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PubMed1999

A case of aortitis syndrome and IgA nephropathy: possible role of human leukocyte antigens in both diseases.

A 51-year-old woman, who had both aortitis syndrome (Takayasu arteritis) and IgA nephropathy, presented with hypertension, fever, a high erythrocyte sedimentation rate, high C-reactive protein and serum IgG levels, proteinuria, and renal dysfunction. Renal arteriography showed stenosis and poststenotic dilatation at the origin of the right renal artery, as well as tortuosity of the left renal artery branches and marked atrophy of the left kidney. Renal biopsy showed IgA nephropathy with deposits of IgA, C3, and fibrinogen in the glomeruli and arteriolosclerosis. The present patient had human leukocyte antigen (HLA)-B 52, which is reported to be related to the aortitis syndrome, as well as HLA-DR 4, which is possibly related to IgA nephropathy, suggesting that HLA status may be involved in the pathogenesis of both diseases.

Adult↗

PubMed1975

[Studies of nephropathies in 168 diabetic patients with over 20-year onset of the disease].

Within a clinical epidemiological investigation 168 diabetics were examined multidisciplinarily who survived the beginning of their disease by at least 20 years. The qualitative proof of protein in the urine was regarded as criterion for the presence of a diabetic nephropathy. 29% of the long-term diabetics showed a proteinuria. In a control group of probands with healthy metabolism, however, only 2.5% proteinurias were found. Statistically ascertained correlations were the results in cases of proteinuria and retinopathy (microangio-pathy). Particularly close were the relations of proteinuria to arteriolosclerosis (macroangiopathy). There were no relations between the proof of a proteinuria and the quality of the control of the carbohydrate metabolism which was pursued during decades.

Adult↗

PubMed2002

Hypertension: a microvascular and tubulointerstitial disease.

The vast majority of patients with essential hypertension have structural changes in their kidneys consisting of preglomerular vascular disease ('arteriolosclerosis') and tubulointerstitial injury. Most authorities have assumed that these structural changes occur secondary to hypertensive renal injury. However, Goldblatt proposed that primary renal microvascular disease might be the cause of some forms of hypertension. In this paper we present recent studies from our group that support a role for both preglomerular vascular disease as well as the tubulointerstitial inflammatory response in mediating salt-sensitivity. We propose that subtle acquired renal injury may underlie the etiology of some forms of salt-sensitive hypertension.

Animals↗

PubMed2002

[Risk factors for subcortical arteriosclerotic encephalopathy].

Subcortical arteriosclerotic encephalopathy (SAE) is a chronic progressive form of brain blood supply deficiency. Risk factors for SAE development were studied in 65 patients (42 men and 23 women, mean age 60.5 +/- 7.5 years). A control group included 31 patients (17 men and 14 women, mean age 59.3 +/- 7.4 years) with isolated clinically meaningful lacunar infarcts. A main risk factor for SAE was arterial hypertension (AH) emerging in 98.5% of the patients, which, according to twenty-four hour monitoring, differed significantly from that in the patients with isolated lacunar infarcts. In SAE, diastolic pressure was higher, systolic AP variability was detected more frequent, physiological AP decreased rarely in the nighttime, but AP fell down extremely more often. A frequency of other risk factors (ischemic disease, atrial fibrillation, diabetes mellitus, smoking, elevation of hematocrit, fibrinogen and platelet aggregation) did not differ significantly comparing to isolated lacunar infarcts. Hypercholesterolemia was detected more frequently in the controls than in the SAE patients. The study revealed that AP with hemodynamic features, pathogenetically crucial for development of disseminated arteriolosclerosis in small brain arteries and arterioles as well as for diffuse white matter damage in brain hemispheres characteristic for SAE, is a main risk factor for SAE.

Dementia, Vascular↗

PubMed1992

IgA associated glomerulonephritis.

Immunohistological analysis of 1146 renal biopsies revealed IgA associated glomerulonephritis (IgAGN) in 83 (7.24%) patients (33 children, 50 adults). Clinical features were unusually severe in a high proportion. Nephrotic syndrome (NS) responding poorly to prednisolone was found in 24%, hypertension (HT) in 39%, and azotemia in 34% of patients. NS was slightly more frequent in children than in adults, but HT and azotemia occurred twice as often in adults as in children. Histologically, extensive glomerular crescents and sclerosis were prominent. In addition, moderate arteriolitis and arteriolosclerosis and marked tubulointerstitial nephropathy were notable features. Thus, a low incidence and marked severity characterized IgAGN in this study.

Adult↗

PubMed2004

[The incidence of renal diseases as diagnosed by biopsy in Hungary].

