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• W2035594703 abstract "•Metabolic acidosis: fall in HCO− concentration with fall in pH•Metabolic alkalosis: rise in HCO− concentration with rise in pH•Respiratory acidosis: rise in CO− concentration with fall in pH•Respiratory alkalosis: fall in CO− concentration with rise in pH •Metabolic acidosis: fall in pH causes increased respiration, reducing CO2•Metabolic alkalosis: rise in pH causes decreased respiration, increasing CO2•Respiratory acidosis: fall in pH causes increased renal H+ secretion, raising HCO3− concentration•Respiratory alkalosis: rise in pH causes diminished renal H+ secretion, lowering HCO3− concentration•See Table 1Table 1Formulae Quantifying the Degree of CompensationDisorderCompensationMetabolic acidosisCO2 decreases by 1.0–1.5 × the decrease in arterial HCO3−Metabolic alkalosisCO2 increases by 0.25–1.0 × the increase in arterial HCO3−Respiratory acidosis AcuteHCO3− increases by about 1 for each 10-mm Hg increase in CO2 ChronicHCO3− increases by about 4 for each 10-mm Hg increase in CO2Respiratory alkalosis AcuteHCO3− decreases by about 1 for each 10-mm Hg decrease in CO2 ChronicHCO3− decreases by about 4 for each 10-mm Hg decrease in CO2 Open table in a new tab Average 1 mEq/kg/d for typical Western diet. •Blood buffering of newly formed acid by bicarbonate, creation of CO2•Less efficient buffering of acid by hemoglobin in red blood cells, Ca2+ exchange in bone•Renal handling of acid: ■Hydrogen excretion by proximal tubule (PT) into lumen leads to reclamation and reabsorption of HCO3−■H+ then combines with either HPO42− or HSo4 (“titratable acids”) or NH3 in tubular lumen; 10 to 40 mEq of H+ excreted each day as titratable acidity, 30 to 60 mEq/d by NH4+■Reclamation of filtered bicarbonate occurs primarily in PT■Under conditions of excessive acid generation (metabolic acidosis), ammoniagenesis is required to enhance acid secretion: ○NH4+ produced by renal tubular cells from metabolism of amino acids (primarily glutamine)○NH4+ reabsorbed in thick ascending loop and recycled as NH3 in renal medulla○NH3 diffuses into tubular lumen, trapped as NH4+ by secreted H+○Glutamine metabolism enhanced by hypokalemia, inhibited by hyperkalemia •To respiratory acidosis: ■Increased PT cell secretion of hydrogen ion due to decreased cell pH■Increased PT cell secretion of H+ via Na+/H+ exchanger, and increased reabsorption of HCO3− via Na+/3HCO3− cotransporter on basolateral surface•To respiratory alkalosis: ■Decreased PT cell activity of carbonic anhydrase■Decreased PT cell secretion of H+ and decreased reabsorption of HCO3− •Increased acid load: ■Lactic acidosis■Ketoacidosis■Ingestions: ○Salicylates○Methanol○Ethylene glycol○Paraldehyde○Sulfur○Toluene○Ammonium chloride○Hyperalimentation fluids•Extrarenal acidosis: ■HCO3− losses via gastrointestinal loss: ○Diarrhea○Intestinal fistula○Ureterosigmoidostomy•Renal acidosis: ■Defect in HCO3− reclamation: ○Type 2 “proximal” renal tubular acidosis (RTA)■Defect in HCO3− regeneration: ○Diminished NH4+ production (renal failure, hypoaldosteronism-type IV RTA)○Diminished H+ secretion (type I RTA)•Utility of plasma and urine anion gap: ■Plasma anion gap: ○[Na+] - ([Cl−] + [HCO3−]); normally 8 to 11 mEq/L (mmol/L)○Buffering of HA (proton-anion) by HCO3− in setting of increased acid load leads to increased unmeasured anions (A−) and increased anion gap■Urine anion gap: ○([Na+] + [K+]) - [Cl−]○In setting of metabolic acidosis with normal plasma anion gap (“hyperchloremic metabolic acidosis”), urine