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PubMed1975

Diabetic glomerulosclerosis without glucose intolerance.

The pathophysiology of the microangiopathy of diabetes mellitus is poorly understood, and the relevance of carbohydrate intolerance remains uncertain. Four patients are presented with renal abnormalities suggestive of diffuse diabetic glomeruloscierosis. These patients have no evidence of carbohydrate intolerance by standard clinical technics. A familial incidence of diabetes mellitus and delayed insulin response to an oral glucose load support a classification of prediabetes or suspected diabetes mellitus for these patients. Early intercapillary nodule formation was seen in only two of the four patients. In the absence of this infrequent pathognomonic finding, an alternate approach to the diagnosis of diabetic glomerulosclerosis is suggested. Diffuse glomerular capillary basement membrane thickening, consistently present with diabetic glomerulosclerosis, is demonstrated by measurements utilizing the latex microsphere technic. The mean glomerular capillary basement membrane thickness of these patients was 4,403 A, compared with the control value of 3.098 A (P less than 0.001). Other pathologic findings suggestive of diabetic nephropathy include efferent arteriolosclerosis and linear immunofluorescence without electron dense deposits or inflammation. Skeletal muscle capillary basement membranes of all four patients also demonstrated significant thickening. The mean value for the patients was 1,510 A, as compared with a control value of 961 A (P less than 0.001). The importance of this muscle capillary basement membrane thickening to the diagnosis of diabetic microangiopathy is discussed. The pathologic alterations in the renal biopsy specimens and the demonstration of muscle capillary basement membrane thickening strongly suggest that diabetic glomerulosclerosis may occur in the absence of overt clinical carbohydrate intolerance.

Adolescent↗

PubMed1992

Effects of hypertension and hyperlipidemia on the myocardium and coronary vasculature of the WHHL rabbit.

This study was undertaken to study the effects of hyperlipidemia and hypertension on the coronary circulation and on the myocardium of Watanabe heritable hyperlipidemic (WHHL) rabbits. Surgery to induce hypertension by the one-kidney, one-clip technique was performed on the WHHL rabbits at 3 months of age. At 3 and 6 months after surgery, the right and left coronary arteries and the left ventricle and posterior papillary muscle from normotensive and hypertensive animals were assessed. Atherosclerotic involvement was found at the coronary origin in 94% of the arteries evaluated. Lesions were usually confined to the proximal 1-2 mm of the coronary artery. The prevalence of coronary atherosclerosis in the WHHL rabbit was found to be higher than previously reported in rabbits of the same age. Hypertension-induced muscular and vascular changes such as left ventricular hypertrophy, medial thickening of the arteries, and hyaline arteriolosclerosis were found in most of the hypertensive animals. These changes were rarely seen in the normotensive rabbits. Characteristics of ischemia and cell injury such as eosinophilic fibers, fiber vacuolization, and contraction band necrosis were found more often in hypertensive than in normotensive WHHL rabbits. Confluent areas of severe necrosis indicative of myocardial infarction were not found; myocardial damage was diffuse and involved individual cells and small microscopic areas. This model may be valuable in further studies of coronary artery disease and myocardial injury that result from the combination of hypercholesterolemia and hypertension.

Animals↗

PubMed1990

Arteriolosclerotic leucoencephalopathy in the elderly and its relation to white matter lesions in Binswanger's disease, multi-infarct encephalopathy and Alzheimer's disease.

