Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic pyelonephritis (c.p.) is by definition an infectious tubulo-interstitial nephritis. It has to be differentiated from other etiologic forms of tubulo-interstitial nephritis. Therefore strict morphological criteria are needed for diagnosis. The characteristic lesion is a large cortico-medullary scar overlying a dilated chronically inflammed calyx. The macroscopic aspect and the histologic survey picture are more important than histologic details. A diagnosis on renal biopsies is therefore not warranted. Vesico-renal reflux and papillary morphology play an important pathogenetic role. Beside the more common focal scar a diffuse form of scarring can be observed. A limited number of conditions only have to be considered in differential diagnosis. The Ask-Upmark kidney seems to be a special form of c.p. related to urinary tract infection and reflux in early infancy. Pelvi-calyceal lithiasis without superimposed infection causes a picture very similar to a pyelonephritic scar. A reliable differentiation between c.p. and analgesic nephropathy may cause problems in endstage kidneys with sloughed off papillae. Various mechanisms of renal damage such as bacterial infection, immunological mediated inflammation, leakage of urinary constituents into the interstitium especially Tamm-Horsfall-protein and ischemia have to be considered. Despite the frequency of urinary tract infections chronic progressive pyelonephritis is rare. Predisposing factors are needed for progression of the disease. These include congenital or acquired urinary tract obstruction, vesico-renal reflux and papillary damage with intrarenal obstruction to the urinary flow. Other important factors are focal and segmental glomerulosclerosis and hypertension.
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PMID:[Chronic pyelonephritis and its differential diagnosis. A disease changing with time]. 248 12

Nuclear magnetic resonance (NMR) has contributed considerably to our understanding of experimental acute renal failure. Changes in energy metabolism which are caused by ischemia, urinary obstruction, and nephrotoxic drugs have been characterized with NMR spectroscopy. Data from our laboratory and others utilizing 31P NMR have demonstrated that levels of adenosine triphosphate fall rapidly with ischemia, and that the ability of the kidney to regenerate ATP correlates with ultimate functional recovery. Additionally, development of intracellular acidosis appears to occur early with ischemia and may, if severe enough, predict poor functional recovery. Urinary obstruction is associated with the rapid development of a large peak resonating in the phosphodiester region of the P-31 NMR kidney spectrum which is attributable to increases in urinary inorganic phosphate. Nephrotoxic acute renal failure with a variety of nephrotoxins is associated with little to no changes in high energy phosphates. Renal transplant allograft rejection is associated with energy metabolic changes similar to those seen with ischemia; however, the intracellular pH remains normal. These findings allow causes of experimental acute renal failure to be differentiated among each other in both native and transplanted kidneys. With recent advances in NMR software and hardware, the application of this methodology to human acute renal failure is now possible.
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PMID:Contributions of nuclear magnetic resonance to study of acute renal failure. 269 84

At the transplantation center of Rigshospitalet , Copenhagen, retrograde pyelography is routinely performed via a ureteral catheter inserted during the operation. Ninety-nine retrograde pyelographies performed within the first days after renal transplantation were reviewed. The clinical records of 30 additional patients who had not been subjected to pyelography were also reviewed. Intrarenal backflow (IRB) was seen in 14 per cent of the pyelograms. Upper urinary tract obstruction (29 cases) was observed with equal frequency in the groups with and without IRB. No relationship was observed between IRB and length of warm and cold ischemia of the graft, urinary tract infection (UTI), donor kidney age and graft function on the day of retrograde pyelography. In 40 per cent of the grafts with irreversible rejection within 60 days after transplantation IRB was found at pyelography in the first days after operation. IRB occurred in only 5 per cent of the kidneys with good long term function. Most frequently IRB was localized to the upper pole but was also observed in other parts of the kidney. IRB may be an early radiographic sign of an impending and irreversible graft rejection. There was no evidence that retrograde pyelography increased the frequency of UTI or the number of episodes of irreversible rejection.
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PMID:Intrarenal backflow during retrograde pyelography following kidney transplantation. 637 67

