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)

Contrast-induced nephropathy (CIN) is regarded as acute tubular necrosis resulting from the cytotoxicity of contrast media and the medullary hypoxia linking to the interplay of vasoconstriction and vasodilatation. Saline infusion may prevent CIN by inhibiting renin release and thus production of angiotensin II (ANG II), a vasoconstrictor, from angiotensin I (ANG I). Yet the use of angiotensin converting enzyme inhibitor (ACEI) yields conflicting results in the prevention of CIN. We hypothesise that ACEI will be useful for CIN prevention when the saline infusion is insufficient, useless when the saline infusion is sufficient, and counterproductive when the saline infusion is excessive, respectively. When the production of ANG I and thus ANG II is insufficiently inhibited by insufficient saline infusion, ACEI may help prevent CIN by conferring extra inhibition on the production of ANG II from ANG I. The counterproductive effect may result from ACEI blocking the generation of angiotensin 1-7, a potent vasodilator, from angiotensin 1-9 whose precursor, ANG I, is excessively diminished by excessive saline infusion. Clinical data suggest that normal saline infusion at a rate of 1 ml/kg/h for 12 h, 1 ml/kg/h for 6 h, and 2 ml/kg/h for 6 h before and after contrast injection provide sufficient, insufficient, and excessive hydration in the prevention of CIN, respectively. The mainstream guideline is to stop ACEI and provide sufficient hydration for CIN prevention. Alternatively one may continue to have ACEI but the use of normal saline infusion must be limited to 1 ml/kg/h for 6 h before and after contrast injection.
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PMID:A hypothesis on the conflicting results of angiotensin converting enzyme inhibitor in the prevention of contrast-induced nephropathy. 2643 30

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