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Results for “Kidney Cortex Necrosis”

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At least 271 records · Page 15Linked to original sources
PubMed2005

Endocytic delivery of lipocalin-siderophore-iron complex rescues the kidney from ischemia-reperfusion injury.

Neutrophil gelatinase-associated lipocalin (Ngal), also known as siderocalin, forms a complex with iron-binding siderophores (Ngal:siderophore:Fe). This complex converts renal progenitors into epithelial tubules. In this study, we tested the hypothesis that Ngal:siderophore:Fe protects adult kidney epithelial cells or accelerates their recovery from damage. Using a mouse model of severe renal failure, ischemia-reperfusion injury, we show that a single dose of Ngal (10 microg), introduced during the initial phase of the disease, dramatically protects the kidney and mitigates azotemia. Ngal activity depends on delivery of the protein and its siderophore to the proximal tubule. Iron must also be delivered, since blockade of the siderophore with gallium inhibits the rescue from ischemia. The Ngal:siderophore:Fe complex upregulates heme oxygenase-1, a protective enzyme, preserves proximal tubule N-cadherin, and inhibits cell death. Because mouse urine contains an Ngal-dependent siderophore-like activity, endogenous Ngal might also play a protective role. Indeed, Ngal is highly accumulated in the human kidney cortical tubules and in the blood and urine after nephrotoxic and ischemic injury. We reveal what we believe to be a novel pathway of iron traffic that is activated in human and mouse renal diseases, and it provides a unique method for their treatment.

Acute-Phase Proteins↗
PubMed1976

Hypertension in end-stage renal disease. The relationship between blood pressure, plasma renin, plasma renin substrate and exchangeable sodium in chronic hemodialysis patients.

Blood pressure (BP), plasma renin concentration (PRC), plasma renin substrate concentration (PRSC) and exchangeable sodium (ES) have been studied in 27 patients undergoing regular hemodialysis because of end-stage renal disease. PRC was significantly higher in the hypertensive than in the normotensive patients. The pattern of PRSC was similar in the groups of patients but with a marked individual variation. ES was slightly lower in the hypertensives than in the normotensives but the difference was not statistically significant. Multiple regression analysis demonstrated a significant correlation between mean BP, the natural logarithm of PRC and ES, but the effect of ES was negligible. PRC was negatively correlated to ES in all patients, including the hypertensives. These results strongly suggest that the renin-angiotensin system is the most important factor involved in the pathogenesis of hypertension in end-stage renal disease, when sodium balance is adequately controlled. A clinical application of the predictive value of PRC concerning the effect of bilateral nephrectomy on hypertension is outlined.

Adolescent↗
PubMed1975

Immunologic enhancement of rat renal allografts. III. Immunopathologic lesions and rejection in long-surviving passively enhanced grafts.

Immunologic enhancement of renal allografts from (Lewis times Brown Norway) F1 to Lewis rats was achieved by administering a single dose of antidonor serum at the time of transplantation. A series of grafts functioning for 1 to 4 months after transplantation were examined by light and immunofluorescence microscopy to evaluate the long-term protective effects of the enhancing serum and to determine if previously unobserved lesions appeared in long survivors. Despite the absence of detectable circulating cytotoxic alloantibody, long-term allografts showed necrotizing glomerular and arterial lesions which resembled those seen in acutely rejecting grafts and were compatible with humoral rejection. Thus, in this model, there is a late decline in the ability of passive enhancement to inhibit humoral rejection. Long-term grafts also developed tubular lesions with deposition of immunoglobulin and complement on the tubular basement membranes (TBM). Anti-TBM antibodies were demonstrated in recipients' sera and found to be organ specific but not major histocompatibility antigen or species specific. This tubular lesion is therefore a unique form of allograft injury in which the immune response is directed against tissue antigen(s) which are distinct from the major histocompatibility antigens that induce rejection.

Animals↗
PubMed1975

Electron microscopic and cytochemical study of the vacuoles of regenerating renal tubular cells.

The structure and acid phosphatase activity of vacuoles observed in regenerating proximal renal tubules were examined ultrastructurally. The sequestration and degradation of organelles were followed in the vacuoles, which obtain the acid phosphatase presumably from the lysosomes, and the limiting membrane of which originates from the endoplasmic reticulum. The vacuoles are regarded as autophagic vacuoles. Their appearance is correlated with the commencing differentiation of the dedifferentiated regenerating cells, which have similar regenerative phenomena.

Acid Phosphatase↗
PubMed2006

Microscopic polyangiitis associated with primary biliary cirrhosis: a causal or casual association?

The association between microscopic polyangiitis (MPA) and primary biliary cirrhosis (PBC) has seldom been reported. We describe a patient with PBC and MPA who presented with polyarthritis and pulmonary nodules followed by pauci-immune crescentic glomerulonephritis and liver dysfunction. Detection of p-ANCA, antimyeloperoxidase, and antimitochondrial antibodies along with liver and renal histopathology allowed a diagnosis of MPA and PBC. We also discuss 2 other cases that could be unrecognized associations of both diseases. Further reports are necessary to clarify if the coexistence between PBC and MPA is causal or casual.

Autoimmune Diseases↗
PubMed1978

[Treatment of acute kidney failure].

By the rapid development of the chronic haemodialysis and the transplantation of kidneys the treatment of the acute renal failure is not so often dealt with in literature, though the haemodialysis since its clinical use in 1944 for 15 years exclusively has been used for the treatment of acute renal failure. Alarming reports on the increase of the mortality up to 80% were the cause to deal with treatment and developmental tendencies in form of a survey. The conclusions were that during the last 6 years in the GDR annually about 300 cases of acute renal failure are constantly treated. The total mortality rate is without any essential variations on an average about 44.9%. In comparison to international statistics these figures are remarkably good. According to the basic etiological cause of the acute renal failure the mortality rate varies between 60% in surgical diseases and about 30% in intoxications with uraemia. Apart from these analyses the author enters indication, causes and prognosis in form of a summary.

Acute Kidney Injury↗