Renal dialysis patient

Once aluminium has reached the circulation, there seems little doubt that it can cross the blood-brain barrier - the best proof being that in renal dialysis patients... 

Roger SD, Harris DCH, Stewart JH. Possible relation between restless legs and anemia in renal dialysis patients. Lancet 1991 337 1551. 

Dedman DJ, Treffry A, Candy JM, et al. 1992. Iron and aluminum in relation to brain ferritin in normal individuals and Alzheimer s-disease and chronic renal-dialysis patients. Biochem J 287 509-514. 

Renal dialysis patients fed semipurified, liquid formulas as a sole nutrition source for 3 weeks showed significantly decreased blood plasma TAC (D6). TAC of blood plasma of children with kwashiorkor, a severe edematous manifestation of malnutrition, was below 50% of that of healthy controls (F4). 

D6. DiSilvestro, R. A., Blostein-Fujii, A., and Watts, B., Low phytonutrient, semipurified liquid diets depress plasma total antioxidant status in renal dialysis patients. Nutr. Res. 19,1173-1177 (1999). 

Erythropoietin [ery throw PO eetin] is a glycoprotein, normally made by the kidney, that regulates red cell proliferation and differentiation in bone marrow. Human erythropoietin, produced by recombinant DNA technology, is effective in the treatment of anemia caused by end-stage renal disease, anemia associated with HIV-infected patients, and anemia in some cancer patients. Supplementation with iron may be required to assure an adequate response. The protein is usually administered intravenously in renal dialysis patients, but in others the subcutaneous route is preferred. Side effects such as iron deficiency and an elevation in blood pressure occur. [Note The latter may be due to increases in peripheral vascular resistance and/or blood viscosity.]... 

Cowper, S.E., Robin, H.S., Steinberg, S.M., etal. (2000) Scleromyxoedema-like cutaneous diseases in renal-dialysis patients. Lancet, 356, 1000-1001. 

Hubbard V, Davenport A, Jarmulowicz M, Rustin M Scleromyxoedema-like changes in four renal dialysis patients. BrJDermatol 148 563-568,2003. 

E331 Flicker, R.F. and Bogavich, M. (1987). Pyridoxal-5-phosphatedepletion in renal dialysis patients causes clinically significant errors in ALT determinations. Clin. Chem. 33, 992, Abstr. 547. 

DEena BA, White GH. Interference with the measurement of intact parathyrin in serum from renal dialysis patients. Clin Chem 1989 35 1543-4. 

Aluminium is poorly absorbed from the GI tract, which is just as well since antacid preparations used by dyspeptic patients may contain as much as 500 mg of aluminium per tablet. Aluminium levels in water supplies are variable and may contain from less than 50 to more than I0(K) jg/l. This is a potential hazard to renal dialysis patients when the aluminium can enter the body across the dialysis membrane, thus bypassing intestinal absoiption. The water used in dialysis is now treated to remove contaminating metals. Acute aluminium toxicity is extremely rare. Aluminium toxicity in patients with renal dysfunc-... 

Dedman, D.J., Treffry, A., Candy, J.M., Taylor, G.A.A., Morris, C.M., Bloxham, C.A., Perry, R.H., Edwardson, J.A. and Harrison, P.M. (1992) Iron and aluminium in relation to brain ferritin in normal individuals and Alzheimer s disease and chronic renal-dialysis patients. Biochem. J. 181 509-514. 

Many types of biological specimens can be analyzed for aluminum. Tissue and bone have been suggested as the specimens of choice to evaluate the true body burden [23-2S]. Since these specimens are not obtainable on a regular basis, blood aluminum levels have been analyzed to reflect a subject s aluminum burden [26-28], Most of these methods use serum or plasma as intUcator specimen. The monitoring of aluminum levels in these specimens is considered to be the most appropriate approach to ensure that aluminum toxicity problems do not develop in individual uremic or renal dialysis patients [27]. Urine samples have been analyzed for aluminum content for the biological monitoring of occupationally exposed persons. 

The absorption and excretion of carbenicillin in man has been reported [396]. The antibiotic is not absorbed intact from the gut intramuscular injection (which is painful) often provides adequate serum levels (approximately 20 Mg/ntl) but infections with Pseudomonas strains having minimum inhibitory concentrations up to, or higher than, 100 Mg/ml require intravenous thbrapy to achieve such levels. No evidence of active metabolite formation has been obtained. Marked reductions in the half-life (and serum levels) of carbenicillin follow extracorporeal dialysis or peritoneal dialysis, the former producing the most striking effect [397]. These results were, of course, obtained in patients with severe renal failure. Patients with normal renal function rapidly eliminate the drug but, as with all penicillins, renal tubular secretion can be retarded by concurrent administration of probenecid. 

Erythropoietin release is stimulated by hypoxia (low PO2). Within hours, the hormone ensures that erythrocyte precursor cells in the bone marrow are converted to erythrocytes, so that their numbers in the blood increase. Renal damage leads to reduced erythropoietin release, which in turn results in anemia. Forms of anemia with renal causes can now be successfully treated using erythropoietin produced by genetic engineering techniques. The hormone is also administered to dialysis patients. Among athletes and sports professionals, there have been repeated cases of erythropoietin being misused for doping purposes. 