anion gap is useful to distinguish between extrarenal and renal acidosis○Urine anion gap greater than 0 suggests failure to excrete acid load (eg, RTA)○Urine anion gap less than 0 suggests extrarenal bicarbonate loss (eg, diarrhea) Hyperchloremic metabolic acidosis, normal serum anion gap, urine anion gap greater than 0. Type I RTA (defect in H+ secretion in distal tubule). •Physiology: ■H+-adenosine triphosphatase (ATPase) located in cortical collecting tubule (intercalated cells only), where H+ secretion influenced by Na+ reabsorption in principal cells, and in medullary collecting duct•Pathophysiology: ■Defect in distal H+-ATPase pump (Sjögren syndrome), increased collecting duct membrane permeability with back-diffusion of H+ (amphotericin B), decreased distal delivery of Na+ with failure to exchange for H+ and K+ (volume depletion), or decreased cortical reabsorption of Na+ with net increase in luminal charges and inhibition of H+ and K+ secretion (“hyperkalemic type I RTA,” as in urinary tract obstruction or sickle cell disease)■Calcium and phosphate release from bone to buffer acidemia leads to propensity for nephrocalcinosis in type I RTA•Diagnosis: ■Urine pH >5.3■Plasma K+ usually low or normal (except with voltage defect)■Plasma HCO3− low (<14 mEq/L [mmol/L])•Treatment: ■HCO3− 1–2 mEq/kg/d Type II RTA (defect in PT HCO3− reclamation). •Physiology: ■Filtered HCO3− reabsorbed primarily in the PT after the addition of a proton in lumen (Na+/H+ antiporter), forming H2CO3, and conversion to CO2 and H2O facilitated by carbonic anhydrase■CO2 diffuses across apical membrane and converted to HCO3− again by carbonic anhydrase■HCO3− then transported to blood by Na+/3HCO3− cotransporter■Distal nephron contributes a trivial amount of HCO3− reabsorption via intercalated cell of collecting duct•Pathophysiology: ■Injury to luminal Na+/H+ antiporter or basolateral Na+-K+-ATPase pump (likely etiologies for type II RTA in multiple myeloma, Fanconi syndrome, ifosfamide therapy) or deficient/inhibited carbonic anhydrase (cystinosis, acetazolamide therapy)■Acidosis milder than type I RTA due to intact reabsorption of HCO3− in distal nephron■Often evidence of generalized PT dysfunction is present, with glycosuria, aminoaciduria, and phosphaturia•Diagnosis: ■Urine pH >5.3 if above reabsorptive threshold, <5.3 in steady state, plasma K+ usually low, plasma HCO3− 14 to 20 mEq/L (mmol/L)•Treatment: ■HCO3− 10 to 15 mEq/kg/d Type IV RTA (aldosterone deficiency or resistance). •Physiology: ■Aldosterone promotes distal Na+ reabsorption, K+ and H+ secretion■Direct effects of aldosterone on Na and K channels in luminal membrane of principal cells in cortical collecting tubule, increased Na+-K+-ATPase pump activity in basolateral membrane, and H+-ATPase pump activity in intercalated cells in cortical collecting duct, medullary collecting tubule cells■Indirect effects of aldosterone in H+ secretion secondary to electrochemical gradient induced by Na+ reabsorption•Pathophysiology: ■Decreased adrenal aldosterone production (heparin, tuberculosis, adrenal insufficiency)■Decreased activity of renin-angiotensin system (diabetes, renal insufficiency, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers)■Resistance to aldosterone (potassium-sparing diuretics, trimethoprim, pseudohypoaldosteronism)■Acidosis exacerbated by hyperkalemia-induced inhibition of glutaminase with diminished ammoniagenesis•Diagnosis: ■Urine pH <5.3, plasma K+ high, plasma HCO3− 14 to 20 mEq/L (mmol/L)•Treatment: ■Correct