Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The experiments referred to in this article point to the fact that relatively low concentrations of Hg2+ (5-10 mM) produce damage to the internal mitochondrial membrane. This damage results in the formation of ionic channels that allow the spontaneous effusion of Ca+2 from the matrix. Together with this, the formation of channels produce the balance of the chemo-osmotic gradient, resulting in the overcoming of the transmembrane potential and the uncoupling of oxidative phosphorylation. The experiments carried out in vivo, point to the fact mercury produces acute tubular necrosis of kidney tissue. These toxic effects produced by Hg2+ in vitro with the addition of 15 microM of the inhibition of the angiotensin converting enzyme, captopril. In vivo experiments show that intraperitoneal infection of captopril (40 mg/kg) completely protects from mitochondrial dysfunction produced by mercurial intoxication.
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PMID:[Captopril protection from the nephrotoxic effects of mercury]. 765 76

The purpose of this study was to determine whether angiotensin converting enzyme inhibition could ameliorate renal ischemic injury. Both a chronic rat model and a rat isolated perfused kidney (IPK) model were used. Adult rats were subjected to 60 min of left hilar crossclamping and right nephrectomy. Captopril (1 mg/kg) was given intravenously 5-10 min prior to clamping (CAP-pre, n = 5), at reperfusion (CAP-post, n = 5), or 30 min after reperfusion (CAP-30 min post, n = 5). Other groups of rats received enalapril (0.8 mg/kg iv) in the same manner (ENAL-pre, n = 5; ENAL-post, n = 5; ENAL-30 min post, n = 4). Serum creatinine in the treated groups was compared to ischemic control (NS, n = 7) for 7 days. In the IPK experiments, kidneys were similarly treated with CAP or ENAL. Vascular resistance (VR) and oxygen consumption (O2 CON) were determined from pressure, flow, and oxygen tension data for 60 min after initial equilibration. In the chronic model, Day 2 serum creatinine was significantly lower in all treated groups vs ischemic control. By Day 7, serum creatinine remained significantly lower in all ENAL-treated groups and in the CAP-30 min post group, although other CAP-treated groups had appreciably, although not significantly, lower creatinines, too. Histologic examination of CAP-pre kidney revealed intact morphology compared to ischemic control where acute tubular necrosis was observed. In the IPK experiments, CAP- and ENAL-treated kidneys had VR values that were significantly lower than those of ischemic controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril amelioration of renal reperfusion injury. 804 Nov 45

Acute renal failure (ARF) associated with idiopathic nephrotic syndrome has been reported in adults with advanced age but is a rare event in children. We have reviewed the literature on this subject and report an additional pediatric case. The pathogenetic mechanisms which may lead to ARF during the course of idiopathic nephrotic syndrome are reviewed with a brief discussion of the role of angiotensin II and angiotensin converting enzyme inhibition in this setting. Although no consensus has emerged for the prevention and treatment of ARF in patients with nephrotic syndrome, a combination of salt-poor albumin and diuretics to reduce interstitial edema may be beneficial as a preventive measure. Once acute tubular necrosis is diagnosed, dialysis may be indicated. In the majority of reports the prognosis for recovery of renal function has been good even in patients in whom long-term dialysis was required.
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PMID:Acute renal failure in idiopathic nephrotic syndrome. 904 53

Comprehensive evaluation of renal transplants has been important in differential diagnosis of medical and surgical complications in the early post-transplantation period and in the long-term follow-up. If performed well, it yields excellent functional and good anatomic information about the graft that can be effectively used in the patient. That includes selection of patients for biopsy and for various drug regimens. This is true especially in patients with anuric acute tubular necrosis (ATN) and in patients with developing chronic rejection. Improving indices of renal function (effective renal plasma flow, uptake of tubular tracers) can indicate resolution of tubular injury (ATN) while there is still no improvement in plasma creatinine. In patients with chronic rejection, plasma creatinine increases only after approximately 30% of renal function is lost due to graft fibrosis. Early recognition of this condition could permit treatment and delay of retransplantation. The protocol recommended at the Copenhagen meeting includes a flow study, scintigram of the kidneys, prevoid and postvoid bladder image, injection site image (quality control), time/activity curves of the graft and bladder, and quantitative data of perfusion, function, and tracer transit. The flow study obtained during the initial transit of the bolus through the graft could be performed either with 99mTc mercaptoacetyltriglycine, or 99mTc diethylenetriaminepentaacetate (DTPA). Quantitative analysis of perfusion facilitates interpretation of the study during the early post-transplantation period. ATN, common in cadaver transplants, typically shows adequate perfusion. The function phase should include images and time/activity curves. Images alone are insufficient. Quantitative data such as clearance or other indices of function and indices of tracer transit are essential for correct interpretation of the results. Normal images and normal graft function reliably exclude clinically important complications. A single scintigram demonstrating prolonged tracer transit with decreased function cannot separate acute rejection and ATN. On serial studies, decline in function and poor perfusion are indicative of acute rejection. A normally appearing scintigram without cortical retention, but with low function, is consistent with chronic rejection. Pharmacological intervention to exclude obstruction (diuretic renogram) or hemodynamically significant renal artery stenosis (angiotensin converting enzyme challenge) should be used whenever indicated.
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PMID:Report of the Radionuclides in Nephrourology Committee for evaluation of transplanted kidney (review of techniques). 1032 28

