ABSTRACT
Phosphorus is a major component of proteins, phospholipids, and nucleotides. The increased uptake of phosphorus by cells during erythropoiesis can result in severe hypophosphatemia. A case of severe hypophosphatemia due to accelerated erythropoiesis in response to Cefotetan-induced hemolytic anemia is described. The hypophosphatemia seen during hemolysis may be the result, rather than the cause, of the hemolysis.
Subject(s)
Anemia, Hemolytic/complications , Anemia, Hemolytic/etiology , Cefotetan/adverse effects , Hypophosphatemia/etiology , Anemia, Hemolytic/physiopathology , Erythropoiesis/drug effects , Female , Humans , Middle AgedABSTRACT
Over a two-year period, 100 venous angiograms were performed on 75 patients because of difficulty with vascular access. Seventy percent of the patients had decreased arterial flow or increased venous resistance. High output failure, sepsis, and aneurysm formation were also found. Venous angiography of the fistula demonstrated significant stenosis in 40% of the cases as well as total occlusion by thrombus in 9%, aneurysm formation in 7%, and abnormal fistula needle placement or anatomic abnormalities in 20% of the cases. Definitive diagnosis with the aid of venous angiography permitted specific surgical intervention in 62% of the cases, and identified new sites for needle placement in 18% of the cases, thus prolonging fistula life and reducing the need for new fistula placement. Our experience with local cellulitis of the fistula site and sepsis is also discussed.
Subject(s)
Arteriovenous Shunt, Surgical/adverse effects , Renal Dialysis/adverse effects , Adult , Aneurysm/etiology , Angiography , Arteriovenous Shunt, Surgical/instrumentation , Arteriovenous Shunt, Surgical/methods , Cellulitis/etiology , Constriction, Pathologic/etiology , Female , Heart Failure/etiology , Humans , Infections/etiology , Male , Needles , Phlebography , Thrombosis/etiology , Time FactorsSubject(s)
Anti-Bacterial Agents/pharmacology , Calcimycin/pharmacology , Calcium/pharmacology , Gluconeogenesis/drug effects , Kidney Cortex/metabolism , Animals , Cyclic AMP/metabolism , Cyclic AMP/pharmacology , Drug Interactions , In Vitro Techniques , Kidney Cortex/drug effects , Parathyroid Hormone/pharmacology , Pentobarbital/pharmacology , RatsABSTRACT
In five patients with Bartter's syndrome, mean (+/-SE) plasma norepinephrine concentrations increased from 324 +/- 75 pg/ml with the patients in the supine position to 550 +/- 100 pg/ml, 753 +/- 104 pg/ml and 808 +/- 116 pg/ml after 2,5 and 10 minutes, respectively, in the standing position, levels significantly higher than normal. Plasma epinephrine concentrations were indistinguishable from normal. One patient was shown to resistant the pressor (but not the metabolic) effects of intravenously administered norepinephrine prior to treatment with reversion to normal pressor responsiveness during indomethacin administration. Similarly, that patient's exaggerated endogenous norepinephrine response to standing (10 minute plasma value of 1,110 pg/ml) reverted to normal (10 minute value of 462 pg/ml) during indomethacin administration. Thus, patients with Bartter's syndrome exhibit a hyperadrenergic state consisten with resistance to endogenous, as well as exogenous, norepinephrine. Since the metabolic responses to intravenously administered norepinephrine were normal in the patient studied, norepinephrine resistance would appear to be limited to the vasculare system. Reversion of norepinephrine resistance during administration of an inhibitor of prostaglandin synthesis suggests that this hyperadrenergic state is not a primary pathogenetic abnormality in Bartter's syndrome.
