

PubMed2005

Essential hypertension, progressive renal disease, and uric acid: a pathogenetic link?

Hypertension and hypertension-associated ESRD are epidemic in society. The mechanisms responsible for renal progression in mild to moderate hypertension and those groups most at risk need to be identified. Historic, epidemiologic, clinical, and experimental studies on the pathogenesis of hypertension and hypertension-associated renal disease are reviewed and an overview/hypothesis for the mechanisms involved in renal progression is presented. There is increasing evidence that hypertension may exist in one of two forms/stages. The first stage, most commonly observed in early or borderline hypertension, is characterized by salt-resistance, normal or only slightly decreased GFR, relatively normal or mild renal arteriolosclerosis, and normal renal autoregulation. This group is at minimal risk for renal progression. The second stage, characterized by salt-sensitivity, renal arteriolar disease, and blunted renal autoregulation, defines a group at highest risk for the development of microalbuminuria, albuminuria, and progressive renal disease. This second stage is more likely to be observed in blacks, in subjects with gout or hyperuricemia, with low level lead intoxication, or with severe obesity/metabolic syndrome. The two major mechanistic pathways for causing impaired autoregulation at mild to moderate elevations in BP appear to be hyperuricemia and/or low nephron number. Understanding the pathogenetic pathways mediating renal progression in hypertensive subjects should help identify those subjects at highest risk and may provide insights into new therapeutic maneuvers to slow or prevent progression.

Disease Progression↗

PubMed2006

White matter changes in elderly people: MR-pathologic correlations.

Magnetic resonance (MR) imaging features of white matter lesions, often seen in the elderly, are correlated with histologic findings. Dilatation of perivascular spaces is seen, especially in the frontal and/or parietal subcortical white matter; the spaces are less than 3 mm in diameter and have sharp margins with no perifocal abnormality. Old lacunar infarcts are larger than 3 mm in diameter and are irregularly shaped and accompanied by perifocal myelin pallor and gliosis. Periventricular hyperintensity, including cap and rim, histologically shows myelin pallor, dilatation of perivascular spaces, discontinuity of the ependymal lining, and subependymal gliosis. Deep and subcortical white matter hyperintensity reflects myelin pallor and dilatation of perivascular spaces. Diffuse white matter lesion, seen in Binswanger's disease, shows myelin pallor and tissue rarefaction associated with loss of myelin and axons. U-fibers are usually well preserved. Severe arteriosclerosis and arteriolosclerosis are usually seen in the white matter. Knowledge of the pathologic features of incidental changes in white matter helps in understanding MR imaging findings.

Aged↗

PubMed1999

Catastrophic antiphospholipid syndromes in systemic lupus erythematosus.

The objective of this study was to look for the occurrence of catastrophic antiphospholipid syndromes (APS) and to try to detect discriminating factors for predicting a worse prognosis, related to Lupus anticoagulant (LA) and antiphospholipid antibodies (aPL), in systemic lupus erythematosus (SLE) with main renal involvement. Regression, recursive partition and logistic regression analyses were applied to our 80 SLE patients prospectively followed up since 1980. Immunologic and other laboratory parameters including beta 2-glycoprotein 1 dependence, resistance to activated protein C caused by a substitution on the coagulation factor V gene, induction of monocyte procoagulant activity. Regression studies demonstrated an overall worse prognosis in term of both thrombosis and death for the group of LA/aPL positive patients (33/80). However, recursive partition analysis was able to isolate a small high risk-subgroup (8/33) characterized by persistent LA/aPL antibodies positive result, widespread signs of noninflammatory vasculopathy (skin, brain, kidney) and renal pathology mimicking that of thrombotic microangiopathy or arteriolosclerosis, also in the absence of classic SLE-nephritis. Only in this subset, three catastrophic APS were recorded, while, in traditional SLE nephritis, even persistent LA/aPL positive results (sometimes after one previous thrombosis) did not seem to imply a particularly severe prognosis. All serologic criteria employed are unable to identify high-risk patients. We conclude that catastrophic APS is a rare event in renal SLE. Before more predictive serologic markers become available, a simple algorithm, dealing with clinical data and renal histologic patterns, may help physicians to identify putatively high risk-LA/aPL antibodies in SLE patients with main renal involvement. This ominous subset does not belong to the group of classic SLE-nephritis.

