Renal replacement therapy toxicity

This particular form of chronic tubulo-interstitial nephritis is characterized by an important cellular infiltration of the interstitium with macrophages, T-cells but also B-cells. Furthermore, after arrest of the drug, there is improvement of the renal function in some cases [26,93]. In those in which there is a delayed diagnosis of renal damage, recovery of renal function does not occur. Instead, several of those patients needed one or another form of renal replacement therapy. An important aspect of this type of toxic nephropathy is the documented persistence of the inflammation of the renal interstitium even several months after arrest of drug intake [28]. 

In a retrospective study of 66 active soldiers without previous renal replacement therapy receiving colistin mostly intravenously, 45 % had some degree of renal dysfunction and 21% stopped treatment because of nephrotoxicity. The authors concluded that the probability of renal toxicity increases with cumulative dose and duration of treatment (a fourfold increase with treatment for more than 14 days) [179. ... 

L A. Nephrotoxicity is the most common and most serious toxicity associated with amphotericin B administration. This is manifested by azotemia (elevated serum blood urea nitrogen and creatinine), and by renal tubular acidosis, which results in the wasting of potassium and magnesium in the urine (leading to hypokalemia and hypomagnesemia, requiring oral or intravenous replacement therapy). Normochromic normocytic anemia is also seen with long-term amphotericin B administration. Elevation of hver enzymes is not associated with the use of amphotericin B. 

Avoidance of salt depletion and a salt load (500-1000 ml of 0.9% saline) reduce the renal toxicity of DAMB (120-126). Also the maintenance of adequate serum potassium concentrations by replacement therapy may be important and may contribute to kidney sparing (127). Other preventive measures, including dopamine infusion, are of no value (128). 

In all patients with chronic renal insufficiency, strict supervision of total aluminium intake is vital. The administration of aluminium should be stopped as soon as the serum concentration exceeds 150 pg/ml or at the appearance of the first symptoms of encephalopathy (81). According to current recommendations, dia-lysate solutions should contain less than 10 pg/l of aluminium (82). There is some controversy about the view that aluminium-containing medications used to control serum phosphate concentrations in uremic subjects should be replaced by calcium-containing phosphate binders (83). Another approach used to reduce the toxic risks of aluminium hydroxide may be to tailor doses to the phosphate concentration in serum, that is individualizing aluminium gel therapy (SED-12, 515). 

After diagnosis, therapy of ohgoanuria depends on the underlying causes. Recovery of renal function may follow rehydration, blood replacement, vasopressor support to improve cardiac output, administration of furosemide, and termination of therapy with toxic drugs such as indomethacin or amphotericin. 

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