AIM AND METHODS: The authors analysed the incidence of renal diseases as diagnosed by biopsy in the population living on the southern Great Hungarian Plain. 798 biopsy specimens were examined between 1990 and 2002. RESULTS: The most common diseases in decreasing order of frequency were IgA nephropathy (15%), membranous nephropathy (12%), thin-basement-membrane nephropathy (8%), minimal change nephropathy (7%), lupus glomerulonephritis (7%), focal sclerosis (6%), hypertensive kidney disease and arteriolosclerosis (5%), diabetic nephropathy (5%), and crescentic glomerulonephritis (4%). The most frequent diseases in decreasing order of frequency in children were minimal change nephropathy, thin-basement-membrane nephropathy, Henoch-Schönlein nephropathy and IgA nephropathy; in adults were IgA nephropathy, membranous nephropathy, lupus glomerulonephritis and thin-basement-membrane nephropathy; and in the elderly were membranous nephropathy, amyloidosis, crescentic glomerulonephritis and diabetic nephropathy. The incidence of the diseases differed significantly between the genders in IgA nephropathy, thin-basement-membrane nephropathy, lupus glomerulonephritis, chronic sclerosing nephropathy and Alport nephropathy. At the time of the biopsy, 69 patients were suffering from diabetes mellitus. 37 patients were diagnosed as having diabetic nephropathy, and 32 as having non-diabetic nephropathy. In 6 cases, the diabetic nephropathy was accompanied by other glomerular disorders. In more than half of the diabetic patients with non-diabetic nephropathy, membranous nephropathy or focal sclerosis was diagnosed. Crescentic glomerulonephritis was diagnosed on 30 occasions, which was due to vasculitis in 20 cases, proliferative glomerulonephritis in 7 cases and anti-glomerular-basement-membrane nephritis in 3 cases. In the middle-aged and the elderly, the renal disease was relatively often a consequence of systemic disease. CONCLUSION: The incidence and the gender distribution of renal diseases diagnosed by biopsy were similar to those reported by other European kidney biopsy centres. IgA nephropathy was the most frequent disease in the biopsy registry of the authors. The high incidence of thin-basement-membrane nephropathy seems to be related to consequent biopsy examinations of glomerular haematuria. In diabetics and the elderly, the diagnosis of the renal disease may be challenging.

Adolescent↗

PubMed2004

[Membranous nephropathy].

Membranous nephropathy (MN) is a frequent cause of nephrotic syndrome in adults. A considerable diversity of prognosis is seen with idiopathic MN. We overview the recent progress of clinicopathological research, especially the initial factors affecting the longterm outcome of idiopathic MN. We studied retrospectively 105 patients with idiopathic MN and could assign the patients to two different groups based on the electron microscopic (EM) findings. In the homogeneous type only one patient developed end-stage renal failure, and earlier remission occurred in this group. With regard to secondary outcome, increased age, focal segmental glomerular sclerosis, arteriolosclerosis, heterogeneous type of EM findings were independent risk factors. Our results suggest that a new EM classification at initial biopsy is an independent indicator of prognosis in human idiopathic MN.

Adult↗

PubMedDate not supplied

The discovery of diabetic nephropathy: from small print to centre stage.

Until the early nineteenth century, diabetes mellitus was regarded as a disease of the kidney, in which there was an increase in the volume of urine and a wasting of the flesh. With the identification of glucose in blood and urine in the late eighteenth century, first it was re-framed as a disease of assimilation and only then became a metabolic disorder. Whilst these changing concepts were debated, it was noted in parallel that diabetics might show coagulable urine containing albumin, even before Bright and others had established this as a sign of kidney disease. Wilhelm Griesinger (1817-1868) was perhaps the first to suggest in 1859 that the diabetes might be causing the Bright's disease, with the latter as a 'complication'. During the next half-century the observation that as albuminuria appeared and increased, so glycosuria improved or might remit, with a parallel or subsequent evolution into uraemia. Glomerulosclerosis and arteriolosclerosis were described in occasional patients during the same period, but text-books of pathology ignored these observations. Thus it was only when diabetics began to survive longer using insulin treatment in the early 1920s that a diabetic nephropathy became widely recognized. After a few isolated descriptions which were ignored, the now famous paper of Paul Kimmelstiel and Clifford Wilson appeared in 1935 detailing nodular renal lesions in just 8 maturity-onset (48-68 year old) diabetics. They barely noted the association with diabetes however, and it was Arthur Allen in 1941 who clarified the association in 105 patients with diabetes, again all aged over 40. Despite the age of the patients in these early studies, diabetic nephropathy became thought of as a disease of young diabetics as a cohort of survivors of juvenile diabetes passed 15 years or more of disease and more than half developed nephropathy. In the 1950s the technique of renal biopsy was rapidly applied to the study of diabetics, and the early lesions defined using electron microscopy as well as optical methods. Then the role of diabetic nephropathy as a cause of renal failure changed: to begin with numbers of young insulin-requiring diabetics were small and infrequently referred for dialysis treatment or transplantation. Then in the 1970s and 1980s the proportion of such juvenile-onset diabetics developing renal failure gradually fell, but at the same time much larger numbers of older diabetics survived their vascular disease and required treatment for renal failure. World-wide, today diabetes accounts for 20-50% of patients entering established renal failure programs, and absolute numbers increase as greater longevity and western-style living has promoted an 'epidemic' of diabetes at all ages.

