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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemic injury to the renal allograft, prior to implantation, is an important cause of delayed graft function. With improved understanding of the pathophysiological mechanisms involved, strategies have been devised to minimize ischemic injury during preservation ex vivo. It is clear that reducing the warm ischemic time, flushing the kidney with hypothermic solution containing cell-impermeant compounds, and maintaining the organ at low temperature ex vivo have increased the duration that the kidney can be preserved. The effectiveness of a number of other components of preservation solutions, as well as the relative merits of continuous perfusion of the organ ex vivo, is more controversial. In this chapter, we review the mechanistic features of ischemic acute renal failure and discuss various preservation strategies and their success in the context of these basic principles of ischemic pathophysiology.
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PMID:Kidney preservation ex vivo for transplantation. 158 Jun 5

A patient with a 12 hour history of headache, breathlessness and hypotension developed acute renal failure necessitating haemodialysis for 12 days. During recovery she developed hypertension, tachycardia and facial flushing. Investigations revealed a right adrenal phaeochromocytoma. Whilst postural hypotension is common in phaeochromocytoma, profound shock with acute renal failure is rare. This may have been precipitated by concomitant drug therapy, myocardial necrosis or by necrosis within the tumour.
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PMID:Phaeochromocytoma presenting with cardiogenic shock and acute renal failure. 333 32

Acute renal failure occurred in a patient with a carcinoid syndrome whenever he developed a flushing episode. Renal biopsy performed during one of these oliguric episodes did not reveal any lesions which could explain this reversible form of renal insufficiency. Urinary indices were not conclusive. Alteration of intrarenal hemodynamics by vasoactive compounds is proposed to be the causative mechanism of this relapsing acute oliguric renal failure.
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PMID:Functional acute renal failure in a patient with carcinoid syndrome. 369 18

In this investigation, we describe a modification of Euro-Collins flushing solution which enables this solution to be effective in preventing normothermic postischemic acute renal failure. The left kidneys of Sprague-Dawley rats were briefly flushed in situ by vascular perfusion with Euro-Collins solution and the renal pedicle clamped to render the kidney ischemic and hold the flushing solution in the kidney. Following 1 h of in situ normothermic ischemia, the pedicle clamp was removed and a contralateral nephrectomy of the right kidney performed. In two other groups of rats the same experimental protocol was followed using Euro-Collins solution in which the dextrose in this solution was replaced with a similar osmolal contribution of either sucrose (64 g/l) or mannitol (35 g/l). Rats with kidneys flushed with the standard Euro-Collins solution containing dextrose (n = 24) exhibited significantly higher postischemic daily serum creatinine levels, a greater degree of tubular necrosis, and a higher mortality (75, versus 31%) than unflushed ischemic controls (n = 22). Rats with kidneys flushed with Euro-Collins, containing either sucrose (n = 25) or mannitol (n = 22) in place of dextrose, all survived, exhibited only focal tubular damage as observed by electron microscopy, and most returned to normal serum creatinine levels within 72 h following ischemia. These findings, together with other reports that mannitol- and sucrose-based flushing solutions provide excellent protection during prolonged cold ischemia, strongly argue for the substitution of sucrose, mannitol or other similar protective impermeant agents for dextrose in flushing solutions such as Euro-Collins.
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PMID:Improving Euro-Collins flushing solution's ability to protect kidneys from normothermic ischemia. 393 Sep 35

