By Kar Neng Lai
This handbook presents useful and available details on all facets of common nephrology, dialysis, and transplantation. It outlines present remedies in undemanding language to assist readers comprehend the therapy purpose, and doesn't suppose wide wisdom of anatomy, biochemistry, or pathophysiology. such as 33 chapters written by way of 31 specialists from 4 continents, this quantity covers all of the sensible advice 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, power renal failure, and renal substitute treatment. it really is therefore a vital resource of quickly reference for nephrologists, internists, renal fellows, and renal nursing experts, and is usually compatible for graduate scholars and examine scientists within the box of kidney ailments.
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Additional info for A Practical Manual of Renal Medicine: Nephrology, Dialysis and Transplantation
Qxd 6/2/2009 3:01 PM Page 25 Acid-Base Disturbances 25 Example A patient with ureterosigmoidostomy has serum [Na+] = 138, [Cl−] = 118, [TCO2] = 10. [AG−] = 138 − 118 − 10 = 10 mEq/L, all of which are due to albumin and other normally present but unmeasured anions. There are no abnormal anions present. The low [TCO2] is due to loss of serum HCO3− in the feces as a result of exchange with urinary Cl− in the colonic lumen. Note the hyperchloremia as a result of the increased colonic absorption of Cl−.
M. 1 Causes of hyperkalemia. Spurious hyperkalemia Ischemic venipuncture, hemolysis, thrombocytosis, leukocytosis, familial pesudohyperkalemia, infectious mononucleosis True hyperkalemia Decreased renal function Prerenal azotemia Renal disorders Acute and chronic kidney failure, hyporeninemia, hypoaldosteronism, interstitial nephritis, systemic lupus erythematosus, sickle cell disease, obstructive uropathy, pseudohypoaldosteronism, post-kidney transplantation, amyloidosis, lead nephropathy Adrenal disorders Addison’s disease, 21-hydroxylase deficiency, corticosteroid methyloxidase deficiency Medications Converting enzyme inhibitors, angiotensin receptor blockers, nonsteroidal anti-inflammatory agents, spironolactone, triamterene, amiloride, heparin, cyclosporine or tacrolimus Increased release from cells Cell lysis: crush injury, tumor lysis, hemolysis, rhabdomyolysis Medications: beta-adrenergic blockers, digitalis, arginine, succinylcholine Insulin deficiency and hyperglycemia Familial hyperkalemic periodic paralysis Acidosis: metabolic and respiratory Hyperosmolality Exercise Increased intake of potassium Potassium salts, aged blood, potassium penicillin, geophagia • At 8 mEq/L, the ECG shows the T wave merging with the markedly widened QRS complex, giving the mistaken impression of a ventricular arrhythmia.
Salts of citrate, lactate, acetate, malate. • Calcium carbonate: milk alkali syndrome. 2 Maintenance Phase This phase is due to (a) enhanced renal HCO3− reclamation as a result of decreased effective circulating volume and Cl− depletion and (b) ongoing generation of metabolic alkalosis. 2 Assessment of Urinary Chloride Urinary [Cl−] is valuable in the evaluation of metabolic alkalosis as a marker of volume depletion and as a means to help sort out the causes of metabolic alkalosis. When blood volume is high, urine [Cl−] will be high (except in diuretic therapy; see below).
A Practical Manual of Renal Medicine: Nephrology, Dialysis and Transplantation by Kar Neng Lai