Patients generally seek medical help because they want relief from disease. They have little interest in diagnosis—except in so far as it helps the doctor treat them more efficiently—and still less in the mechanism of their illness. Nevertheless, clinical chemistry traditionally has been more concerned with diagnosis and the elucidation of the mechanism of disease than with treatment. In only a few circumscribed areas, such as management of water and electrolyte imbalance, diabetic coma, and renal dialysis, has clinical biochemistry proved indispensable for treatment, the overall raison d etre of the health industry. 

Chronic renal dialysis Although serum ferritin is usually a good guide to body iron stores, the correlation of body iron stores and serum ferritin may not be valid in patients on chronic renal dialysis who are also receiving iron dextran complex. 

Slow IV injection In chronic renal failure patients, iron sucrose may be administered by slow IV injection into the dialysis line at a rate of 1 ml (20 mg iron) undiluted solution per minute (ie, 5 min/vial) not exceeding 1 vial of iron sucrose (100 mg elemental iron) per injection. Discard any unused portion. 

Patients with CRF not requiring dialysis Patients with CRF not yet requiring dialysis may require lower maintenance doses of darbepoetin than patients receiving dialysis. Predialysis patients may be more responsive to the effects of darbepoetin, and require judicious monitoring of blood pressure and hemoglobin. Also closely monitor renal function and fluid and electrolyte balance. 

Renal function impairment Renal failure or dialysis patients may require smaller doses closely supervise to prevent cardiac failure or exacerbation of renal failure. Carcinogenesis Dietary administration of minoxidil to mice for up to 2 years was associated with an increased incidence of malignant lymphomas in females at all dose levels (10, 25, and 63 mg/kg/day) and an increased incidence of hepatic nodules in males (63 mg/kg/day). 

High-risk patients Hypertensive patients at risk of excessive hypotension include those with the following concurrent conditions or characteristics Heart failure, hyponatremia, high-dose diuretic therapy, recent intensive diureses or increase in diuretic dose, renal dialysis, or severe volume or salt depletion of any etiology. Single doses of enalaprilat as low as 0.2 mg have produced excessive hypotension in normotensive patients with these diagnoses. Because of the potential for an extreme hypotensive response in these patients, initiate therapy under very close medical supervision. The... 

Renal function impairment Admn s er 1.25 mg every 6 hours for patients with Cor greater than 30 mL/min. For Ccr 30 mL/min or less, initial dose is 0.625 mg. If there is inadequate clinical response after 1 hour, the 0.625 mg dose may be repeated. May give additional 1.25 mg doses at 6-hour intervals. For dialysis patients, initial dose is 0.625 mg or less administered over 5 minutes or more, preferably longer (no more than 1 hour). 

Use in patients with impaired renal function - Perindoprilat elimination is decreased in renally impaired patients, with a marked increase in accumulation when Ccr drops below 30 mL/min. In patients with Ccr less than 30 mL/min, safety and efficacy have not been established. For patients with lesser degrees of impairment (Ccr more than 30 mL/min), the initial dosage should be 2 mg/day, and dosage should not exceed 8 mg/day because of limited clinical experience. During dialysis, perindopril is removed with the same clearance as in patients with normal renal function. 

Renal function impairment - In patients with a creatinine clearance less than 30 mL/min, increase the dosing interval to 12 hours, with a maximum daily dose of 200 mg. Because hemodialysis only removes 7% of an administered dose, dialysis patients can receive their regular dose on the day of dialysis. 

Renal function impairment Use rizatriptan and sumatriptan with caution in dialysis patients because of a decrease in the clearance. 

Renal function impairment- In end-stage renal disease patients maintained on hemodialysis or peritoneal dialysis, the recommended dosing is 100 mg every 6 to 8 hours. 

Renal function impairment An additional 200 mg dose of nevirapine following each dialysis treatment is indicated in patients requiring dialysis. Patients with Ccr 20 mL/min or greater do not require an adjustment in nevirapine dosing. 

However, in patients with renal failure there is a strange and currently unexplained observation in relation to non-renal clearance. If this is measured for some compounds it also is found to be depressed even though it is the kidney that is diseased and not the liver The picture becomes a little clearer if the same non-renal (presumed hepatic) clearance is measured again in patients after renal dialysis when the hepatic clearance has been found to have risen to control values. Recent animal experiments have demonstrated that the circulating inhibitor of hepatic cytochrome P450 may be parathyroid hormone. Parathyroidectomy of rats with chronic renal failure prevented the reduction in liver cytochrome activity (see Michaud et al., 2006). 

Staphylococcal vascular shunt infections in persons undergoing renal dialysis have been successfully treated with vancomycin. Vancomycin in oral form can also be used in patients in whom C. difficile colitis is not responding to metronidazole. 

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