Albuminuria↗

PubMed2006

[Clinical and morphological characteristics of lupus nephritis in systemic lupus erythematosus with antiphospholipid syndrome].

AIM: To ascertain clinical and morphological features of lupus nephritis (LN) in systemic lupus erythematosus (SLE) associated with antiphospholipid syndrome (APS). MATERIAL AND METHODS: Immunological markers of SLE and APS, clinical picture, urine indices were examined in 138 patients with SLE, APS and renal dysfunction. RESULTS: LN associated with APS is characterized with marked arterial hypertension, such patients had arterial thromboses more frequently than patients with isolated LN. Patients with anticardiolipin antibodies have arteriolosclerosis, in APS - diffuse interstitial sclerosis. CONCLUSION: Renal impairment in SLE may run not only with LN but also with thrombotic microangiopathy modifying clinical symptoms and course of the disease.

Adolescent↗

PubMed1992

Lymphatic diseases.

The microcirculation is the keystone of bodily homeostasis. Although it may be altered organically as in arteriolosclerosis and diabetic angiopathy, its unique architecture makes it prone to spasticity. This article discusses vasospasticity and diagnostic approaches and treatment for Raynaud's vasospasticity, acrocyanosis, and livedo reticularis.

Humans↗

PubMedDate not supplied

[Focal segmental glomerulosclerosis].

Focal and segmental glomerulosclerosis accounted for 4.1% of all primary glomerulopathies. Typical signs of focal and segmental glomerulosclerosis were striking arteriolosclerosis on histological examination, the urinary syndrome of high proteinuria with mild haematuria and frequent nephrotic syndrome. The ten-year cumulative percentage of remissions was 30%. Patients with remission had at the time of biopsy a normal serum creatinine level and no or minimal regressive tubulointerstitial changes. The ten-year cumulative percentage of renal failure was 40%. Presence of nephrotic syndrome, extracapillary proliferation and advanced tubulointerstitial changes, tended to shorten a kidney survival. In one third of the patients the serum creatinine level rose by more than 50 mol/1/year.

Adult↗

PubMed1991

The spectrum of lacunar infarction in the elderly.

Lacunar infarcts are small subcortical ischemic brain lesions caused by occlusion of a perforating arteriole. The occlusion results from thickening of the arteriolar wall (arteriolosclerosis), is related to aging, and is accelerated by arterial hypertension. The infarction is usually associated with one of several clinical lacunar syndromes, depending on the exact location of the lesion. Patient evaluation should include the documentation of infarct size and location with imaging studies and the search for uncommon hematologic derangements that predispose to thrombosis. Recovery from a single lacunar infarction is usually very good. Most important in prevention of lacunar infarction recurrence is control of hypertension. Aspirin therapy also appears to be beneficial.

Aged↗

PubMed1991

[Color-coded duplex sonography of dysfunctional kidney transplants. Correlation of the resistive index with the histopathologic results of biopsy].

The resistive index (RI) is used as a measure of the vascular resistance in renal allografts. The sample volume for the measurement can be positioned much more exactly with color duplex US than with duplex US, resulting in more precise values for the RI. To find out which pathologic changes lead to an increase of the RI, we correlated the RI with the histopathological results obtained in 43 biopsies. Our results show that it is not possible to differentiate between vascular and interstitial rejection on the basis of the RI because there is no statistically significant difference between the RI values caused by the two types of rejection. Distinct interstitial infiltration, edema of any origin, vascular changes and also chronic rejection and arteriolosclerosis lead to elevated RI. A good correlation was found between the elevation of RI and the severity of the vascular changes. Severe tubular and glomerular changes, cyclosporine toxicity, tubular necrosis, cytomegaly infection, glomerulonephritis and dysfunctions of other causes did not lead to elevation of the RI.

