A practical approach to the management of patients with chronic renal failure.

The number of patients with significant chronic renal failure is expanding rapidly in the United States. All physicians and medical-care providers will have an increasingly important role in the detection and management of renal failure in patients who are not undergoing dialysis. Patients with diabetes or hypertension should be carefully monitored for the development of renal insufficiency by using screening tools such as blood pressure measurement, determination of serum creatinine, urinalysis, and determination of 24-hour urinary microalbuminuria. In order to slow the progression of renal disease, attenuate uremic complications, and prepare patients with renal failure for renal replacement therapy, all medical-care providers should "take care of the BEANS." Blood pressure should be maintained in a target range lower than 130/85 mm Hg, and in many patients, angiotensin-converting enzyme inhibitors may be beneficial. Erythropoietin should be used to maintain the hemoglobin level at 10 to 12 g/dL. Access for long-term dialysis should be created when the serum creatinine value increases above 4.0 mg/dL or the glomerular filtration rate declines below 20 mL/min. Nutritional status must be closely monitored in order to avoid protein malnutrition and to initiate dialysis before the patient's nutritional status has deteriorated. Nutritional care also involves correction of acidosis, prevention and treatment of hyperphosphatemia, and administration of vitamin supplements to provide folic acid. Specialty referral to nephrology should occur when the creatinine level increases above 3.0 mg/dL or when the involvement of a nephrologist would be beneficial for ongoing management of the patient.

Clinical experience with desferrioxamine in dialysis patients with aluminium toxicity.

A desferrioxamine (DFO) infusion test, using a DFO dose of 36.9 +/- 11.2 mg/kg (mean +/- SD), was performed in 50 consecutive dialysis patients undergoing diagnostic bone biopsy. In 30 patients whose bones stained positively for aluminium the serum aluminium level increased by an average of 373 +/- 250.4 ng/ml. The increase in 20 aluminium-negative patients was 231 +/- 179.2 ng/ml (p less than 0.05). Aluminium-positive patients had lower levels of immunoreactive parathyroid hormone (336 +/- 442 muleq/ml) than aluminium-negative patients (1278 +/- 1400 muleq/ml; p less than 0.05). A change in serum aluminium level of greater than 200 ng/ml after the administration of DFO was 73 percent sensitive and 50 percent specific, and had a positive predictive value of 69 percent for detecting positive bone aluminium staining. The combination of a baseline immunoreactive parathyroid hormone level less than 200 muleq/ml and a change in serum aluminium of greater than 200 ng/ml after DFO was 90 percent specific and had a positive predictive value of 85 percent. In the second phase of our study, 28 dialysis patients with aluminium toxicity received long-term therapy (11.0 +/- 4.3 months) with DFO at an average starting dose of 41.7 +/- 17.1 mg/kg, administered once weekly. The four deaths which occurred during this treatment involved the only patients who had advanced dialysis dementia. Seven patients with less severe neurological symptoms responded favourably. Fractures decreased from 1.7 fractures/patient/year to 0.1 fracture/patient/year. Muscular strength and overall functional class were improved or stable in 25 patients; myalgias and arthralgias were also stable or improved in 19 patients. After 5-7 months of treatment, serum aluminium levels decreased from 401 +/- 262 ng/ml to 245 +/- 217 ng/ml (p less than 0.01); erythrocyte mean corpuscular volume increased from 86.3 +/- 10.91 fl to 94.1 +/- 9.23 fl (p less than 0.02); and serum calcium decreased from 10.4 +/- 0.94 mg/dl to 9.9 +/- 0.70 mg/dl (p less than 0.02). Serum immunoreactive parathyroid hormone levels remained stable in 25 patients, but severe hyperparathyroidism developed rapidly in three patients. Eight patients with transfusional iron overload had no change in serum ferritin levels. Iron depletion developed in six patients, with a decrease in serum ferritin from 251 +/- 229.8 micrograms/l to 45 +/- 29.3 micrograms/l, and they required parenteral iron supplementation. Significant side-effects occurring during long-term DFO administration were hypotension (11 patients), gastrointestinal upset (seven patients), porphyria cutaneous tarda-like lesions (three patients), and transient visual disturbance (one patient). There was a decrease in stainable bone aluminium in all nine patients with paired bone biopsy specimens (pre- and post-DFO).(ABSTRACT TRUNCATED AT 400 WORDS)

Hemosiderosis in a dialysis patient: treatment with hemofiltration and deferoxamine chelation therapy.

Although the highly permeable membranes utilized in hemofiltration are theoretically more permeable to deferoxamine-chelated iron than the standard cuprophan membranes used in conventional hemodialysis, no clinical data support this contention. Ours are the first published results of a preliminary short-term trial of combined therapy with deferoxamine and hemofiltration in a dialysis patient with hemosiderosis. An average of 15.3 mg of iron was mobilized with a 19.5-liter exchange over only 4 1/2 hours of postdilution hemofiltration. This compares favorable with previous reports in which 8 to 12 hours of dialysis were performed with Kiil dialyzers, and also with the 24-hour urinary excretion of chelated iron in iron-overloaded patients with normal renal function. We conclude that combined therapy with deferoxamine and hemofiltration offers promises as an effective means of iron mobilization in dialysis patients with hemosiderosis.