This review evaluates the various causes and management of acute renal failure (ARF) in children. ARF is defined as an abrupt decline in the renal regulation of water, electrolytes and acid-base balance, and continues to be an important factor contributing to the morbidity and mortality of critically ill infants and children. The common causes of ARF in children include acute tubular necrosis secondary to various causes (including congestive heart failure and sepsis), haemolytic uremic syndrome, and glomerulonephritis and urinary tract obstruction. Ischaemia, toxins (including drugs) as well as primary parenchymal disease, have to be considered and ARF can also be a complication of systemic disease. The basic principles of management are avoidance of life-threatening complications, maintenance of fluid and electrolyte balance, and nutritional support. Only a few patients require specific management of the underlying disorder, although it is important to diagnose these conditions. Knowledge about the use of drugs for the prevention of ARF is scarce. Mannitol, low-dose dopamine, calcium channel antagonists, atrial natriuretic peptide and albumin have been evaluated and, where possible, meta-analyses are cited. Mannitol treatment appears to be warranted prophylactically after paediatric renal transplantation. Albumin infusion can reverse prerenal ARF in children with nephritic syndrome. For treatment of the complications of hyperkalaemia and volume overload, salbutamol, insulin and glucose infusion and diuretics such as furosemide and sodium bicarbonate, are discussed. All of the major dialysis modalities (peritoneal dialysis, haemodialysis and continuous haemofiltration) can be used to provide equivalent solute clearance and ultrafiltration. The indication for, and the choice of the modality depend on the patient requirements and on local resources, and should involve the care of a paediatric nephrologist. Peritoneal dialysis requires minimal equipment and infrastructure, is easy to perform and remains the favoured modality of renal replacement therapy in children. However, continuous haemofiltration is an excellent alternative to peritoneal dialysis in patients with ARF and severe fluid overload. Dialysis remains the most important tool to bridge the time needed for recovery of renal function. There is increasing evidence that more intense use of dialysis may improve the overall prognosis.
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PMID:Acute renal failure in children: aetiology and management. 1173 64

Obstructive nephropathy refers to the mechanical or functional changes in the urinary tract that interfere with normal urinary flow. Once obstruction is set, it leads to progressive renal damage that is mainly characterized with tubulointerstitial fibrosis. Here we reviewed the pathophysiology of urinary tract obstruction and indicated future therapeutic options. Following complete unilateral ureteral obstruction, there is a progressive fall in renal blood flow and glomerular filtration rate, and is a increase in intratubular pressure. These events activate the plasma and tissue renin-angiotensin systems (RAS). It has been proved that upregulated angiotensin II is one of the crucial factors those are responsible for the subsequent deleterious process. Angiotensin II induces transforming growth factor-beta, which causes overproduction of extracellular matrix (ECM) proteins like collagen, fibronectin, etc. The ECM proteins are dominantly accumulated in tubulointerstitium and result in deterioration of renal function. Along with the activation of the RAS, tissue ischemia and mononuclear leukocyte infiltration also modulate the fibrotic changes. The process from the RAS activation to renal fibrosis is observed not only in obstructive nephropathy but also in other renal diseases and is called the Final Common Pathway. Mechanical release of the obstruction is to perform in terms of the treatment, however, several promising pharmaceutical options are now under investigation.
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PMID:[Pathophysiology and clinical implication of obstructive nephropathy]. 1467 94

Inflammation plays a major role in the pathophysiology of acute renal failure resulting from ischemia. In this review, we discuss the contribution of endothelial and epithelial cells and leukocytes to this inflammatory response. The roles of cytokines/chemokines in the injury and recovery phase are reviewed. The ability of the mouse kidney to be protected by prior exposure to ischemia or urinary tract obstruction is discussed as a potential model to emulate as we search for pharmacologic agents that will serve to protect the kidney against injury. Understanding the inflammatory response prevalent in ischemic kidney injury will facilitate identification of molecular targets for therapeutic intervention.
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PMID:Ischemic acute renal failure: an inflammatory disease? 1525 93

Acute renal allograft dysfunction in the first weeks after transplantation primarily requires examination for acute rejection, drug-associated injury, pre-renal failure due to exsiccosis/dehydration, and post-renal problems such as urinary tract obstruction. In rare instances, main renal artery or vein thrombosis may be found, e.g. due to acute rejection of the vessels. Herein, we describe the clinical course of a patient with a recent renal transplantation who presented with an acute enigmatic renal allograft failure which, after intensive diagnostic efforts, emerged as paradoxical embolism with extensive allograft ischemia in consequence of a venous thrombosis and a patent foramen ovale - a so far unreported case.
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PMID:Organ transplants do not escape paradoxical embolisms. 2221 7