An in situ flushing solution was evaluated with regard to the following: (1) its ability to protect the kidney during 60, 90, and 120 minutes of normothermic ischemia; (2) the effects of using an intracellular versus extracellular electrolyte composition in the flushing solution; and (3) the ability of the flushing solution to complement in situ hypothermia as a protective measure during long-term ischemia. Rat kidneys were briefly flushed in situ with an isotonic phosphate buffered solution (pH 7.2) containing 50 milliosmole of sucrose. The left renal pedicle was then immediately clamped to render the kidney ischemic and to hold the flushing solution in the kidney. Following removal of the pedicle clamp, a contralateral nephrectomy of the right kidney was performed and daily serum creatinine levels determined to evaluate postischemic renal function. The results indicate the following: (1) the flushing procedure is very effective in preventing postischemic acute renal failure following 60 minutes of normothermic ischemia, but is considerably less effective for ischemic times of 90 minutes or more; (2) an intracellular electrolyte composition in the flushing solution does not improve the protective effects of this solution; and (3) the flushing procedure can significantly improve on the protection otherwise provided by in situ hypothermia.
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PMID:Evaluation of a flushing solution designed to protect kidneys from in situ ischemia. 402 28

Rat kidneys were flushed in situ with selected preservation solutions prior to clamping the renal vessels for 1 hour. Collins and Euro-Collins flushing solutions did not appear to protect the physiologic or morphologic status of rat kidneys when examined 2 days after the ischemic insult. These experimental groups exhibited serum creatinine levels similar to those seen in ischemic controls, correspondingly low urine creatinine levels, anuria, and significant deterioration of the uriniferous tubules as revealed by light and electron microscopy. In situ flushing with hypertonic Sacks or isotonic phosphate-buffered sucrose solutions, however, resulted in significant improvements in serum and urine creatinine levels, prevented anuria, and dramatically improved the morphologic integrity of the uriniferous tubules. Flushing with a phosphate-buffered sucrose solution that contained ATP-MgCl2 further improved the physiologic and morphologic status of ischemic kidneys to the point that they were indistinguishable from the nonischemic controls. The degree of protection obtained by flushing kidneys with the isotonic phosphate-buffered sucrose solution plus ATP-MgCl2 is greater than that provided by any other single pretreatment or posttreatment for ischemia that is currently available. We, therefore, believe that the use of this procedure can provide a valuable approach to surgical situations in which postischemic acute renal failure is a potential problem.
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PMID:Protection of kidneys from acute renal failure resulting from normothermic ischemia. 660 9

Experiments were performed to determine whether furosemide, given in doses high enough to induce a strong diuresis and to inhibit the mechanism of tubuloglomerular feedback, offers any protection from acute renal failure induced by a nephrotoxin or ischaemia. Microperfusion of the loop of Henle revealed that a tubular furosemide concentration of 5 x 10(-5) mol x 1(-1) was necessary to fully inhibit the tubuloglomerular feedback response to a raised sodium chloride concentration at the macula densa. The infusion of furosemide systemically to achieve such concentrations in the tubule resulted in an improvement in renal function when given before or after the nephrotoxin but was without effect when given before or after ischaemia. Measurements of furosemide concentrations in the urine, however, confirmed that sufficient amounts were applied to inhibit the feedback mechanism. It is concluded from this and similar studies that furosemide is only beneficial in models of acute renal failure with an obstructive or nephrotoxic pathogenesis, in which it acts by flushing out the noxious material and not by inhibiting the mechanism of tubuloglomerular feedback.
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PMID:The early phase of experimental acute renal failure. VI. The influence of furosemide. 732 42

Extensive skeletal muscle injury, whether caused by mechanical crush or by extreme physical exertion, is incompatible with life, unless treated early and vigorously. The immediate cause of morbidity is leakiness of the sarcolemmal membrane to cardiotoxic or nephrotoxic cations and metabolites (K, PO4, myoglobin and urate) of the sarcoplasma, and rapid massive uptake by the muscles of extracellular fluid, sodium and calcium, leading to profound hypovolemic and hyocalcemic shock. Casualties who survive the early steep of hyperkalemia and arterial hypotension are susceptible to myoglubinuric acute renal failure owing mainly to the combination of renal vasoconstriction, nephrotoxicity, and tubular obstruction by myoglobin plugs and urate. Management includes immediate (prehospital) intravenous volume replacement followed by mannitol-alkaline diuresis. The alkali regimen ameliorates the acidosis associated with shock and the hyperkalemia, and protects against the nephrotoxicity of myoglobin and urate by alkalinization of the urine. Mannitol, through its impermeant hyperoncotic properties, decompresses and mobilizes muscle edema and promotes renal tubular flow, thus flushing myoglobin plugs and enhancing urinary elimination of nephrotoxic metabolites. With this regimen and when necessary also with the use of dialysis, a substantial salvage of lives, limbs, and kidney function has been achieved recently compared with invariable mortality for casualties who were buried for 3 to 4 hours or more in the early 1940s (World War 2).
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PMID:Acute renal failure complicating muscle crush injury. 975 9