Arteriolosclerotic leucoencephalopathy in the elderly (ALE) is characterized by white matter lesions associated with atherosclerosis and arteriolosclerosis. Mild lesions are focal and probably represent early status cribosus or incomplete lacunar infarcts. Moderate and severe lesions are diffuse areas of demyelination in the centrum semiovale in which lacunar infarcts are seldom observed. The incidence of ALE in a consecutive necropsy series of 50 cases (mean age 62.6 +/- 13.1 years) was 52%, it was rare in the fourth and fifth decades but increased thereafter to reach a prevalence of 100% at the age of 80 years. Mild lesions occurred in 19 patients and lesions were moderate or severe in 7 (14%). The mean age was higher in this group (74.7 +/- 7.6 years) than in patients with white matter changes as a whole. Dementia occurred only in 3 patients with moderate or severe ALE. These data suggest that (a) ALE is common in old age and is probably the cause of leuko-araiosis in most CT scans in the elderly; (b) ALE may be asymptomatic; (c) the severity of white matter changes may be not related to the severity of neurological deficits; and (d) multiple lacunar infarcts or associated degenerative diseases (i.e., Alzheimer's disease) may be the main cause of dementia in patients with ALE. White matter lesions in ALE, Binswanger's disease, transition areas in multi-infarct encephalopathy (MIE) and Alzheimer's disease (AD) are similar in morphology and are probably the result of a subacute hypoperfusion/hypoxic process. Increased arterial blood pressure is a frequent risk factor in ALE, Binswanger's disease and MIE, whereas congophilic angiopathy of the meningeal and cortical vessels, in addition to mild or moderate arteriolar hyalinosis in the white matter, may play a role in the pathogenesis of incomplete infarctation of the white matter in patients with AD.

Aged↗

PubMedDate not supplied

The vascular endothelium as a regulator of the ocular circulation: a new concept in ophthalmology?

The endothelium influences local vascular tone by releasing endothelium-derived relaxing factors such as nitric oxide, prostacyclin and a putative hyperpolarizing factor. In isolated ophthalmic arteries and the perfused eye, all endothelial factors importantly contribute to vascular regulation. In larger ophthalmic vessels, this is due to their effects on vascular smooth muscle cells; in smaller vessels, pericytes can be influenced as well. Contracting factors formed include peptide endothelin-1 and cyclooxygenase products, such as thromboxane A2 and prostaglandin H2. In the peripheral circulation endothelial dysfunction occurs under pathological conditions, both in conduit arteries and the microcirculation. An imbalance of endothelium-derived relaxing and contracting factors could be important for the development of vascular ophthalmic complications like hypertension, diabetes, arteriolosclerosis and retinal ischemia. Endothelial dysfunction may also contribute to vasospastic events in retinal migraine and some forms of low tension glaucoma associated with Raynaud phenomenon and migraine.

Animals↗

PubMed1994

Renal protective effect of efonidipine hydrochloride (NZ-105), a new calcium antagonist, in spontaneously hypertensive rats.

1. We investigated the renal protective effect of efonidipine hydrochloride (NZ-105) in spontaneously hypertensive rats (SHR). SHR were given a diet containing 0.075% NZ-105 from 8 weeks old for 20 weeks. 2. 24-hr urinary protein excretion in the control SHR (drug-free diet) increased with age (from 77.3 mg/kg/day at 8 weeks old to 385.4 mg/kg/day at 28 weeks old), while that in NZ-105-treated SHR was maintained at almost the same level as that in Wistar-Kyoto rats (WKY), matched control animals throughout the experimental period. 3. The histological changes of the kidney were examined by light microscopy at the end of the treatment period. In control SHR, swelling and hyalinization of glomeruli, dilatation of renal tubules containing hyaline casts and arteriolosclerosis were revealed. The long-term administration of NZ-105 markedly suppressed these changes. 4. The kidney weights and plasma creatinine concentration in control SHR were higher than those in WKY, while they were significantly reduced in NZ-105-treated SHR. The long-term administration of NZ-105 also suppressed the elevation of systolic blood pressure and the increases of plasma renin activity and aldosterone concentration. 5. These findings suggest that NZ-105 inhibits the development of proteinuria and progressive kidney damage in SHR and may become a useful antihypertensive drug with the renal protective effect.

Animals↗

PubMed2005

A unifying pathway for essential hypertension.

We present the hypothesis that most cases of essential hypertension occur via two phases. The first phase is initiated by episodes of renal vasoconstriction induced by a hyperactive sympathetic nervous system, activation of the renin-angiotensin system, or hyperuricemia resulting from diet or genetics. During this phase the hypertension is salt resistant and renin dependent, and the kidney normal. Over time, preglomerular vascular disease develops (arteriolosclerosis), associated with tubulointerstitial inflammation; this shifts the hypertension to a salt-sensitive, volume-dependent, and renal-dependent pathway. This pathway unites many of the previous hypotheses on the etiology of hypertension, and offers insights into ways to prevent, ameliorate, or cure the underlying process.