Human immunodeficiency virus-associated nephropathy (HIVAN) is a clinicopathological entity characterised by proteinuria, rapidly developing azotemia and histologically by collapsig variant of focal and segmental glomerulosclerosis with acute tubular necrosis and mild interstitial inflammation. Untreated, it may result in end stage renal disease (ESRD) in as little as four months. The incidence of HIVAN continues to increase and is the single most common cause of chronic renal disease in HIV-1 seropositive patients. It affects predominantly black individuals. Exact pathogenesis is still not clear but a great deal of progress has been made in the recent past by studies on transgenic mouse model, renal cell cultures and from study of human biopsy material. Current considerations revolve around the role of HIV or protein in renal epithelium and the effects of cytokines, including transforming growth factor-beta and basic fibroblast growth factor on renal structures. Different modalities of treatment with corticosteroids, zidovudine or angiotensin converting enzyme inhibitors have been tried with modest success.
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PMID:Human immunodeficiency virus-associated nephropathy. 1183 70

Chronic heart failure (CHF) is often associated with impaired renal function due to hypoperfusion. Such patients are very sensitive to changes in renal perfusion pressure, and may develop acute tubular necrosis if the pressure falls too far. The situation is complicated by the use of diuretics, ACE inhibitors and spironolactone, all of which may affect renal function and potassium balance. Chronic renal failure (CRF) may also be associated with fluid overload. Anaemia and hypertension in CRF contribute to the development of left ventricular hypertrophy (LVH), which carries a poor prognosis, so correction of these factors is important.
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PMID:Influence of progressive renal dysfunction in chronic heart failure. 1195 39

Nephrotic syndrome (NS) is frequent in renal transplant recipients and may be related to a large variety of glomerular lesions. In some of these cases, the transplant biopsy showed no significant glomerular changes and the NS was reversible, but the primary renal disease was not minimal change disease (MCD), suggesting that MCD may develop de novo in renal transplant setting. Knowledge of this entity, however, is limited. Among 67 cases of post-transplant NS encountered in a 12-yr period, five were found to be associated with de novo MCD. A critical review of the literature revealed nine additional cases of de novo MCD. The data from these 14 cases show that patients with de novo MCD had a large variety of primary renal diseases but MCD or focal segmental glomerulosclerosis was not among them. Eight of the 14 transplanted kidneys (60%) were from living related donors, suggesting this as a risk factor. Nephrotic range proteinuria (3-76 g/d) developed immediately or shortly after transplantation (within 4 months for all reported cases, except for one at 24 months). The serum creatinine when NS was first diagnosed was normal or mildly elevated, but acute renal failure occurred in three patients. On biopsy, the glomeruli were normal or, more frequently, displayed mild, focal segmental mesangial sclerosis, hypercellularity, deposition of IgM/C3, or accumulation of mononuclear inflammatory cells in some glomerular capillaries. The tubulointerstitial compartment was normal in cases with normal renal function; displayed mild acute and/or chronic rejection that correlated with a mildly elevated serum creatinine; or showed acute changes including acute rejection, acute tubular necrosis, or acute cyclosporin A toxicity, which accounted for both acute renal failure at presentation and its subsequent reversibility. Under various treatments, including increased steroids, angiotensin converting enzyme inhibitors, calcium channel blockers and angiotensin receptor blockers, sustained remission of NS was achieved in 13 cases, within a year (0.5-12 months) in 10 and later (24, 34 and 98 months, respectively) in three. In the remaining case, the patient died of septic shock 2 months after transplantation. After remission of the NS, the grafts functioned well without or with minimal proteinuria for several years. De novo MCD has characteristic clinical and pathologic features. It represents an important but hitherto underemphasized cause of post-transplant NS, which is potentially reversible and does not adversely affect the renal transplants.
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PMID:De novo minimal change disease associated with reversible post-transplant nephrotic syndrome. A report of five cases and review of literature. 1222 32

Despite major advances in nutritional support, membrane technology and dialytic techniques, the mortality of patients with acute renal failure (ARF) who require dialysis is still almost 50% (1). Increased patient age and co-morbidity confer a poorer prognosis, and the condition is certainly commoner in this patient group. Hence, one study showed that the age-related annual incidence of ARF increased from 17 per million in adults under 50 years to 949 per million in the 80-89 age group (2). Over 60% of cases of ARF ultimately result from renal hypoperfusion and consequent intra-renal ischaemic damage, which leads to acute tubular necrosis (ATN) (3). Ischaemic ARF may thus result from a diversity of systemic and intra-renal circulatory stresses including acute losses of blood and extra-cellular fluids, from low cardiac output states such as following ischaemic or toxic myocardial damage, and even from drug-induced renal perfusion shutdown (ACE inhibitors, non-steroidal anti-inflammatory agents). Many cases of ARF have a multi-factorial aetiology (e.g. post-surgical sepsis with hypovolaemia, hypotension and injudicious antibiotic use), and these patients, who often have other organ failure, fit into the poorer prognostic category. A large number of patients with ischaemic ARF pass through a phase of potentially reversible pre-renal oliguria; early recognition and prompt, appropriate treatment of these pre-renal factors can prevent progression to established ARF, with the genuine prospect of improved patient morbidity and mortality, and this is the main scope of this article. Early diagnosis in other patients with ARF, such as those with acute inflammatory renal disease (e.g. vasculitis) or urinary tract obstruction, will allow appropriate prompt treatment and the possibility for reversal of the ARF. The following account, which is composed of personal experience, that of colleagues, and the literature (1,4), is not intended to provide a comprehensive guide to the management of ARF, but seeks to highlight important common pitfalls and fundamental principles in the recognition and subsequent preventive treatment of these patients.
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PMID:Early management and prevention of acute renal failure. 1237 20

