By Kar Neng Lai
This guide offers useful and available info on all points of basic nephrology, dialysis, and transplantation. It outlines present remedies in straight forward language to aid readers comprehend the therapy motive, and doesn't suppose wide wisdom of anatomy, biochemistry, or pathophysiology. which includes 33 chapters written by way of 31 specialists from 4 continents, this quantity covers the entire sensible suggestions within the emergency and long term administration of sufferers with electrolyte disturbance, acid-base disturbance, acute renal failure, universal glomerular ailments, high blood pressure, pregnancy-related renal issues, continual renal failure, and renal alternative treatment. it really is therefore an important resource of speedy reference for nephrologists, internists, renal fellows, and renal nursing experts, and is additionally compatible for graduate scholars and learn scientists within the box of kidney ailments.
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Extra info for A Practical Manual of Renal Medicine: Nephrology, Dialysis and Transplantation
Timely hemodialysis after a plasmapheresis procedure in a renal dysfunction patient can avert the alkalosis caused by citrate given during the plasmapheresis procedure. • Intermittent hemodialysis with a high [HCO3−] dialysate (used to achieve a predialysis serum [HCO3−] > 22 mmol/L) often results in transient metabolic alkalosis post-dialysis. qxd 6/2/2009 3:01 PM Page 35 Acid-Base Disturbances 35 • The ingestion of nonabsorbable antacids (magnesium hydroxide, aluminum hydroxide, or calcium carbonate), combined with a cation exchange resin (sodium polysterene sulfonate), by renal insufficiency patients may lead to metabolic alkalosis.
The causes for metabolic acidosis can be classified in terms of: (a) a high H+ production rate, (b) excessive loss of HCO3−, and (c) inability to excrete the amount of acids generated as a result of normal metabolism. In practical terms, differentiation among the various types of acidosis usually relies on the anion gap, as depicted in Fig. 1. A high anion gap acidosis is almost always due to increased acid generation (the only exception being that of advanced renal insufficiency), whereas excess urine HCO3− loss or stool HCO3- (and/or HCO3− precursor) loss and decreased renal acid excretion can lead to a normal anion gap acidosis.
Metabolic acidosis in dialysis patients has been associated with muscle wasting and hypoalbuminemia. Other negative effects include increased bone resorption, worsening hypertriglyceridemia, and stunted growth in children. The US National Kidney Foundation K/DOQI guidelines recommend maintaining a serum [HCO3−] of ≥22 mmol/L in end-stage renal disease (ESRD) and CKD patients. • Sevelamer hydrochloride decreases serum [HCO3−] due to the provision of an increased acid load as HCl is released in exchange for bound phosphate and bile acids.