Animals↗

PubMed2005

Hemodynamics of hyperuricemia.

Prolonged hyperuricemia is associated with the development of hypertension, renal arteriolosclerosis, glomerulosclerosis, and tubulointerstitial injury. It confers a greater risk than proteinuria for developing chronic renal disease and is associated with the development of hypertension. Mild chronic hyperuricemia without intrarenal crystal deposition was induced in rats by inhibiting uricase with oxonic acid. Hyperuricemic rats developed hypertension, afferent arteriolar thickening, and mild renal interstitial fibrosis. Additionally, hyperuricemia accelerated renal damage and vascular disease in rats undergoing renal ablation. To better understand the role of hyperuricemia in the kidney, micropuncture studies were performed. Hyperuricemia resulted in renal cortical vasoconstriction (single nephron glomerular filtration rate (SNGFR) 35%, P < .05) and glomerular hypertension (P < .05). The possibility that hyperuricemia could modify renal hemodynamic disturbances during progression of renal disease was tested in rats with 5/6 nephrectomy. Hyperuricemia accentuated the renal vascular damage and caused cortical vasoconstriction (SNGFR 40%, P < .05) and persistent glomerular hypertension. In conclusion, hyperuricemia impairs the autoregulatory response of preglomerular vessels, resulting in glomerular hypertension. Lumen obliteration induced by vascular wall thickening results in severe vasoconstriction. The resulting ischemia is a potent stimulus that induces tubulointerstitial inflammation and fibrosis as well as arterial hypertension.

Animals↗

PubMed1977

Conduction system in a patient with Prinzmetal's angina and transient atrioventricular block.

His bundle recordings obtained during and between attacks of Prinzmetal's variant angina and transient atrioventricular (A-V) block were followed by a comprehensive serial section study of the conduction system in a 33 year old woman. Recordings between attacks showed normal A-H and H-V intervals. During an attack there was block proximal to the His bundle recording site. Pathologic studies revealed severe narrowing of the right coronary artery. Arteriolosclerosis of the heart was diffuse. Insignificant changes were found in the approaches to the A-V node and the A-V node itself. Major changes found in the left bundle branch had no counterpart in the electrocardiogram; the discordance in these findings is discussed.

Adolescent↗

PubMed2002

The pathology of ischemic-vascular dementia: an update.

In Western memory clinic-based series, ischemic-vascular dementia (IVD) is seen in 8-10% of cognitively impaired elderly subjects. Its prevalence in autopsy series ranges from 0.03% to 58% with reasonable values of 4-10%, while in Japan, IVD is seen in 22-35% and mixed-type dementia (MTD) (Alzheimer disease/AD+IVD) in 6-11%. In a large Viennese autopsy series, "pure" IVD was observed in 9.4% of demented elderly and in 2.9% of those clinically diagnosed as possible/probable AD MTD was observed in 3.1% and 1.3% respectively. The major morphological types of IVD are multi-infarct encephalopathy (MIE), small vessel infarct type-strategic infarct dementia (SID), subcortical arteriosclerotic leukoencephalopathy (Binswanger), multilacunar state, mixed cortico-subcortical type, granular cortical atrophy, and post-ischemic encephalopathy. In contrast to previous suggestions that IVD is mainly the result of large hemispheral infarcts or losses of over 100 ml of brain tissue, recent data indicate that cognitive decline is commonly associated with widespread small ischemic or vascular lesions (microinfarcts, lacunes) throughout the brain with predominant involvement of the basal ganglia, white matter, and hippocampus. The lesion pattern of "pure" IVD, which is related to arteriolosclerosis and hypertensive microangiopathy, differs from that in mixed-type dementia, more often showing large infarcts. Although recent studies suggest that concomitant small cerebral infarcts do not significantly influence the overall rate of cognitive decline in AD patients or may be important for mental decline in early AD, both mild AD pathology and microvascular cerebral lesions appear to be common and may interact in "unmasking" or promoting dementia.

