Acid-Base/Electrolytes
Andrew J. Klein, M.D.
Chi-yuan Hsu, M.D., M.Sc.
Algorithm for acid-base disorders
1. Establish database: ABG, chem-7, anion gap (remember to correct anion gap for hypoalbuminemia. For every 1 g/dl decline in serum albumin, a ~2.5 mEq/L decrease in anion gap will occur).
2. Identify the main disorder:
|
Disorder |
pH |
pCO2 (mmHg) |
HCO3 (mEq/L) |
|
respiratory alkalosis |
> 7.40 |
< 40 |
|
|
respiratory acidosis |
< 7.40 |
> 40 |
|
|
metabolic alkalosis |
> 7.40 |
|
> 24 |
|
metabolic acidosis |
< 7.40 |
|
< 24 |
3. Evaluate compensation using formulas (see below). For respiratory disorders, this will determine chronicity. If compensation does not match expected values, there is a mixed acid-base disorder.
4. Determine the anion gap (AG, normal = 12). If the AG is 20 or greater, then a metabolic acidosis almost certainly exists regardless of pH or HCO3.
5. If there is an AG, determine whether this alone accounts for the change in HCO3. Calculate the gap-gap (delta-gap) = patient’s anion gap – 12 (normal anion gap). Then calculate the delta HCO3 = normal HCO3 (use 25) – the patient's HCO3. The delta-gap ÷ delta HCO3 should normally be between 1-2 (because of non-bicarbonate buffers). A value < 1 suggests a combined non-gap and gap acidosis. A value > 2 suggests a concomitant metabolic alkalosis.
6. Compensation formulas:
· Metabolic acidosis:
- pCO2 decreases 1.2 for each mmol/L change in HCO3 or
- pCO2 = last two digits of pH
· Metabolic alkalosis: pCO2 increases 0.6 for each mmol/L change in HCO3
· Respiratory acidosis:
- Acute: HCO3 increases 0.1 for every mmHg change in pCO2
- Chronic: HCO3 increases 0.35 for every mmHg change in pCO2
· Respiratory alkalosis:
- Acute: HCO3 decreases 0.22 for every mmHg change in pCO2
- Chronic: HCO3 decreases 0.5 for every mmHg change in pCO2
7. Differential diagnosis for each disorder:
· Respiratory alkalosis: CNS disorders, hypoxia, pulmonary receptor stimulation (asthma, pneumonia, pulmonary edema, PE), anxiety, drugs (ASA, theophylline), liver failure, sepsis.
· Respiratory acidosis: respiratory center inhibition (opiates, O2 in CO2 retainer), neuromuscular disorder (Guillain–Barré, myasthenia gravis, hypokalemia), chest wall disorder, airway obstruction, acute and chronic lung disease.
· Metabolic alkalosis:
- Chloride–responsive (urine Cl < 10): vomiting, NG drainage, diuretics, post–hypercapneic, cystic fibrosis, villous adenoma, congenital chloride diarrhea.
- Chloride–resistant (urine Cl > 20): hypokalemia, primary aldosteronism, secondary aldosteronism (CHF, cirrhosis & ascites), Cushing’s, Gitelman’s Liddle’s, licorice.
- Miscellaneous: poorly resorbed anion (high dose carbenicillin or other PCN derivative), refeeding alkalosis, administration of alkali (e.g. overshoot from treatment of acidosis, massive transfusions with citrate anticoagulant, milk alkali).
· Metabolic acidosis (gap acidosis) - there is an unmeasured anion:
· Metabolic acidosis (non-gap acidosis): Clinically, the major distinction is between renal and extrarenal (usually GI) causes. To differentiate, calculate the urine anion gap (UAG) = UNa + UK – UCl. A negative UAG (more Cl than Na + K) implies the kidney is appropriately compensating for acidosis by secreting NH4+ (the unmeasured cation), further implying a nonrenal cause. A highly positive UAG implies deficiencies in excretion of acid.
- Nonrenal causes of non-gap metabolic acidosis – HCO3 wasting: GI causes (diarrhea, ileus, fistula, villous adenoma), urinary tract diversions (ureterosigmoidostomy, ileal conduit), administration of chloride: dilutional acidosis, NH4Cl, TPN, cholestyramine.
- Renal causes of non-gap metabolic acidosis: renal failure, renal tubular acidosis.
Haber RJ. A practical approach to acid-base disorders. West J Med 1991 Aug;155(2):146-51
Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000 Feb;11(2):369-75.
|
|
Type I |
Type II |
Type IV |
|
Location |
Distal |
Proximal |
Distal |
|
Defect |
Distal acidification |
Diminished HCO3 resorption |
Aldosterone deficiency or resistance |
|
Urine Ph |
> 6.0 |
Variable |
Usually < 5.3 |
|
Plasma K+ |
Low or normal |
Low or normal |
High |
|
Plasma HCO3 |
Very low (may be < 10 mEq/L) |
Moderately low (14-20) |
Usually >15 |
1. Common causes:
· Type I RTA: primary, amphotericin, Sjogren’s, myeloma, marked volume depletion.
· Type II RTA: primary, myeloma, acetazolamide, heavy metals (Pb, Cd, Hg, others), Fanconi syndrome.
· Type IV RTA: most commonly diabetes mellitus. Also commonly caused by heparin, Addison's disease, NSAIDs,. The main problem here is hyperkalemia and not acidosis.
2. Urinary anion gap (See Acid-Base/Electrolytes: Algorithm for acid-base disorders): only applicable to type I and IV RTA. Not validated for type II RTA.
3. Note: Does the patient have renal insufficiency? Renal insufficiency is a much more common cause of “renal acidosis” than RTA among hospitalized adults.