Adolescent↗

PubMed1994

[A clinicopathological study of senile dementia of Alzheimer's type (SDAT) and white matter lesions of Binswanger's type].

A clinicopathological study of senile dementia of Alzheimer's type (SDAT) accompanied by the white matter lesions of Binswanger's type was carried out. Fifty-seven patients, who were diagnosed as suffering from SDAT based on clinical and pathological criteria, were classified into two groups based on the white matter lesions of Binswanger's type. Namely, group 1 consisted of the SDAT patients without any subcortical or white matter lesions (30 cases); group 2 consisted of those with white matter lesions of Binswanger's type (11 cases). The other 9 cases included those with vascular lesions and 4 with some of the same pathological changes found in Parkinson's disease. Clinically, group 2 patients showed subcortical symptoms such as urinary incontinence, Parkinsonian gait, being accompanied by hypertension and arrhythmias. Periventricular lucency (CT) were common in group 2. Macroscopically, both groups showed moderately to severe atrophy, and the width of the corpus callosum of group 2 was narrower than that of group 1. There was no difference in cerebral arteriosclerosis between the groups. In microscopic findings, patients in group 2 showed diffuse distribution of cortical changes such as senile plaques as well as Alzheimer's senile plaques as well as Alzheimer's neurofibrillary tangles while those in group 1 showed various types of diffuse or local distribution. Arteriolosclerosis of the white matter were found in both groups. There was no difference in aortic atherosclerosis and/or heart disease. The complication of white matter lesions of Binswanger's type was not a rare finding in SDAT.

Aged↗

PubMed1996

[Clinico-pathological evaluation of leukoaraisosis in Alzheimer's disease].

Patients with multi-infarct dementia often have periventricular low density lesions on computed tomography and periventricular hyper-intensity lesions on computed tomography and periventricular hyper-intensity lesions on magnetic resonance imaging. Hachinski called this condition leukoaraiosis and results of previous studies that in multi-infarct dementia leukoaraiosis correlates with cerebral hypoperfusion. Periventricular low-density lesions in the white matter also occur, but their origin and clinical significance insuch patients is unknown. We studied when these lesions develop in patients with Alzheimer's dementia, and whether their presence correlates with clinical findings and cerebral blood flow. The subjects were 37 patients with a probable diagnosis of Alzheimer's dementia, as based on the Neuroepidermilogy Branch of the National Institute of Neurological Disorders and Stroke and the Alzheimer's disease and Related Disorders Association system. Autopsy findings were also available for 2 patients. Patients at higher Functional Assessment Staging of Senile Dementia of Alzheimer Type stages had more extensive periventricular low-density lesions. Patients with the lesions were more likely to have grasp reflex and sucking relex. Blood flow to the frontal and parietal cortices was significantly less in patients with the lesions than in those without the lesions. Neither of the 2 autopsies cases yielded evidence of arteriolosclerosis. Periventricular low-density lesions in Alzheimer's dementia may be closely associated with a degenerative process different from that seen in multi-infarct dementia.

Alzheimer Disease↗

PubMed2002

Factors associated with progression of IgA nephropathy are related to renal function--a model for estimating risk of progression in mild disease.