hyperkalemia, HCO3− 1 to 2 mEq/kg/d RTA of renal insufficiency (reduction in nephron mass). •Physiology: ■Under normal conditions, ammonium excretion increases in response to an acid load, as described earlier in the Physiology/Response to Acid Generation subsection; this increase can be up to 3 to 4 times normal, but is limited by glomerular filtration rate (GFR)•Pathophysiology: ■Fibrosis that occurs with chronic kidney disease leads to diminished functional nephron number and diminished capacity for ammoniagenesis■At GFR less than 40 to 50 mL/min (0.67 to 0.83 mL/s), total ammonium excretion diminishes■H+ is retained but a reduction in HCO3− is stabilized at serum levels of 12 to 20 mEq/L by calcium buffering from bone•Diagnosis: ■Measurement of GFR•Treatment: ■NaHCO3 therapy can be used to minimize bone buffering of acidemia and delay development of osteopenia, but this benefit must be weighed against risks of sodium retention■Indications for use of alkali include: ○Dyspnea/inability to maintain respiratory compensation○Chronic kidney disease in children (at risk of growth retardation)○Severe acidosis with plasma HCO3− less than 12 mEq/L (mmol/L) Anion gap acidosis. •Treat underlying disease process•With saline hydration, NaCl + HA → kidney excretes NaA rather than NH4+•Transition from “anion gap” to “nonanion gap” acidosis in the hydrated patient during treatment Lactic acidosis and ketoacidosis. •Treat underlying disease process•Controversies surround use of bicarbonate-containing fluids in ketoacidosis and lactic acidosis due to potential risk of worsening intracellular acidosis and lack of clinical benefit Ingestions. •Competitive inhibition of alcohol dehydrogenase with ethanol or fomepizole for alcohol ingestions•Indications for hemodialysis treatment under conditions of ethylene glycol, methanol, and salicylate ingestion Rhabdomyolysis. •Enhancement of myoglobin excretion with alkalinization of urine with bicarbonate-containing fluids, hemodialysis Renal tubular acidosis. •Identify type of RTA by urine pH, serum potassium•Calculate bicarbonate deficits, replacement needs, and maintenance dosing of bicarbonate in cases of RTA types I, II, and IV Two phases of metabolic alkalosis: Generation phase. Factors that generate a metabolic alkalosis: •Loss of hydrogen due to gastrointestinal losses: ■Gastric suction■Vomiting■Antacid therapy■Chloride-losing diarrhea•Renal losses: ■Diuretics■Mineralocorticoid excess■Hypercalcemia/milk-alkali syndrome■Low chloride intake•H+ shift into cells: ■Hypokalemia■Refeeding•Retention of bicarbonate: ■Massive blood transfusions■NaHCO3 administration•Contraction alkalosis: ■Diuretics■Sweat losses in cystic fibrosis Maintenance phase. Factors that permit maintenance of metabolic alkalosis: •Decreased GFR (due to volume depletion or renal failure) or•Increased tubular reabsorption of HCO3− (due to volume depletion, chloride depletion, hypokalemia, hyperaldosteronism) Urinary chloride measurement in diagnosis of metabolic alkalosis. •Urine Cl− <10 mEq/L (mmol/L): ■Vomiting■Nasogastric suction■Diuretics•Urine Cl− >20 mEq/L (mmol/L): ■In hypertension: ○Cushing syndrome○Primary hyperaldosteronism○Hypokalemia○Glucocorticoid remediable aldosteronism○Conditions of apparent mineralocorticoid excess■With normal/low blood pressure: ○Bartter syndrome○Gitelman syndrome •Metabolic alkalosis with low urinary chloride: ■Normal saline or ½ normal saline lowers plasma HCO3− by reversing the stimulus to renal Na+ retention, permitting NaHCO3 excretion, and increasing distal