Aged↗

PubMed2000

The contribution of MRI in the differential diagnosis of posterior fossa damage.

In multiple sclerosis patients, magnetic resonance imaging (MRI) frequently detects lesions in the brain stem and cerebellum. However various pathologies that have a predelection to occur in posterior fossa parenchyma may share similar features with inflammatory-demyelinating lesions. In this paper, we review the contribution of MRI to the differential diagnosis of posterior fossa pathology. Vascular lesions due to chronic hypoperfusion and arteriolosclerosis or occlusion of the main supplying arteries of the posterior circulation leading to acute infarction frequently produce characteristic pontine or cerebellar lesions. Neoplastic disease, in particular pontine gliomas in younger patients may have similar MRI features and may be difficult to distinguish from inflammatory-demyelinating lesions. Central pontine myelinolysis usually occurs in severely ill patients but the pontine MRI changes have an overlapping profile with inflammatory demyelination. Diffuse axonal injury of the midbrain and brainstem after head trauma and atrophy of posterior fossa structures in degenerative diseases may appear similar on MRI to tissue changes also seen frequently in MS. Analysis of the MRI appearance and clinical information is most often useful to narrow the fairly long list of differential diagnoses of posterior fossa pathology.

Brain Diseases↗

PubMed2000

Outcome of IgA nephropathy in adults graded by chronic histological lesions.

This prognostic study of primary immunoglobulin A (IgA) nephropathy focused on chronic irreversible glomerular sclerosis and interstitial fibrosis, based on the premise that this disease is characterized by a protracted and, for many, progressive course. We used a chronicity-based histological grading system to assess the biopsy specimens of 126 adults with IgA nephropathy over a median follow-up of 10 years. Our grading system included a glomerular grading (GG) of 1 to 3 based on the extent of glomerular sclerosis, a tubulointerstitial grading (TIG) of 1 to 3 based on the degree of tubular loss or interstitial fibrosis, and the evaluation of hyaline arteriolosclerosis (HA). These three histological parameters were correlated with each other and with serum creatinine level, degree of proteinuria, and blood pressure at the time of renal biopsy. Univariate analysis showed that these three histological and three clinical parameters were significantly correlated with renal survival. By multivariate analysis using the Cox regression model, GG, serum creatinine level, and degree of proteinuria represented independent prognostic factors of renal survival. For a subset of patients at a relatively early stage of disease with a serum creatinine level less than 130 micromol/L at the time of biopsy, all three histological features and degree of proteinuria were significantly correlated with renal survival, and GG was the only independent prognostic factor for renal outcome. This study shows that glomerular sclerosis represents the most important prognostic factor in adult patients with primary IgA nephropathy and has a strong predictive value. Our chronicity-based histological grading system not only correlates well with the natural history of IgA nephropathy but is also reproducible and relatively simple to apply.

Adolescent↗

PubMed1997

Myofibroblasts and arteriolar sclerosis in human diabetic nephropathy.

We examined the biopsy specimens of 62 patients with diabetic nephropathy to establish whether the myofibroblast (MF) has a role in progressive interstitial fibrosis and to ascertain whether a relationship existed between MF activity and severity of arteriolosclerosis. MF were identified by morphology and alpha smooth muscle actin (alpha SMA) immunostaining. Analysis of vascular injury was performed by counting the number of interstitial arterioles after staining endothelial cells with von Willebrand factor (VWF) antibody. Arteriosclerosis was quantified by using a computer-aided image analyzer to measure the arteriolar wall surface and total arteriolar surface area, and the ratio of wall to total surface area was expressed as the index of arteriosclerosis (IA). Fractional area of interstitium (IFA), alpha SMA, and collagen III (Coll III) were quantitated by point counting. Results were related to structural and functional parameters using rank correlation coefficients. There was a strong correlation between IFA and Coll III staining (r = 0.83; P < 0.001). The alpha SMA staining correlated with IFA (r = 0.56; P < 0.001) and Coll III (r = 0.47; P < 0.001), and there were significant correlations between alpha SMA and total urinary protein (r = 0.47; P < 0.001), renal function (plasma creatinine) at time of biopsy (r = 0.51; P < 0.001), and the percent change in plasma creatinine after 4 years (delta Cr) (r = 0.37; P = 0.01). The IA correlated significantly with Coll III (r = 0.29; P = 0.02), glomerular filtration rate (GFR) (r = 0.39; P = 0.008), and creatinine (r = 0.33; P = 0.01), but no correlation was observed between alpha SMA and IA (r = 0.16; P = 0.23) or IA and delta Cr (r = -0.04; P = 0.6). Strong correlations could be shown between arteriolar density, IFA (r = 0.75; P < 0.001), alpha SMA (r = -0.36; P = 0.034), and Coll III (r = -0.66; P < 0.0001). The MF appears to have a significant role in the progression of diabetic nephropathy. Ischemia secondary to arteriosclerosis may contribute to interstitial fibrosis through fibroblast modulation into MF.