Intravenous immunoglobulin (IVIg) is administered for various indications and generally considered a safe therapy. Most of the adverse effects (AEs) associated with IVIg administration are mild and transient. The immediate AEs include headache, flushing, malaise, chest tightness, fever, chills, myalgia, fatigue, dyspnea, back pain, nausea, vomiting, diarrhea, blood pressure changes, tachycardia, and anaphylactic reactions, especially in IgA-deficient patients. Late AEs are rare and include acute renal failure, thromboembolic events, aseptic meningitis, neutropenia, and autoimmune hemolytic anemia, skin reactions, and rare events of arthritis. Pseudohyponatremia following IVIg is important to be recognized. Renal failure, usually oliguric and transient, occurs mostly on using sucrose-containing products owing to osmotic injury. Among high-risk patients who have a previous renal disease, dehydration, diabetes mellitus, advanced age, hypertension, hyperviscosity, or are treated by other nephrotoxic medications, administration of a non-sucrose-containing IVIg product after accomplishing hydration, in a low concentration and a slow infusion rate while supervising urine output and kidney function, is recommended. Thromboembolic complications occur because of hyperviscosity especially in patients having risk factors including advanced age, previous thromboembolic diseases, being bedridden, diabetes mellitus, hypertension, dyslipidemia, or those receiving high-dose IVIg in a rapid infusion rate. Immediate AEs can be treated by the slowing or temporary discontinuation of the infusion and symptomatic therapy with analgesics, nonsteroidal anti-inflammatory drugs, antihistamines, and glucocorticoids in more severe reactions. Slow infusion rate of low concentration of IVIg products and hydration, especially in high-risk patients, may prevent renal failure, thromboembolic events, and aseptic meningitis.
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PMID:Intravenous immunoglobulin: adverse effects and safe administration. 1639 92

Intravenous immunoglobulin (IVIg) is administered both for the treatment of immunodeficiencies and for an expanding list of autoimmune diseases. Most adverse effects are mild and transient including headaches, flushing, fever, chills, fatigue, nausea, diarrhea, blood pressure changes and tachycardia. IgA deficiency-related anaphylactic reactions are largely preventable. Late adverse events are rare and include acute renal failure and thromboembolic events. Acute renal failure, usually oliguric and transient, occurs generally in insufficiently hydrated patients and with sucrose-stabilized products due to osmotic injury. Thromboembolic complications occur due to hyperviscosity especially in patients having risk factors including advanced age, previous thromboembolic events, immobilization, diabetes mellitus, hypertension, dyslipidemia or those receiving high-dose IVIg in a rapid infusion rate or excessive dose. Slow infusion rate and good hydration may prevent renal failure, thromboembolic events and aseptic meningitis. In our experience in more than 200 patients receiving IVIg for different autoimmune diseases and near 10000 infusions for relapsing-remitting multiple sclerosis patients, the occurrence of adverse effects was 24-36% after high dose IVIg, most were headaches and all were mild adverse events. We conclude that IVIg is a safe therapy when given in a slow infusion rate in well-hydrated patients, better avoiding patients with known risk factors.
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PMID:Safety of intravenous immunoglobulin (IVIG) therapy. 1731 19


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