Cl− delivery, which promotes HCO3− secretion (“saline-responsive alkalosis”)•Metabolic alkalosis with high urinary chloride: ■Treatment of underlying disorder (eg, adrenal adenoma resection) and repletion of potassium •Inhibition of respiratory drive: ■Opiates■Anesthetics■Sedatives■Central sleep apnea■Obesity■Central nervous system lesions•Disorders of respiratory muscles: ■Muscle weakness: ○Myasthenia gravis○Periodic paralysis○Aminoglycosides○Guillain-Barré syndrome○Spinal cord injury○Acute lateral sclerosis○Multiple sclerosis■Kyphoscoliosis•Upper airway obstruction: ■Obstructive sleep apnea■Laryngospasm■Aspiration•Lung disease: ■Pneumonia■Severe asthma■Pneumothorax■Acute respiratory distress syndrome■Chronic obstructive pulmonary disease■Interstitial lung disease •Elevated Pco2 in PT leads to decreased intracellular pH, enhances H+ secretion in PT, leading to increased HCO3− generation over 5 days (3 to 5 mEq/L [mmol/L] HCO3− for every 10-mm Hg increase in Pco2) •Ventilatory support•NaHCO3− therapy controversial in this disorder: ■Perhaps beneficial in severely acidemic patient (eg, status asthmaticus) versus■Hazards of therapy in patients with reversible hypercapnea (eg, chronic obstructive pulmonary disease in which respiratory drive is depressed) •Hypoxemia ■Pulmonary diseases: ○Pneumonia○Interstitial fibrosis○Emboli○Edema■Congestive heart failure■Anemia•Stimulation of the medullary respiratory center: ■Hyperventilation■Hepatic failure■Septicemia■Salicylate intoxication■Pregnancy■Neurologic disorders•Mechanical ventilation •Lightheadedness•Paresthesias•Cramps•Carpopedal spasm •Decreased Pco2 in PT leads to increased intracellular pH, inhibits H+ secretion in the PT, leading to decreased HCO3− generation over 5 days (reduces serum concentration of HCO3− 3 to 5 mEq/L [mmol/L] for every 10-mm Hg decrease in Pco2) •Correction of underlying disorder•Increasing Pco2 in inspired air (breathing into paper bag) in setting of acute respiratory alkalosis •Identified by inappropriate or inadequate correction using the formulae for renal and respiratory compensation described in Table 1 •Mixed respiratory acidosis and metabolic alkalosis (eg, chronic obstructive pulmonary disease and diuretic therapy)•Mixed metabolic acidosis and metabolic alkalosis (eg, ketoacidosis and vomiting)•Mixed respiratory alkalosis and metabolic acidosis (salicylate intoxication) •Use of ΔAG to determine if mixed acid-base disturbance is present•The ΔAG = measured anion gap - expected anion gap•The ΔAG is most useful to distinguish concomitant metabolic alkalosis and anion gap metabolic acidosis•If ΔAG + measured bicarbonate is greater than physiologic bicarbonate concentrations (eg, 21 to 27 mEq/L [mmol/L]), an underlying metabolic alkalosis is present 1Arbus GS, Hebert LA, Levesque PR, Etsten BE, Schwartz WB: Characterization and clinical application of the “significance band” for acute respiratory alkalosis. N Engl J Med 280:117–123, 19692Batlle DC: Segmental characterization of defects in collecting tubule acidification. Kidney Int 30:546–554, 19863Batlle DC, Hizon M, Cohen E, et al: The use of the urinary anion gap in the diagnosis of hyperchloremic metabolic acidosis. N Engl J Med 318:594–599, 19884Brent J, McMartin K, Phillips S, et al: Fomepizole for the treatment of ethylene glycol poisoning. Methylpyrazole for Toxic Alcohols Study Group. N Engl J Med 340:832–838, 19995Caruana RJ, Buckalew VM Jr: The syndrome of distal (type 1) renal tubular acidosis: Clinical and laboratory findings in 58 cases. Medicine (Baltimore) 67:84–99, 19886Field M, Rao MC, Chang EB: Intestinal electrolyte transport and diarrheal disease (1). N Engl J Med 321:800–806, 19897Foster DW, McGarry JD: The metabolic derangements and treatment of diabetic ketoacidosis. N Engl J Med 309:159–169, 19898Gabow PA, Kaehny WD, Fennessey PV, Goodman SI, Gross PA, Schrier RW: Diagnostic importance of an increased anion gap. N Engl J Med 303:854–858, 19809Graf H, Leach W, Arieff AI: Evidence for a detrimental effect of bicarbonate therapy in hypoxic lactic acidosis. Science 227:754–756, 198510Jacobson HR, Seldin DW: On the generation, maintenance, and correction of metabolic alkalosis. Am J Physiol 245:F425-F432, 198311Karet FE, Finberg KE, Nelson RD, et al: Mutations in the gene encoding B1 subunit of H+-ATPase cause renal tubular acidosis with sensorineural deafness. Nat Genet 21:84–90, 199912Krapf R, Beeler I, Hertner D, Hulter HN: Chronic respiratory alkalosis: The effect of sustained hyperventilation on renal regulation of acid-base equilibrium. N Engl J Med 324:1394–1401, 199113Kurtz I, Maher T, Hulter HN, Schambelan M, Sebastian A: Effect of diet on plasma acid-base composition in normal humans. Kidney Int 24:670–680, 198314Levy LJ, Duga J, Girgis M, Gordon EE: Ketoacidosis associated with alcoholism in nondiabetic subjects. Ann Intern Med 78:213–219, 197315Narins RG, Cohen JJ: Bicarbonate therapy for organic acidosis: The case for its continued use. Ann Intern Med 106:615–618, 198716Pierce NF, Fedson DS, Brigham KL, Mitra RC, Sack RB, Mondal A: The ventilatory response to acute base deficit in humans: Time course during development and correction of metabolic acidosis. Ann Intern Med 72:633–640, 197017Roth KS, Foreman JW, Segal S: The Fanconi syndrome and mechanisms of tubular transport dysfunction. Kidney Int 20:705–716, 198118Sherman RA, Eisinger RP: The use (and misuse) of urinary sodium and chloride measurements. JAMA 247:3121–3124, 198219Szylman P, Better OS, Chaimowitz C, Rosler A: Role of hyperkalemia in the metabolic acidosis of isolated hypoaldosteronism. N Engl J Med 294:361–365, 197620Widmer B, Gerhardt RE, Harrington JT, Cohen JJ: Serum electrolyte and acid-base composition: The influence of graded degrees of chronic renal failure. Arch Intern Med 139:1099–1102, 197921White PC: Disorders of aldosterone biosynthesis and action. N Engl J Med 331:250–258, 1994 Total body K determined by internal and external K balance: Factors that regulate: •Acid-base/metabolic acidosis: differences between organic (limited K shifts) and inorganic hyperchloremic acidosis•Insulin: K moves from extracellular to intracellular sites•Tonicity: hyperglycemia, mannitol moves K from intracellular to extracellular sites•B2 adrenergic receptor: Catecholamines through B2 adrenergic receptor move K into cells; α adrenergic receptor prevents K movement from extracellular to cellular compartments•Clinical correlate: “stress hypokalemia” Renal K physiology: •K freely filtered•Filtered K reabsorbed in proximal convoluted tubule and proximal straight tubule•K added to distal loop of Henle (at least in deep glomeruli) so that, at tip of loop, fractional excretion of K (FEK) 150% of filtered load•K reabsorbed in ALH (Na, K2Cl cotransporter) so that, at beginning of distal convoluted tubule, FEK 15% of filtered load•K added to lumen of cortical collecting tubule so that, at end of this tubule, FEK 100% of filtered load•K secretion mediated by Na reabsorption through Na channel followed by Na extrusion by basolateral Na, K ATPase, resulting in