Adult↗

PubMed1999

Idiopathic nodular glomerulosclerosis.

Idiopathic nodular glomerulosclerosis is an unusual entity with light microscopic and ultrastructural features similar to those of nodular diabetic glomerulosclerosis but without evidence of abnormal glucose metabolism. We report 2 patients whose renal biopsies showed nodular glomerulosclerosis with afferent and efferent arteriolosclerosis, glomerular basement membrane thickening, focal mesangiolysis and capillary microaneurysm formation, and who had no evidence of abnormal glucose metabolism or other features of diabetes mellitus. Review of the literature shows that, of the 27 reported cases of idiopathic nodular glomerulosclerosis (not including the 2 cases reported herein), 11 showed evidence of abnormal glucose metabolism or were frankly diabetic. Of the remaining 16 cases with normal serum blood glucose measurements, 3 had diabetic retinopathy and 1 had a delayed insulin response curve. The cause and pathogenesis of the glomerular nodules are discussed, and it is suggested that arteriolar stenosis and glomerular ischemia may be involved in the development these lesions.

Aged↗

PubMed1991

The pathogenesis of chronic renal failure in diabetic nephropathy. Investigation of 488 cases of diabetic glomerulosclerosis.

Investigation of renal biopsy specimens from 488 patients with diabetic glomerulosclerosis (DGS) of varying severity revealed the following: 1) The severity of DGS increases with the duration of the diabetes. 2) As the severity of DGS increases, it is complicated with increasing frequency by exudative changes, which correspond in detail to hyperperfusion lesions described in the literature. 3) As the severity of DGS increases, the severity of arteriolosclerosis and the incidence of nephrotic syndrome increase significantly. 4) The 5- and 10-year renal survival rates are highest for those diabetic patients in whom the tubules and renal cortical interstitium are of normal appearance. These survival rates are diminished if any of the following are present at the time of biopsy: a) interstitial fibrosis; b) hyperperfusion lesions; c) nephrotic syndrome; d) elevation of the serum creatinine concentration to more than 1.3 mg%. 5) No significant correlation was found between renal survival rate and age, sex, or type of diabetes. 6) The inflammation of the renal interstitium seen in diabetes does not differ from that seen in chronic glomerulonephritis. Monocytes, macrophages, T lymphocytes, fibroblasts and fibrocytes play the major role in this inflammation. This inflammatory process is considered to represent not pyelonephritis, but rather an auto-immune process. In other words, it is proposed that the diabetic kidney fails not only as a result of non-specific glomerular lesions (hyperperfusion lesions) but also because of non-specific tubulointerstitial changes, whereas diabetic glomerulosclerosis alone does not lead to chronic renal failure.

Adult↗

PubMed1998

Osteopontin expression, tubulointerstitial disease, and essential hypertension.

A role has recently been proposed for the tubulointerstitium in the pathogenesis of salt-dependent essential hypertension. In this study, biopsies from patients with essential hypertension with either minimal ("benign") or severe ("decompensated") tubulointertitial injury were analyzed for the expression of osteopontin, a protein known to modulate tubulointerstitial damage and nitric oxide production. In biopsies from patients with decompensated arteriolosclerosis, osteopontin mRNA and protein were increased in tubules in association with expression of alpha-smooth muscle actin by interstitial fibroblasts and increased type IV collagen deposition. The relevance of these findings to the pathogenesis of essential hypertension is discussed.

