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

Mercury chloride (HgCl2) has a potent nephrotoxic effect. Most of Hg2+ existing in plasma following HgCl2 exposure forms a complex with sulfhydryl-containing ligands such as albumin and glutathione (GSH). The Hg(2+)-GSH complex is filtered in the glomeruli of the kidney and degraded into Hg(2+)-cysteine in the proximal tubules by the combined action of gamma-glutamyl transpeptidase and dipeptidase present in the epithelial cells. The degradation product is then incorporated and accumulated into the proximal tubule epithelial cells. The accumulated Hg2+ in the epithelial cells finally causes acute tubular necrosis (ATN) by its cytotoxic effect. At present, it is believed that tubular obstruction resulting from ATN triggers the onset of HgCl2-induced acute renal failure (ARF). A progressive fall in glomerular filtration rate (GFR) contributes to the progression of HgCl2-induced ARF. The fall in GFR may be caused by an increment in afferent arteriole resistance (RA) and a decrement in the ultrafiltration coefficient (Kf) due to mesangial cell contraction. These changes in RA and Kf may be attributed to the increased action of the vasoconstrictors, angiotensin II and endothelin-1 and to the decreased action of the vasodilator, nitric oxide observed at the glomerulus level of HgCl2-induced ARF. Accordingly, the imbalance between these vasoactive substances appears to play an important role in the progression of HgCl2-induced ARF due to reducing GFR. Further studies, however, remain to elucidate the mechanisms involved.
 ...
PMID:[HgCl2-induced acute renal failure and its pathophysiology]. 952 59

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.
 ...
PMID:Acute renal failure in children: aetiology and management. 1173 64

There are no multifactorial studies of complications after renal transplant in the Hispanic population. The objective of this study was to identify which factors are associated with the development of complications after renal transplantation. This retrospective study was performed on all patients transplanted in the Puerto Rico Transplant Program during 2002. Independent variables included preoperative albumin, white blood cell (WBC) count, hemoglobin, creatinine, weight, height, body mass index (BMI), type of dialysis, time on dialysis, and urine production after transplant. Dependent parameters included posttransplant diuresis, wound infection, wound dehiscence, lymphoceles, acute tubular necrosis, length of stay, postoperative weight, graft survival, and patient survival. Data were analyzed with parametric and nonparametric techniques using STAT 200 software. Sixty-four patients were included in the study: 37 male, 27 female. No significant differences in complication rate or length of stay were found with age, preoperative albumin, WBC count, hemoglobin, creatinine, weight, height, dialysis modality, and donor type. Significant factors included type of dialysis, time on dialysis, and BMI. Preoperative albumin if > 3 was not a prognostic indicator for the development of surgical complications following renal transplantation. Only preoperative weight, BMI, and dialysis duration were significant factors in the development of postoperative complications and prolonged hospital stay in this sample Hispanic transplant population. These data are important in formulating selection, education, and transplant management policy.
 ...
PMID:Study of factors that affect complications after renal transplantation. 1664 7

Renal failure in patients with liver disease is mostly none-organic: prerenal failure or hepatorenal syndrome (HRS). In addition there is organic renal failure, mostly acute tubular necrosis (ATN). In order to avoid functional renal failure cautious diuretic treatment as well as intravenous albumin substitution following paracentesis are pivotal. For prophylaxis of HRS patients with spontaneous bacterial peritonitis shall be given albumin infusions in addition to antibiotic treatment. Patients with HRS type I exhibit a very poor prognosis. Liver transplantation is the only established therapy with long-term success. To bridge the time to transplantation TIPS or terlipressin and albumin can be used.
 ...
PMID:[Renal impairment in liver diseases]. 1704 10

In patients with cirrhosis, acute renal failure is due to prerenal failure (a result of decreased renal perfusion) and tubular necrosis. There are 3 main causes of prerenal failure: 'true hypovolemia' (which complicates hemorrhage, gastrointestinal or renal fluid losses), sepsis, and type 1 hepatorenal syndrome (HRS). Prerenal failure may also be due to the administration of non-steroidal antiinflammatory drugs, or intravascular radiocontrast agents. Prerenal failure is reversible after restoration of renal blood flow. Treatments target the cause of hypoperfusion, and fluid replacement is used to treat 'non-HRS' prerenal failure. In patients with type 1 HRS with very low short-term survival rate, liver transplantation is the ideal treatment. Systemic vasoconstrictor therapy with terlipressin (combined with intravenous human albumin), noradrenaline (combined with albumin and furosemide) or midodrine (combined with octreotide and albumin) may improve renal function in patients with type 1 HRS waiting for liver transplantation. MARS (for Molecular Adsorbent Recirculating System) and the transjugular intrahepatic portosystemic shunt may also improve renal function in these patients. In patients with cirrhosis, acute tubular necrosis is mainly due to an ischemic insult to the renal tubules. Studies are needed on the natural course and treatment (e.g., renal-replacement therapy) of acute tubular necrosis in patients with cirrhosis.
 ...
PMID:Diagnosis and treatment of acute renal failure in patients with cirrhosis. 1722

