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)

Magnesium is an essential cation, involved in many enzymatic reactions, as a cofactor to adenosine triphosphatases. It is critical in energy-requiring metabolic processes, as well as protein synthesis and anaerobic phosphorylation. Serum Mg concentration is maintained within a narrow range by the kidney and small intestine since under conditions of Mg deprivation both organs increase their fractional absorption of Mg. If Mg depletion continues, the bone store contributes by exchanging part of its content with extracellular fluid (ECF). The serum Mg can be normal in the presence of intracellular Mg depletion, and the occurrence of a low level usually indicates significant Mg deficiency. Hypomagnesemia is frequently encountered in hospitalized patients and is seen most often in patients admitted to intensive care units. The detection of Mg deficiency can be increased by measuring Mg concentration in the urine or using the parenteral Mg load test. Hypomagnesemia may arise from various disorders of the gastrointestinal tract, conditions affecting Mg renal handling, or cellular redistribution of Mg. The gastrointestinal causes include the following: protein-calorie malnutrition, the intravenous administration of Mg-free fluids and total parenteral nutrition, chronic watery diarrhea and steatorrhea, short bowel syndrome, bowel fistula, continuous nasogastric suctioning, and, rarely, primary familial Mg malabsorption. The renal causes include Bartter's and Gitelman's syndrome, post obstructive diuresis, post acute tubular necrosis, renal transplantation, and interstitial nephropathy. Many therapeutic agents cause renal Mg wasting and subsequent deficiency. These include loop and thiazide diuretics, aminoglycosides, cisplatin, pentamidine, and foscarnet. Magnesium deficiency is seen frequently in alcoholics and diabetic patients, in whom a combination of factors contributes to its pathogenesis. Hypomagnesemia is known to produce a wide variety of clinical presentations, including neuromuscular irritability, cardiac arrhythmias, and increased sensitivity to digoxin. Refractory hypokalemia and hypocalcemia can be caused by concomitant hypomagnesemia and can be corrected with Mg therapy. The dose and route of administration of Mg in the treatment of hypomagnesemia is dictated by the clinical presentation, the degree of Mg deficiency, and the renal function.
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PMID:Magnesium deficiency: pathophysiologic and clinical overview. 777 97

Acute renal failure is a very rare complication seen during the course of non- fulminant hepatitis A. Several mechanisms have been postulated in the pathogenesis of renal failure. Firstly, there is insufficiency of renal blood flow due to developing endotoxemia or cryoglobulinemia, secondly mesangial proliferative glomerulonephritis or interstitial nephritis occurs due to immune complexes and finally there is acute tubular necrosis caused by the direct cytopathic effect of the virus or due to immune complexes. The following case report describes a 17 year old male patient admitted with complaints of appetite loss and severe weight loss due to anorexia nervosa. During the second week of admission, he developed hepatitis A infection which was complicated by acute renal failure requiring hemodialysis therapy. Hepatorenal parameters returned to normal values by the fifth week of admission in this case of biopsy proven acute tubular necrosis. In this case, the possible negative effects of malnutrition on the liver and kidneys were not observed. The present authors emphasize that during the course of non- fulminant hepatitis A, renal functions should be closely monitored and renal biopsy should be performed if acute renal failure occurs.
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PMID:Acute oligo-anuric renal failure during the course of non-fulminant hepatitis A in a patient with anorexia nervosa. 1637 99

Acute renal failure (ARF) is one of the common emergencies in pediatric practice. In the Indian subcontinent, its etiology, clinical features and outcome vary from other parts of the world. We decided to perform a prospective study of ARF in 180 pediatric patients admitted to our institute between August 2006 and March 2008. Our study included children, neonates 7.8%, <1 year 16.7%, 1-5 years 30.5% and >5 years comprised 52.8%. The male:female ratio was 2.3:1. Acute tubular necrosis remains the major cause of ARF; other intrinsic renal disease accounted for almost 30% of the patients. In all patients of ARF who required dialysis, peritoneal dialysis was offered as the first-line management. Six patients were offered hemodialysis. Mortality below one year age was higher compared with those who were more than one year of age (40% vs 11.3%). The overall mortality in the present study was 17.7%. ARF in pediatric nephrology is not uncommon. In our setup, peritoneal dialysis (PD) is an effective and safe modality of renal replacement therapy in most of the cases. Delayed referral, malnutrition, infections, age less than one year and multiorgan involvement were bad prognostic features.
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PMID:Acute renal failure in the pediatric age group - single center prospective study of 180 cases. 2191 53

Kidney transplant patients (KTPs), and particularly those with advanced chronic kidney rejection, may be affected by opportunistic infections, metabolic alterations and vascular and oncologic diseases that promote clinical conditions that require a variety of treatments, the combinations of which may predispose them to hyponatremia. Salt and water imbalance can induce abnormalities in volemia and/or serum sodium depending on the nature of this alteration (increase or decrease), its absolute magnitude (mild or severe) and its relative magnitude (body sodium:water ratio). Hyponatremia appears when the body sodium:water ratio is reduced due to an increase in body water or a reduction in body sodium. Additionally, hyponatremia is classified as normotonic, hypertonic and hypotonic and while hypotonic hyponatremia is classified in hyponatremia with normal, high or low extracellular fluid. The main causes of hyponatremia in KTPs are hypotonic hyponatremia secondary to water and salt contraction with oral hydration (gastroenteritis, sepsis), free water retention (severe renal failure, syndrome of inappropriate antidiuretic hormone release, hypothyroidism), chronic hypokalemia (rapamycin, malnutrition), sodium loss (tubular dysfunction secondary to nephrocalcinosis, acute tubular necrosis, tubulitis/rejection, interstitial nephritis, adrenal insufficiency, aldosterone resistance, pancreatic drainage, kidney-pancreas transplant) and hyponatremia induced by medication (opioids, cyclophosphamide, psychoactive, potent diuretics and calcineurinic inhibitors). In conclusion, KTPs are predisposed to develop hyponatremia since they are exposed to immunologic, infectious, pharmacologic and oncologic disorders, the combinations of which alter their salt and water homeostatic capacity.
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PMID:Hyponatremia in kidney transplant patients: its pathophysiologic mechanisms. 3009 23