Actins↗

PubMed1998

Blood flow differences between leuko-araiosis with and without lacunar infarction.

BACKGROUND: The present study was designed to find the differences in regional cerebral blood flow and cerebrovascular acetazolamide reactivity between leuko-araiosis with and without lacunar infarction. METHODS: Fifteen cases of leuko-araiosis with lacunar infarction, 15 cases of leuko-araiosis without lacunar infarction and 15 age-matched controls in which leuko-araiosis and cerebrovascular diseases are absent (control group) were studied. The regional cerebral blood flow was measured using the stable xenon computed tomography method before and 20 minutes after intravenous injection of 17 mg/kg acetazolamide. RESULTS: The blood flows in the leuko-araiosis area and the lacunar area were significantly lower than the blood flow in the cerebral white matter. The blood flows in the cerebral cortex and the cerebral white matter were significantly lower in the leuko-araiosis with lacunar infarction group than in the leuko-araiosis without lacunar infarction group and the control group. The cerebrovascular acetazolamide reactivity in the leuko-araiosis area and the lacunar area was significantly lower than that in the cerebral white matter. The cerebrovascular acetazolamide reactivity in the cerebral cortex and the cerebral white matter was significantly lower in the leuko-araiosis with lacunar infarction group than in the leuko-araiosis without lacunar infarction group and the control group. CONCLUSIONS: The degree of arteriolosclerosis is considered to be more severe and the rate of association of hypertension was higher in leuko-araiosis with lacunar infarction than in leuko-araiosis without lacunar infarction.

Acetazolamide↗

PubMed2000

Hypertensive renovasculopathies and the rise of blood pressure with age in Japan and USA.

Arterial intimal fibroplasia in renal interlobular arteries but not arteriolar hyalinization was reported to be proportional to the rise of blood pressure with age in the data from all populations examined so far. New findings from Japan offer further insights into the disparities between the two types of renovasculopathy, both of which are called by the same name, 'arteriolosclerosis'. PAS stained paraffin sections were prepared from specimens obtained at autopsy in Tokyo and New Orleans, emphasizing basal subjects, i.e. those with no cause of death known to be related to hypertension. Severities of fibroplastic vasculopathy, in units of intimal thickness as % of outer diameter, and hyaline vasculopathy, in units of affected arterioles per cm2 of tissue sectional area, were measured morphometrically. Blood pressure data were taken from published population surveys. Fibroplastic renovasculopathy was found to provide a proxy for mean blood pressure (MBP) when comparing groups of men and women of various age groups in the USA and Japan. Hyaline renovasculopathy did not reproduce these patterns. Some of these findings confirm similar results from prior studies, and this reproducibility increases confidence that a true biological difference may exist between these populations.

Adult↗

PubMed2001

[Age-related macular degeneration (AMD)--therapeutic possibilities and new approaches].

Age related macular degeneration (ARMD) is one of the leading causes of irreversible vision loss in patients over 65 years of age. Nearly 30 percent of persons over 75 years of age will suffer from ARMD. The etiology is not yet fully understood. Besides age, many risk factors such as gender, arterial hypertension, arteriolosclerosis, elevated serum lipids, smoking, alcohol abusus, and exposure to UV light are being discussed. Genetic factors are certainly involved as well; familiar predisposition is assumed in more than 50 percent of cases. White individuals are more affected than colored ones. Predisposing ocular signs are macular drusen, focal hyperpigmentation, and light eyes. In this review, anatomical, pathophysiological and fluorescein-angiographic features and the clinical classification of exudative and dry stages of ARMD are described. Concepts of management of ARMD include pharmacological measures, laser treatment, photodynamic therapy, and surgery including excision of submacular choroidal neovascular membranes and macular translocation. Success rates of any therapeutic method are very limited. Low vision aids are promising by improving quality of life in many cases.

Aged↗