enalapril and Kidney-Neoplasms
enalapril has been researched along with Kidney-Neoplasms* in 3 studies
Other Studies
3 other study(ies) available for enalapril and Kidney-Neoplasms
Article | Year |
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Inhibition of tyrosine kinases by sunitinib associated with focal segmental glomerulosclerosis lesion in addition to thrombotic microangiopathy.
Sunitinib is an orally administered inhibitor of tyrosine kinases and has become the standard of care for many patients with metastatic renal cell carcinoma. Its use has been associated with renal toxicity in some patients. We report a patient with a metastatic clear-cell renal carcinoma who showed arterial hypertension, nephrotic syndrome and azotaemia 10 months after treatment with sunitinib. The renal biopsy revealed focal segmental glomerulosclerosis (FSGS) in addition to thrombotic microangiopathy (TMA), and the complete syndrome disappeared 6 months after sunitinib withdrawal. To our knowledge, this is the first case of FSGS associated to TMA secondary to sunitinib treatment. We discuss the possible glomerular pathomechanism. Topics: Aged; Antineoplastic Agents; Biopsy; Carcinoma, Renal Cell; Enalapril; Glomerulosclerosis, Focal Segmental; Humans; Indoles; Kidney; Kidney Neoplasms; Lung Neoplasms; Male; Protein-Tyrosine Kinases; Pyrroles; Sunitinib; Thrombotic Microangiopathies | 2010 |
Pathogenesis of acute renal failure: new aspects.
Based on 2 case presentations - acute renal failure (ARF) due to myeloma kidney and due to angiotensin-converting enzyme inhibitor administration in the presence of transplant artery stenosis - new aspects in the pathogenesis of ARF are presented and discussed. The multifactorial pathogenesis of ARF includes (a) a disturbance of glomerular microcirculation (afferent and perhaps mesangial constriction, inadequate efferent dilatation); (b) a disturbance of medullary microcirculation (medullary capillary congestion) attributed to a combination of endothelial damage and tubular dilatation; (c) tubular cell damage which, though rarely in humans justifying the term 'acute tubular necrosis', promotes both backleak of glomerular filtrate and shedding of brush border vesicles; (d) the latter promotes tubular obstruction by casts which consist of Tamm-Horsfall protein and brush border components. Once ARF is established, repair processes set in which appear to depend on growth factors such as epidermal growth factor and insulin-like growth factor 1, of which there is a relative shortage in established ARF. Experimental therapeutic approaches focus on the restitution of microcirculation (endothelin receptor antagonists, atriopeptins), interference with cast formation (integrin receptor blockers), and the promotion of recovery by growth factors. Topics: Acute Kidney Injury; Aged; Angioplasty, Balloon; Angiotensin-Converting Enzyme Inhibitors; Antineoplastic Agents; Arteriosclerosis; Enalapril; Female; Glomerular Filtration Rate; Humans; Kidney; Kidney Glomerulus; Kidney Neoplasms; Kidney Transplantation; Male; Multiple Myeloma; Postoperative Complications; Renal Circulation | 1997 |
Angiotensin-converting enzyme inhibitor and anemia in a patient undergoing hemodialysis.
Topics: Aldosterone; Anemia; Blood Pressure; Enalapril; Erythropoietin; Hematocrit; Humans; Hypertension; Kidney Failure, Chronic; Kidney Neoplasms; Male; Middle Aged; Polycystic Kidney Diseases; Renal Dialysis; Renin-Angiotensin System | 1991 |