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At least 1,315 records · Page 73Linked to original sources
PubMed1967

Acute necrotic myelitis and perivenous encephalomyelitis associated with hypertension and renal infection.

The case reported showed acute necrotic myelopathy and acute perivenous encephalomyelitis against a background of renal infection, malignant hypertension, and a history of injury. Death from renal disease and pneumonia halted the neurological pathology in the acute stage, thus allowing a more detailed histological examination than is possible in the later stages. The pathogenesis of acute necrotic myelopathy, together with the effects of oedema and vascular compression in the cord, are discussed briefly.

Acute Disease↗
PubMed1972

The role of fibrin deposition in diabetic glomerulosclerosis: a light, electron and immunofluorescence microscopy study.

The possible role of fibrin deposition in the development of diabetic glomerulosclerosis has been investigated by light, immunofluorescence, and electron microscopy examination of renal tissue obtained by percutaneous biopsy from seven diabetic patients having minimal clinical evidence of renal involvement and at necropsy on nine diabetic patients. Although the biopsy specimens showed only early to moderate diffuse glomerulosclerosis without either nodular or exudative lesions, approximately 70% of glomeruli examined showed specific fluorescence for fibrinogen in a discontinuous linear pattern along the capillary basement membrane and diffusely in the mesangium. Moreover the immunofluorescence findings correlated well with the distribution patterns of material thought to be fibrin both in the light microscopy studies, by virtue of its staining properties, and by electron microscopy, because of periodicity, texture, and electron density. It is suggested that electron-dense granular deposits seen on electron microscopy may represent intermediate compounds in the fibrinogen to fibrin conversion, and that endothelial and mesangial trapping of fibrinogen or other macromolecules may initiate or accelerate mesangial enlargement, nodule formation, and irregularity of the basement membrane.

Adult↗
PubMed1975

Necropsy study on glomerulonephritis in the elderly.

The necropsy reports and clinical observations of 44 cases of glomerulonephritis occurring in patients over 55 years old were reviewed. Two-thirds of the patients died from a rapidly progressive renal disease with focal necrotizing and fibrosing glomerular lesions; half of these exhibited a granulomatous splenic trabeculitis; an associated vasculitis was found in only a minority of these cases. Another important group consisted of cases of acute diffuse glomerulonephritis which, as a rule, occurred in association with a major infection. There were only four cases of chronic sclerosing glomerulonephritis.

Acute Disease↗
PubMed1988

Vitronectin (serum spreading factor): its localisation in normal and fibrotic tissue.

The distribution of vitronectin and fibronectin in normal and fibrotic tissue was directly compared using indirect immunofluorescence. Both glycoproteins were ubiquitiously localised to loose connective tissue. Vitronectin, unlike fibronectin, was not detected in basement membranes, in normal renal glomeruli, or around smooth muscle cells of both musculares mucosae and propria of the gastrointestinal tract. The presence of vitronectin could not be shown in washed permeabilised platelets. Vitronectin was very much increased in reactive and fibrotic tissue, as was fibronectin. This was observed in lymph nodes affected by both nodular sclerosing Hodgkin's disease and by metastatic carcinoma as well as in myelofibrotic bone marrow and sclerotic glomeruli. These findings suggest that vitronectin may have an important role in the processes of inflammation and repair.

Blood Proteins↗
PubMed2006

Salt loading produces severe renal hemodynamic dysfunction independent of arterial pressure in spontaneously hypertensive rats.

We have previously shown that salt excess has adverse cardiac effects in spontaneously hypertensive rats (SHR), independent of its increased arterial pressure; however, the renal effects have not been reported. In the present study we evaluated the role of three levels of salt loading in SHR on renal function, systemic and renal hemodynamics, and glomerular dynamics. At 8 wk of age, rats were given a 4% (n = 11), 6% (n = 9), or 8% (n = 11) salt-load diet for the ensuing 8 wk; control rats (n = 11) received standard chow (0.6% NaCl). Rats had weekly 24-h proteinuria and albuminuria quantified. At the end of salt loading, all rats had systemic and renal hemodynamics measured; glomerular dynamics were specially studied by renal micropuncture in the control, 4% and 6% salt-loaded rats. Proteinuria and albuminuria progressively increased by the second week of salt loading in the 6% and 8% salt-loaded rats. Mean arterial pressure increased minimally, and glomerular filtration rate decreased in all salt-loaded rats. The 6% and 8% salt-loaded rats demonstrated decreased renal plasma flow and increased renal vascular resistance and serum creatinine concentration. Furthermore, 4% and 6% salt-loaded rats had diminished single-nephron plasma flow and increased afferent and efferent arteriolar resistances; glomerular hydrostatic pressure also increased in the 6% salt-loaded rats. In conclusion, dietary salt loading as low as 4% dramatically deteriorated renal function, renal hemodynamics, and glomerular dynamics in SHR independent of a minimal further increase in arterial pressure. These findings support the concept of a strong independent causal relationship between salt excess and cardiovascular and renal injury.

Albuminuria↗
PubMed2002

Combination therapy with benazepril and oral adsorbent ameliorates progressive renal fibrosis in uremic rats.