Adult↗

PubMed1991

[Clinico-pathological study of focal glomerular sclerotic lesions in idiopathic membranous nephropathy].

Sixty-one patients with idiopathic membranous nephropathy (MN) were studied clinicopathologically to determine the significance of focal glomerular sclerotic lesions (FGSL). Renal biopsy specimens were examined by light and immunofluorescence microscopy. The light microscopic specimens were cut into 20 serial sections and odd-numbered ones were stained with Masson trichrome staining. The histopathological findings were scored and statistically analyzed. The patients were divided into two groups: Group I consisted of 15 MN patients with FGSL; the other 46 MN patients without FGSL composed Group II. Group I showed higher systolic blood pressure (p less than 0.01), longer duration of proteinuria (0.05), and higher levels of serum creatinine (p less than 0.001) than Group II. In Group I, the stage of membranous lesions was more advanced (p less than 0.01), and tubular atrophy, interstitial fibrosis and arteriolosclerosis were more severe than in Group II (p less than 0.05). The above results suggest that FGSL in MN may be related to the impairment of the renal function, but an only explanation for the cause of FGSL by the glomerular hyperfiltration theory is unlikely. Further investigations are required to clarify the full pathogenesis of FGSL.

Adult↗

PubMedDate not supplied

The effects of hypertension on the nervous system.

With 60 million Americans meeting criteria for either essential or secondary hypertension, elevated arterial pressures remain a major health problem. While efforts to find etiologies for essential hypertension continue, clinicians battle its effects on organ systems, including the nervous system. Hypertensive changes in the nervous system may be acute, chronic, or both. The intracerebral vasculature is commonly affected. Not infrequently, acute changes including hemorrhage, encephalopathy, and cerebral edema are superimposed on chronic changes of hyaline and fibrinoid arteriolosclerosis. Chronic vascular changes sacrifice vascular lumina. The resulting ischemia is responsible for cystic (lacunar) lesions and subcortical ischemic white matter lesions consistent with Binswanger's disease.

Acute Disease↗

PubMed1990

An autopsy case of cardiomyopathy with restrictive physiology in a child.

An autopsy case of cardiomyopathy with restrictive physiology associated with subendocardial myocardial necrosis and fibrosis in a seven-year-old child is described. Cardiac catheterization showed high left ventricular end-diastolic pressure with a dip-and-plateau pattern. Macroscopically, marked dilatation with fibroelastosis in both atria and mild dilatation in both ventricles were observed. Histologic examination revealed extensive subendocardial necrosis with marked disorganization of myocardial cells and moderate arteriolosclerosis. We speculate that these extensive myocardial lesions, which contributed to the restrictive hemodynamic changes, could have been induced by anoxia or a Ca2+ transport abnormality of unknown cause.

Cardiomyopathy, Restrictive↗

PubMed1990

[Type I and III membranoproliferative glomerulonephritis. Clinical picture and prognosis].

Membranoproliferative glomerulonephritis (CN) of types I and III was diagnosed in 154 patients (15.5% out of primary CN). Out of this number 60% were men. During biopsy, one third of the patients were normotensive, 40% were slightly hypertensive and one third suffered from severe hypertension. Mean proteinuria was 6.5 +/- 5.5 g/24 h. In two thirds of the patients erythrocyturia was higher than 35 mil. in Addis' sediment and the findings in the urine were characterised by the proportion between proteinuria and erythrocyturia (p less than 0.001). During biopsy in one half of the patients, the serum creatinine level was already elevated. The presence of creatininemia was found to be directly linked to blood pressure, proteinuria, the degrees of extracapillary proliferation, tubulointerstitial regression and vascular arteriolosclerosis. The cumulative duration of the kidney function within the period of 10-20 years was 41 or 28%, the cumulative cure amounted to 14% 10 years after biopsy.

Adolescent↗

PubMed1986

[Early morphologic changes in the myocardium after a wound of the heart complicated by hemopericardium (experimental study)].

The myocardia of 20 dogs with penetrating injuries of the right ventricles were studied morphologically and histochemically. Microcirculatory disorders found in the myocardium included overfilled venous and capillary bed that eventually led to capillary stasis, interstitial edema, hemorrhagic foci, arteriolosclerosis. For the first time focal disseminated injuries of cardiomyocytes of a segmental, zonal, and contractural type were detected. In line with these lesions, earlier cardiomyocytic changes were found, such as margination of nuclear chromatin, clarification of karyoplasm, interfibrillar edema of sarcoplasm with subsequent loosening and aggregation of myofibrils. This complex of morphologic changes was invariably found in the myocardia of both ventricles in the dogs dead 10-90 minutes after cardiac injury.

Animals↗