The aim of this experimental study was to investigate the pathological effects of gentamicin in birds. Broiler chicks at 1 day of age were intramuscularly administered gentamicin at dose levels varying from 0 to 180 mg/kg. Clinical signs comprising of depression, decreased feed consumption, increased water intake, loose watery droppings and reduced body weights appeared in a dose-related manner in chicks administered 30 mg/kg or higher dose levels. Mortality was 0% and 20% in chicks given 40 mg and 50 mg/kg gentamicin. It increased in a dose-related manner and was 100% in 100mg/kg or higher dose groups. The LD50 calculated at total deaths in 5 weeks duration was 77.56 mg/kg. Kidneys and livers of chicks given 50mg/kg or higher doses of gentamicin were congested, enlarged and had hemorrhages on the surfaces. Microscopically kidneys exhibited acute tubular necrosis. Livers showed fatty change, vacuolar degeneration, necrotic areas and cellular infiltration around portal triads. Serum total proteins and albumin decreased while creatinine and ALT increased in chicks given 20mg/kg and higher doses. The no observable effect level (NOEL) of a single intramuscular administration of gentamicin in day-old broiler chicks was 10mg/kg body weight.
 ...
PMID:Pathological effects of gentamicin administered intramuscularly to day-old broiler chicks. 1904 12

Acute kidney injury (AKI) is an important cause of death among hospitalized patients. The 2 most common causes of AKI are acute tubular necrosis (ATN) and prerenal azotemia (PRA). Appropriate diagnosis of the disease is important but often difficult. We analyzed urine proteins by 2-dimensional gel electrophoresis from 38 patients with AKI. Patients were randomly assigned to a training set, an internal test set, or an external validation set. Spot abundances were analyzed by artificial neural networks to identify biomarkers that differentiate between ATN and PRA. When the trained neural network algorithm was tested against the training data, it identified the diagnosis for 16 of 18 patients in the training set and all 10 patients in the internal test set. The accuracy was validated in the novel external set of patients where conditions of 9 of 10 patients were correctly diagnosed including 5 of 5 with ATN and 4 of 5 with PRA. Plasma retinol-binding protein was identified in 1 spot and a fragment of albumin and plasma retinol-binding protein in the other. These proteins are candidate markers for diagnostic assays of AKI.
 ...
PMID:Identification of diagnostic urinary biomarkers for acute kidney injury. 2022 35

Acute deterioration in kidney function often occurs in patients with acute and chronic liver disease admitted to hospital. The true incidence of acute kidney injury (AKI) is unknown due to the difficulty in accurately measuring kidney function in patients with liver failure, and the lack of a consensus definition of AKI. There is a current consensus definition of hepatorenal syndrome (HRS), but in current clinical practice, volume-unresponsive AKI or acute tubular necrosis are much more common causes of AKI in patients with liver disease. Due to arterial vasodilatation and compensatory neuroendocrine activation, these patients are more prone to AKI due to a combination of changes in renal autoregulation and a sudden reduction in effective plasma volume or hypotension. The key management strategy is to prevent the development of HRS, by avoiding nephrotoxins, and preventing infective complications, and maintaining an effective circulating volume. In patients with HRS, treatment centres around daily plasma volume expansion, typically with albumin, in combination with vasopressors, typically vasopressin analogues, such as terlipressin, or noradrenaline. If renal function does not recover, then renal support with dialysis may be appropriate.
 ...
PMID:Management of acute kidney injury in liver disease. 2042 70

Acute kidney injury (AKI), defined as an abrupt increase in the serum creatinine level by at least 0.3 mg/dL, occurs in about 20% of patients hospitalized for decompensating liver cirrhosis. Patients with cirrhosis are susceptible to developing AKI because of the progressive vasodilatory state, reduced effective blood volume and stimulation of vasoconstrictor hormones. The most common causes of AKI in cirrhosis are pre-renal azotemia, hepatorenal syndrome and acute tubular necrosis. Differential diagnosis is based on analysis of circumstances of AKI development, natriuresis, urine osmolality, response to withdrawal of diuretics and volume repletion, and rarely on renal biopsy. Chronic glomerulonephritis and obstructive uropathy are rare causes of azotemia in cirrhotic patients. AKI is one of the last events in the natural history of chronic liver disease, therefore, such patients should have an expedited referral for liver transplantation. Hepatorenal syndrome (HRS) is initiated by progressive portal hypertension, and may be prematurely triggered by bacterial infections, nonbacterial systemic inflammatory reactions, excessive diuresis, gastrointestinal hemorrhage, diarrhea or nephrotoxic agents. Each type of renal disease has a specific treatment approach ranging from repletion of the vascular system to renal replacement therapy. The treatment of choice in type 1 hepatorenal syndrome is a combination of vasoconstrictor with albumin infusion, which is effective in about 50% of patients. The second-line treatment of HRS involves a transjugular intrahepatic portosystemic shunt, renal vasoprotection or systems of artificial liver support.
 ...
PMID:Kidneys in chronic liver diseases. 2279 39

A case of locally advanced non-small-cell lung carcinoma (NSCLC) was inadequately controlled with cisplatin, bevacizumab and pemetrexed chemotherapy. Following identification of a mutation of the echinoderm microtubule-associated protein like 4-anaplastic lymphoma kinase (EML4-ALK) gene, crizotinib was then administered as targeted treatment. Kidney function was normal at diagnosis and during the first line therapy. The administration of crizotinib coincided on two occasions with a conspicuous rise in the serum creatinine level. Urinary protein over creatinine ratio was 0.31 g/g with 22% albumin and macroscopic hematuria. A kidney biopsy was performed at the time of the second episode of renal impairment which showed acute tubular necrosis (ATN) indicating recent renal injury together with a mononuclear cell infiltrate consistent with ongoing repair related to a previous insult. The renal lesions were closely related temporally to crizotinib administration, supporting a causative role for crizotinib in the acute renal injury and this phenomenon has not previously been described.
 ...
PMID:Acute kidney injury following crizotinib administration for non-small-cell lung carcinoma. 2400 42


<< Previous 1 2 3 4 Next >>