We report a case of a 46-year-old white male with renal graft artery stenosis who developed acute renal shutdown with total anuria while on the ACE inhibitor lisinopril, one week following the discontinuation of aspirin. The serum creatinine was 8.5 mg/dl. Doppler ultrasound and MAG3 scintigraphy of the grafted kidney were highly suggestive of a viable but nonfunctioning kidney. A femoro-femoral bypass for total thrombosis of the right common iliac artery was performed distal to the occlusion. Immediate diuresis was obtained after establishing the bypass. Serum creatinine dropped to 1.35 mg/dl three days later. In this case we believe that the collateral circulation played a significant role in immediate recovery of kidney function by maintaining renal perfusion pressure and preventing acute tubular necrosis (ATN). We also believe that the ACE inhibitor might have contributed to salvaging the kidney by improving medullary oxygen balance and maintaining adequate medullary blood flow.
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PMID:A transplanted kidney surviving total vessel occlusion and anuria. 1611 94

Positron emission tomography (PET) is perfectly suited for quantitative imaging of the kidneys, and the recent improvements in detector technology, computer hardware, and image processing software add to its appeal. Multiple positron emitting radioisotopes can be used for renal imaging. Some, including carbon-11, nitrogen-13, and oxygen-15, can be used at institutions with an on-site cyclotron. Other radioisotopes that may be even more useful in a clinical setting are those that either can be obtained from radionuclide generators (rubidium-82, copper-62) or have a sufficiently long half-life for transportation (fluorine-18). The clinical use of functional renal PET studies (blood flow, glomerular filtration rate) has been slow, in part because of the success of concurrent technologies, including single-photon emission computed tomography (SPECT) and planar gamma camera imaging. Renal blood flow studies can be performed with O-15-labeled water, N-13-labeled ammonia, rubidium-82, and copper-labeled PTSM. With these tracers, renal blood flow can be quantified using a modified microsphere kinetic model. Glomerular filtration can be imaged and quantified with gallium-68 EDTA or cobalt-55 EDTA. Measurements of renal blood flow with PET have potential applications in renovascular disease, in transplant rejection or acute tubular necrosis, in drug-induced nephropathies, ureteral obstruction, before and after revascularization, and before and after the placement of ureteral stents. The most important clinical application for imaging glomerular function with PET would be renovascular hypertension. Molecular imaging of the kidneys with PET is rather limited. At present, research is focused on the investigation of metabolism (acetate), membrane transporters (organic cation and anion transporters, pepT1 and pepT2, GLUT, SGLT), enzymes (ACE), and receptors (AT1R). Because many nephrological and urological disorders are initiated at the molecular and organelle levels and may remain localized at their origin for an extended period of time, new disease-specific molecular probes for PET studies of the kidneys need to be developed. Future applications of molecular renal imaging are likely to involve studies of tissue hypoxia and apoptosis in renovascular renal disease, renal cancer, and obstructive nephropathy, monitoring the molecular signatures of atherosclerotic plaques, measuring endothelial dysfunction and response to balloon revascularization and restenosis, molecular assessment of the nephrotoxic effects of cyclosporine, anticancer drugs, and radiation therapy. New radioligands will enhance the staging and follow-up of renal and prostate cancer. Methods will be developed for investigation of the kinetics of drug-delivery systems and delivery and deposition of prodrugs, reporter gene technology, delivery of gene therapy (nuclear and mitochondrial), assessment of the delivery of cellular, viral, and nonviral vectors (liposomes, polycations, fusion proteins, electroporation, hematopoietic stems cells). Of particular importance will be investigations of stem cell kinetics, including local presence, bloodborne migration, activation, seeding, and its role in renal remodeling (psychological, pathological, and therapy induced). Methods also could be established for investigating the role of receptors and oncoproteins in cellular proliferation, apoptosis, tubular atrophy, and interstitial fibrosis; monitoring ras gene targeting in kidney diseases, assessing cell therapy devices (bioartificial filters, renal tubule assist devices, and bioarticial kidneys), and targeting of signal transduction moleculas with growth factors and cytokines. These potential new approaches are, at best, in an experimental stage, and more research will be needed for their implementation.
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PMID:Future direction of renal positron emission tomography. 1635 95


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