Acute kidney injury is a common complication in hospitalized patients and is associated with substantially increased morbidity and mortality. Frequently, it is caused by impaired renal perfusion, ischemia and reperfusion injury, sepsis or urinary tract obstruction, but often its etiology is multifactorial. In this context, the contribution of nephrotoxic medications to the development of AKI plays an important role. This review begins with an attempt to evaluate the importance of drug-related acute kidney injury in general. Then, a selected list of 7 classes of drugs or compounds, namely aminoglycosides, aristolochic acid, cytostatic drugs, nonsteroidal anti-inflammatory drugs, osmotic agents, radiocontrast, and phosphate salts are discussed in depth, including their epidemiology, pathophysiology, clinical features and treatment. While not attempting to be exhaustive, this review attempts to provide an overview with additional in-depth information on certain classes of drugs that are either of general importance or have recently emerged in the literature.
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PMID:Drugs and AKI. 2240 17

Acute life-threatening conditions in oncology patients may develop either because of underlying malignancy or as a complication from treatment. Oncologic emergencies can be categorized as metabolic, hematologic, and structural conditions. Metabolic and hematologic emergencies are mainly diagnosed on the basis of clinical and laboratory findings. Structural pathologic conditions that result in bleeding, mechanical compression, or obstruction to the hollow organs, such as the trachea and bowel loops, may first be suspected because of clinical findings, including decreasing hematocrit levels, difficulty in breathing, and abdominal pain; however, performance of imaging studies is critical for timely diagnosis and management. Life-threatening conditions of the central nervous system (such as cerebral herniation, carcinomatous meningitis, and spinal cord compression), thoracic emergent conditions (such as central airway obstruction, esophagorespiratory fistula, massive hemoptysis, pulmonary embolism, superior vena cava syndrome, and pericardial tamponade), and abdominopelvic emergencies (such as uncontrolled intraabdominal hemorrhage, bowel obstruction, intestinal perforation, bowel ischemia, intussusception, and urinary tract obstruction) can be definitively diagnosed on the basis of projectional or cross-sectional imaging findings in appropriate clinical scenarios. Select emergent conditions in cancer patients related to chemotherapy and radiation treatment, as well as iatrogenic emergencies secondary to either surgery or placement of central venous catheters, may also demonstrate characteristic findings at imaging studies. In addition, interventional procedures are of great help in the treatment of acute superior vena cava syndrome, massive hemoptysis, and uncontrolled intraabdominal hemorrhage. Radiologists should be aware of these select, "not to be missed" imaging findings of oncologic emergencies to make an accurate, timely diagnosis and provide appropriate patient care.
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PMID:Imaging of oncologic emergencies: what every radiologist should know. 2410 50

Maldevelopment of the collecting system resulting in urinary tract obstruction (UTO) is the leading identifiable cause of CKD in children. Specific etiologies are unknown; most cases are suspected by discovering hydronephrosis on prenatal ultrasonography. Congenital UTO can reduce nephron number and cause bladder dysfunction, which contribute to ongoing injury. Severe UTO can impair kidney growth in utero, and animal models of unilateral ureteral obstruction show that ischemia and oxidative stress cause proximal tubular cell death, with later development of interstitial fibrosis. Congenital obstructive nephropathy, therefore, results from combined developmental and obstructive kidney injury. Because of inadequacy of available biomarkers, criteria for surgical correction of upper tract obstruction are poorly established. Lower tract obstruction requires fetal or immediate postnatal intervention, and the rate of progression of CKD is highly variable. New biomarkers based on proteomics and determination of glomerular number by magnetic resonance imaging should improve future care. Angiotensin inhibitors have not been effective in slowing progression, although avoidance of nephrotoxins and timely treatment of hypertension are important. Because congenital UTO begins in fetal life, smooth transfer of care from perinatologist to pediatric and adult urology and nephrology teams should optimize quality of life and ultimate outcomes for these patients.
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PMID:Congenital urinary tract obstruction: the long view. 2608 76


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