increases in cell K and K extrusion into the lumen through K channels•K secretion regulated by aldosterone secretion (regulated by angiotensin II and total body K) and action (regulated by 11 B-oH steroid dehydrogenase and mineralocorticoid receptor) as well as distal nephron Na delivery and concentration•K reabsorbed by collecting tubule, through K/H exchange (regulated by decreases in total body K)•Urine K is independent of GFR above 30 mL/min (0.50 mL/s)•Increases in urinary K are due to increases in K secretion or decreases in K reabsorption 1Brown MJ, Brown DC, Murphy MB: Hypokalemia from beta2-receptor stimulation by circulating epinephrine. N Engl J Med 309:1414–1419, 19832Struthers AD, Whitesmith R, Reid JL: Prior thiazide diuretic treatment increases adrenaline-induced hypokalemia. Lancet 1:1358–1360, 19833Williams ME, Rosa RM, Silva P, Brown RS, Epstein FH: Impairment of extrarenal potassium disposal by alpha-adrenergic stimulation. N Engl J Med 311:145–149, 19844Giebisch G, Malnic G, Berliner RW: Control of renal potassium excretion, in Brenner BM, Rector FC (eds): The Kidney. Philadelphia, Saunders, 2000, pp 417–4545Giebisch G: Renal potassium transport: Mechanisms and regulation. Am J Physiol 274:F817-F833, 19986Scheinman S, Guay-Woodford LM, Thakker RV, Warnock DG: Genetic disorders of renal electrolyte transport. N Engl J Med 340:1177–1187, 1999 •Serum K less than 3.5 mEq/L (mmol/L) Normal total body K/transcellular shift. •Alkalemia•Insulin excess•“Stress” (eg, asthma attack, acute coronary syndrome, drug intoxication [cocaine] or withdrawal [alcohol], B2 adrenergic drugs)•Hypokalemic periodic paralysis•Thyrotoxicosis•Refeeding syndromes•Barium•Cesium hypothermia Decreased total body K. •Decreased K intake, or•Increased K losses: ■Gastrointestinal■Renal Spurious. •Extreme leukocytosis To decreases in total body K: use of urine K concentration, 24-hour urine K, transtubular K gradient: Low 24-hour urine K (<20 mEq [mmol]/d): extrarenal losses. •Metabolic acidosis: gastrointestinal losses•Normal pH: decreased intake, gastrointestinal losses•Metabolic alkalosis: gastrointestinal losses High 24-hour urine K (>20 mEq [mmol]/d): renal losses. •Metabolic alkalosis: ■Low urine chloride (<10 mEq [mmol]/d): vomiting, diuretics■High urine chloride (>20 mEq [mmol]/d): hypertension: ○“Normal” aldosterone: Cushing syndrome, Liddle syndrome, apparent mineralocorticoid excess syndrome○High aldosterone: primary aldosteronism, glucocorticoid remediable aldosteronism○Normal or low blood pressure: diuretics (during therapy), severe K depletion, Bartter syndrome, Gitelman syndrome•Variable pH: ■Magnesium depletion■Anionic drugs•Metabolic acidosis ■RTA types I and II •Cardiovascular: ■Arrhythmias■Digitalis toxicity•Neuromuscular: ■Smooth muscle: ○Ileus■Skeletal muscle: ○Weakness○Paralysis○Rhabdomyolysis•Endocrine: ■Glucose intolerance•Renal/electrolyte: ■Vasopressin resistance■Increased ammonia production■Metabolic alkalosis•Structural changes: ■Renal cysts■Interstitial changes■PT dilation, vacuolization •Estimate of K deficit: serum K may not reflect total body K•Reverse source of K loss•Symptomatic: intravenous K (rate, complications)•Asymptomatic: ■Metabolic acidosis: ○K plus citrate, or○HCO3■Metabolic alkalosis: ○K plus NaCl (chloride responsive)○Role of spironolactone, amiloride (chloride resistant)■Importance of magnesium therapy 1Osorio FV, Linas SL: Disorders of potassium metabolism, in Schrier RW (ed): Atlas of Diseases of the Kidney (vol 1; section 1, Disorders of Water, Electrolytes