BACKGROUND: A number of factors are linked to the outcome of IgA nephropathy (IgAN). However, it has been difficult to compare results of studies since patient populations have varied greatly. There were 3 aims in the study reported here, namely to compare factors associated with renal outcome in IgAN patients with different levels of renal function on diagnosis; to determine factors which were independently associated with progression of renal disease in initially mild IgAN; and to create a model for the estimation of the risk of progression in individual IgAN patients with normal renal function on diagnosis. METHODS: Two hundred and fifty-nine IgAN patients who had been followed on average for 9.1 (SD 4.5) after diagnosis were divided into 2 groups on the basis of renal function on diagnosis. In group 1 (98 patients), Ccr (creatinine clearance, estimated by the Cockcroft-Gault formula) was < 85 ml/min, in group 2 (161 patients) > or = 85 ml/min. Univariate analyses were used to find significant differences between progressors and non-progressors in both groups. Logistic regression analysis was used to determine factors independently associated with progression in group 2. RESULTS: Several factors were found to be associated with outcome in both groups, such as hypertension, level of Ccr, serum cholesterol, proteinuria, and also histopathological changes. Factors associated with progression in patients with initially decreased renal function (group 1), were predictable, such as male sex, absence of episodes of macroscopic hematuria, serum urate level and degree of tubular atrophy. Surprisingly, in patients with initially normal renal function (group 2), numbers of urinary erythrocytes were associated with outcome. The factors independently associated with progression in this group were number of urinary erythrocytes, existence of hypertension and in histopathology arteriolosclerosis and the level of glomerular score. A model for estimating risk of progression on the basis of various combinations of factors found to be independently associated with outcome is presented. CONCLUSIONS: We concluded that association between variable and outcome in IgAN depends partly on renal function at the time of assessment of the factor. Since there are factors which are independently associated with the outcome of early and apparently mild disease, early diagnosis of IgAN is desirable: outcome in mild IgAN can be predicted reliably on the basis of factors found to be independently associated with outcome.

Adrenal Cortex Hormones↗

PubMed2003

Schnabel cavernous degeneration: a vascular change of the aging eye.

CONTEXT: Schnabel cavernous degeneration is a histologic finding originally attributed to glaucoma; however, its cause and significance have been controversial. OBJECTIVE: To determine the basic cause of the formation of cavernous spaces in the proximal optic nerve and its clinical significance. METHODS: A retrospective analysis of 4500 autopsy eyes processed for histologic evaluation between 1967 and 1991. RESULTS: Ninety-three (2.1% of eyes examined) cases of Schnabel cavernous optic atrophy were identified. The majority of the eyes were from women (81%). The mean age of the entire group was 88 years (reference range, 54-103 years). Severe vascular anomalies were present in 75% of the individuals. Cavernous degeneration was unilateral in 82% of the cases. Loss of ganglion cells and nerve fiber layer consistent with glaucoma was found in 23.7% of the individuals. Clinical information was available for 15 individuals (16%). Half of them were thought to have some clinical optic nerve damage; in the remainder, no specific optic disc abnormalities were noted. Histologic findings of arteriolosclerosis in the optic nerve circulation were common. The prevalence of glaucoma was low. CONCLUSIONS: Schnabel cavernous optic atrophy appears to be a unilateral condition of elderly women with systemic vascular disease and few characteristic ocular features. Our data indicate that a chronic vascular occlusive disease of the proximal optic nerve is more involved in cavernous atrophic pathogenesis than is a sustained increase of intraocular pressure.

Aged↗

PubMed1991

Duplex Doppler sonography in renal parenchymal disease. Histopathologic correlation.

To evaluate the histopathologic changes influencing Doppler measurements of the resistive index (RI) in renal arteries in renal parenchymal diseases, 68 kidneys in 34 consecutive patients with various forms of renal parenchymal diseases were studied by duplex Doppler ultrasound (duplex US) immediately before percutaneous renal biopsy. The RI, renal length, and renal cortical echogenicity were correlated with the amount of glomerular, interstitial, and vascular changes graded on a scale from 0 to 100. The renal vascular resistance and therefore the RI are significantly correlated with the prevalence of arteriolosclerosis, glomerular sclerosis, arteriosclerosis, edema, and focal interstitial fibrosis. There was no significant difference of the RI in five groups of different renal parenchymal diseases. Of 34 patients, 24 presented with an RI less than 0.7, which was thought to be within the normal range so far. Additionally, the RI increases as the patient's age increases, due to higher incidence of arteriosclerosis. Of our patients, 44% presented with normal cortical echogenicity. Quantitative duplex US using the RI does not reliably distinguish different types of renal medical disorders.

Adult↗