BACKGROUND/AIMS: The administration of an angiotensin-converting enzyme (ACE) inhibitor or an oral adsorbent, AST-120 (Kremezin), prevents the progression of renal failure. This study was designed to determine the additional effects of AST-120 combined with an ACE inhibitor, benazepril, on the progression of renal fibrosis in uremic rats. METHODS: 5/6-nephrectomized uremic rats were divided into control uremic rats (CRF group), benazepril-treated uremic rats (CRF+B group) and uremic rats receiving benazepril and AST-120 (CRF+BK group). After 14 weeks of treatment renal function and pathological changes were investigated. RESULTS: The progression of renal dysfunction was delayed in both the CRF+B and CRF+BK groups as compared with the CRF group. In the CRF+BK group, the level of serum and urinary indoxyl sulfate and the tubular accumulation of indoxyl sulfate decreased. Both the CRF+B and CRF+BK groups showed lower glomerular sclerosis indices than the CRF group. In the CRF+BK group, but not the CRF+B group, the interstitial fibrosis area and the expression of transforming growth factor (TGF) beta1 and tissue inhibitor of metalloproteinases (TIMP) 1 were decreased as compared with the CRF group. Furthermore, the CRF+BK group showed a smaller interstitial fibrosis area and a lower renal osteopontin expression than the CRF+B group. CONCLUSION: Combination therapy of benazepril and AST-120 is more effective than benazepril alone in retarding the progression of interstitial fibrosis by reducing the expression of TGF-beta 1, TIMP-1 and osteopontin.

Adsorption↗
PubMed2002

Multifactorial determination of hypertensive nephroangiosclerosis.

Essential hypertension causes renal injury. Hypertensive nephroangiosclerosis (HN) or hypertensive nephropathy are terms most commonly used to describe this renal pathology. Although specific histological lesions occurring in affected kidneys are well known, pathogenesis of hypertension-related renal scarring is not completely understood. Evidence exists to support the theory that other factors such as aging, black race or smoking, beside blood pressure, contribute to the development and progression of HN. Metabolic disturbances, cocaine and nonsteroidal anti-inflammatory drug abuse, ochratoxin A exposure, dietary salt intake, heavy metal toxicity, hantavirus infection and perinatal programming are also considered risk factors. Renal susceptibility genes may determine whether hypertension-induced progressive renal damage occurs and how severe it is. Determination of all risk factors may identify patients at high risk of renal failure and help tailor an appropriate management. In the present paper, the knowledge available on this clinically important objective is discussed.

Humans↗
PubMed2005

Inhibitory effect of pravastatin on transforming growth factor beta1-inducible gene h3 expression in a rat model of chronic cyclosporine nephropathy.

BACKGROUND/AIMS: Overexpression of transforming growth factor beta1-inducible gene h3 (betaig-h3) is associated with renal scarring in several models of renal disease. We investigated the inhibitory effect of pravastatin on betaig-h3 expression in a rat model of chronic cyclosporin A (CsA)-induced nephropathy. METHODS: Adult Sprague Dawley rats kept on a low salt diet (0.05% sodium) were treated daily for 4 weeks with vehicle (olive oil, 1 ml/kg), CsA (15 mg/kg) or both CsA and pravastatin (20 mg/kg in drinking water). The effect of pravastatin on betaig-h3 expression was evaluated using in situ hybridization, immunohistochemistry, and immunoblotting. Functional parameters, histopathology (tubulointerstitial fibrosis, TIF, and arteriolopathy), and levels of transforming growth factor beta1 (TGF-beta1) and endothelial nitric oxide synthase were compared for the different treatment groups. RESULTS: Co-administration of pravastatin significantly inhibited betaig-h3 mRNA production and gene expression within the tubulointerstitium of the CsA-treated kidneys, and this paralleled an attenuation of TIF (12.7 +/- 2.2 vs. 35.9 +/- 5.4%, p < 0.01 vs. CsA) and the expression of TGF-beta1 mRNA (279 +/- 40 vs. 719 +/- 85%, p < 0.01 vs. CsA). Pravastatin treatment reduced endothelial nitric oxide synthase protein levels and reversed the renal dysfunction caused by CsA. Neither CsA nor pravastatin affected total serum cholesterol or triglyceride levels in the treatment groups. CONCLUSION: Pravastatin thus effectively abrogated the upregulation of betaig-h3 gene expression and associated TGF-beta1 production, and this was associated with attenuated TIF in this model of chronic CsA-induced nephropathy.

Animals↗
PubMed1996

Inappropriately high plasma renin activity accompanies chronic loss of renal function.

Stimulation of both the systemic and local renin-angiotensin systems participates in the pathogenesis of tissue injury observed in experimental renal disease. However, substantial information demonstrating excessive activation of the renin-angiotensin system in patients with chronic renal disease is not available in spite of the well-established role of this system in the progression of renal damage. This investigation examined the plasma renin activity (PRA) and the ratio of this parameter to the simultaneously measured glomerular filtration rate (PRA/GFR) in normal volunteers (mean values 3.2 ng/ml/h and 3.0 ng/ml/h/100 ml GFR, respectively) and in patients with chronic renal disease (1.6 ng/ml/h and 28.5 ng/ml/h/100 ml GFR, respectively). A mean tenfold increase in the PRA/GFR ratio was observed in patients with chronic renal disease as compared to normal volunteers. The observed augmentation in PRA was not caused by physiologic mechanisms aimed at conserving urinary sodium since a positive correlation was found between PRA/GFR and the fractional excretion of sodium (y = 2.75 + 2.23x; r = 0.781, p < 0.01), as opposed to that of normal controls (y = 5.3 - 1.46x; r = -0.640, p < 0.01). Consequently, our results support the existence of inappropriate activation of the renin-angiotensin system in humans with chronic renal disease. Such stimulation might play a critical role in the pathophysiology of advanced renal injury.

Adult↗
PubMedDate not supplied

Managing acute myocardial infarction in a renal transplant recipient.

We describe the management of a patient, with a 13-year-old cadaveric renal transplant, who presented with acute myocardial infarction. Successful primary angioplasty was performed to the left anterior descending artery. It was complicated by transient renal failure and pseudoaneurysm of the femoral artery which was managed conservatively.

Acute Kidney Injury↗