and Acid-Base). Philadelphia, Current Medicine, 1998, pp 2–172Weiner ID, Wingo CS: Hypokalemia: Consequences, causes, correction. J Am Soc Nephrol 8:1179–1188, 19973Ganguly A: Primary aldosteronism. N Engl J Med 339:1828–1834, 19984Galla JH: Metabolic alkalosis. J Am Soc Nephrol 11:369–375, 2000 •Serum K ≥5.0 mEq/L (mmol/L) Normal total body K: transcellular shift. •Exercise, especially in setting of β adrenergic receptor blockade and mineral acidosis•Hyperchloremic metabolic acidosis•Insulin deficiency•Hypertonicity•α adrenergic receptor stimulation•Tissue breakdown or ischemia, for example: ■Rhabdomyolysis■Gastrointestinal■Brain Increased total body K. •Increased intake: rare as sole cause•Decreased renal K excretion Spurious. •Thrombocytosis•Leukocytosis•Ischemic blood draw To increases in total body K: use of urine K concentration, 24-hour urine K, and/or transtubular K gradient (SK/Urine K ÷ Sosm/Uosm): Normal to high 24-hour urinary K (>40 to 60 mEq [mmol]/d): •Relative increase in K intake Low 24-hour urinary K (<20 to 40 mEq [mmol]/d): •Decrease renal K excretion: ■GFR >20 mL/min (0.33 mL/s): ○Decreased distal nephron Na delivery○Decreased mineralocorticoid production or action○Decreased total body Na○Increased total body Na: □heart failure□cirrhosis○Decreased production: □Addison disease□Isolated hypoaldosteronism (hereditary, acquired, drugs [angiotensin-converting enzyme inhibitors, heparin, nonsteroidal anti-inflammatory drugs, COX2 inhibitors], infection [human immunodeficiency virus], chronic kidney disease [diabetes, tubular interstitial diseases, others])○Decreased action: □Hereditary (pseudohypoaldosteronism types I and II)□Acquired (drugs [angiotensin receptor blockers, amiloride, spironolactone, triamterene] and pseudohypoaldosteronism [hereditary, acquired: sickle cell disease, renal allograft disease, obstruction])■GFR <20 mL/min (0.33 mL/s): ○Endogenous or exogenous K○Drugs that impair K excretion •May be disproportionately greater than level of serum K•Cardiovascular: ■T-wave abnormalities■Lengthened segments■Bradyarrhythmias•Neuromuscular: ■Ileus■Paresthesias■Weakness■Paralysis•Renal/electrolyte: ■Decreased ammonia production■Metabolic acidosis •Who requires emergent therapy: ■Electrocardiogram abnormalities■Ileus■Paralysis•Emergent therapies: ■Doses, pharmacology■Stabilize cell membrane: Ca■Shift K from extra to intracellular compartments: ○Insulin (± glucose)○HCO3○Albuterol (B2 adrenergic receptor agonist)■Decrease total body K ○K exchange resin (oral or rectal)○Hemodialysis•Prevention of hyperkalemia: ■Importance of diet■Recognition of drugs that decrease K secretion■Role of adequate distal Na delivery■K exchange resins 1Weiner ID, Wingo CS: Hyperkalemia: A potential silent killer. J Am Soc Nephrol 9:1535–1543, 19982Weiner ID, Linas SL, Wingo CS: Disorders of potassium metabolism, in Johnson RJ, Feehally J (eds): Comprehensive Clinical Nephrology. St. Louis, MO, Mosby, 2003, pp 109–1233Greenberg A: Hyperkalemia: Treatment options. Semin Nephrol 18:46–57, 19984Palmer BF: Current concepts: Hyperkalemia caused by inhibitors of the renin-angiotensin-aldosterone systems. N Engl J Med 351:585–592, 20045Halperin ML, Kamel KS: Electrolyte quintet: Potassium. Lancet 352:135–140, 19986Allon MT, Copkney C: Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients. Kidney Int 38:869–872, 19907Allon M: Hyperkalemia in end-stage renal disease: Mechanisms and management. J Am Soc Nephrol 6:1134–1142, 1995" @default.
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