Vitamin B6 and hemodialysis: the impact of high-flux/high-efficiency dialysis and review of the literature.

High-flux/high-efficiency (HF/HE) dialysis is associated with improved clearance for larger molecules, which include a wide variety of middle molecules and water-soluble vitamins. Our study attempted to measure in vivo clearances of serum pyridoxal-5'-phosphate (PLP), the active metabolite of vitamin B6, on standard cuprophan versus cellulose triacetate HF/HE dialysis for patients maintained on 10 mg daily pyridoxine supplements. A longitudinal evaluation of PLP after 3 months on HF/HE dialysis was performed simultaneously. The average in vivo PLP clearance for six patients on standard hemodialysis increased by more than 50%, from 86 +/- 61.7 mL/min using a cuprophan membrane to 173 +/- 90.2 mL/min using a cellulose triacetate dialyzer, at average blood flows of 375 mL/min (P < 0.05). Levels of PLP decreased from a baseline of 50 +/- 13.8 ng/mL to 24 +/- 9.7 ng/mL (P < 0.05) after 3 months of HF/HE treatments; the levels returned to 45 +/- 6.4 ng/mL on resumption of standard dialysis treatments. Although not achieving statistical significance, the average hematocrit increased from 31.2% +/- 1.66% to 32.7% +/- 1.24% while on HF/HE dialysis without an increase in erythropoietin requirements. We conclude that HF/HE dialysis treatments can have a dramatic impact on vitamin B6 homeostasis. Further investigation to evaluate the effects of different membranes and reprocessing should be performed on more heterogeneous patient populations in whom compliance problems with diet and vitamin supplementation may exist. The increased clearance of vitamin B6 may have significantly more detrimental effects in these settings.

Renal and electrolyte complications associated with antibiotic therapy.

Adverse effects of antibiotics generally are minimal, but it is necessary to remain vigilant for potentially serious sequelae, such as unusual forms of renal failure, acidosis and electrolyte abnormalities. Avoiding potentially nephrotoxic drug combinations and monitoring drug levels of nephrotoxic agents such as vancomycin and aminoglycosides should be routine. However, with prolonged use of certain antibiotics, levels of electrolytes, creatinine and blood urea nitrogen should be periodically checked. Elderly and debilitated patients or patients with preexisting renal insufficiency are at particularly high risk for unexpected complications from antimicrobial therapy. All antibiotics have the potential to cause acute interstitial nephritis, which may be manifested by acute renal failure.

The de novo diagnosis of systemic lupus erythematosus in a hemodialysis patient.

We present the first reported case of a patient who developed de novo systemic lupus erythematosus (SLE) after the initiation of dialysis for chronic renal failure. The etiology of his renal failure was secondary to biopsy-proven idiopathic membranoproliferative glomerulonephritis in conjunction with accelerated hypertension. The physical, biochemical or serologic findings of SLE did not become apparent until 4 years after the initiation of hemodialysis. This deviates from the natural history of SLE; typically, once dialysis is initiated, disease and serologic activity diminish with time to the point where therapy is no longer required. Therefore, this first diagnosis of SLE after years on dialysis represents a novel observation.

Effects of intracellular magnesium on calcium, potassium and chloride channels.

Intracellular free magnesium activity approximates 0.6-0.8 mM. Variations in concentration around this physiologic range profoundly affect current flow through calcium, potassium and chloride channels. These effects are exerted on both inwardly and outwardly directed currents and appear to be independent of the state of phosphorylation of the channel. In the heart, these effects are manifested in changes in action potential duration, which may help to explain postulated links between hypomagnesemia and arrhythmias. In the kidney, effects of magnesium on ion channels may subserve a protective role and may explain how potassium balance is altered in magnesium depletion syndromes.