Smulders YM, Frissen PH, Slaats EH, Silberbusch J. Renal tubular acidosis. Pathophysiology and diagnosis. Arch Intern Med. 1996 Aug 12-26;156(15):1629-36.
1. Definition: A water disorder due to excess water retention in relation to solute. Na+ less than 130 meq/L; the most common electrolyte abnormality seen in hospitalized patients.
2. Symptoms: confusion, seizures, coma.
3. Initial diagnostics: assess volume status, check serum osmolality, urine osmolality, urine Na+:
· Isoosmotic hyponatremia (pseudohyponatremia, Sosm 280-295): lab artifact due to hyperproteinemia or hyperlipidemia (rarely seen with modern assays).
· Hyperosmotic hyponatremia (Sosm >295): due to hyperglycemia (no osmolar gap) or IV infusions (mannitol, glycine – assess with osmolar gap).
· Hypoosmotic hyponatremia (“true” hyponatremia, Sosm < 280): except for polydipsia and beer potomania these disorders are characterized by high ADH levels and inappropriately high urine osms (verify urine Osm > serum Osm). First assess volume status:
- Hypovolemic: “appropriate” ADH secretion in an effort to maintain intravascular volume.
a. Extrarenal salt loss (UNa < 10): GI (emesis, diarrhea), skin (burns), hemorrhage, surgical drains. Also remote diuretic use. Note that patients will have to continue drinking free water in order to dilute themselves down.
b. Renal salt loss (UNa > 20): diuretics, cerebral salt wasting syndromes.
- Euvolemic: preserved sodium/volume regulation.
a. Hypothyroidism: check TSH.
b. Adrenal insufficiency: check cortisol or cosyntropin stimulation test.
c. Psychogenic polydipsia and beer potomania: check simultaneous urine and serum osms. (These are low ADH states with low urine osms.)
d. SIADH: diagnosis of exclusion, usually with urine Na > 20 and low serum uric acid. Differential diagnosis:
· Pulmonary: pneumonia, TB, etc.
· CNS processes: trauma, CVA, SAH, brain tumor, meningitis, Guillain-Barre,
etc.
· Neoplastic: Small cell lung cancer is a classic example.
· Drugs: increased ADH secretion (chemotherapy agents such as cyclophosphamide, vincristine; carbamazepine; neuroleptics), potentiated action of ADH (chlorpropamide, cyclophosaphamide).
· Postoperative states: hypotonic fluid load plus pain-induced increased ADH.
· Others: pain, numerous other stressors
- Hypervolemic: third-spacing with functional intraarterial volume depletion. Differential diagnosis: cirrhosis, CHF, nephrotic syndrome.
4. Hyponatremia in HIV: seen in 50% of patients hospitalized for HIV and in 20% of ambulatory patients, and is often associated with pneumonia and/or CNS processes. If hyponatremia is present at admission, it is just as likely to be due to hypovolemic GI loss as to euvolemic SIADH. However, if hyponatremia occurs after admission, most patients have euvolemic SIADH. In end-stage HIV, always consider adrenal insufficiency as a cause of hyponatremia.
5. Treatment: Note—correction too fast may result in central pontine myelinolysis (flaccid paralysis, dysarthria, and dysphagia).
· Equation for correction: To estimate the change in serum Na+ by 1liter of any IVF:
Change in serum Na+ per liter of fluid = (IVF[Na+] + IVF[K+]) – serum Na+
TBW(liters) + 1
- Estalish hemodynamic stability: replete with normal saline.
- Correct hyponatremia: maximum rate of correction: 8-10 mmol/day, though if symptomatic, correct at 1-2 mmol/hour until symptoms resolves.
- Choice of fluids: 3% NaCl: 513 mEq Na+, 0.9% NaCl (NS): 154 mEq Na+
- Symptomatic: 3% NaCl + furosemide
- Asymptomatic: fluid restriction to 1.0 liters/day
- Demeclocycline is rarely indicated, but may be used if patients cannot adhere to H20 restriction or need additional therapy.
- H20 restriction: 1.0-1.5 liters/day
- Diuretics: furosemide
- Emergent dialysis, esp if indicated for volume
- Note: hypertonic saline is not routinely recommended.
Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med. 2000 May 25;342(21):1581-9.
a. Central DI: (Uosm increase with DDAVP): CNS trauma or infection, tumors, aneurysms, Sheehan’s, granulomatous disease (sarcoid, histiocytosis X).l
b. Nephrogenic DI: DI (no change in Uosm with DDAVP): drugs (lithium, demeclocycline), hypercalcemia, hypokalemia.
- Note: because most patients with DI sense thirst and have access to water, they are usually not hypernatremic at baseline).
3. Causes:
· Hypotonic fluid loss:
- Renal causes (hypovolemic, urine output > 1L/day, Uosm > 500; UNa > 20): osmotic diuresis.
- Gastrointestinal causes (hypovolemic, urine output < 500 ml/day, Uosm > 500; UNa < 10): vomiting, NG drainage, diarrhea, osmotic cathartics (lactulose), enterocutaneous fistulas.
- Cutaneous causes (hypovolemic, urine output < 500 ml/day, Uosm > 500; UNa < 10): burns, excessive sweating (exercise, heat exposure).
- Causes: hypertonic NaCl or NaHCO3 infusions, hypertonic feedings. Each amp of HCO3 is 50 mEq so to make an isotonic HCO3 solution add D5W to 3 amps HCO3 to get a solution that has 150 mEq/L Na+. Do not give D5NS with the 3 amps of HCO3 as this creates a hypertonic solution.
4. Treatment:
· Main concern: cerebral edema if correction is too rapid. Hypernatremia ® flux of fluid from brain to ECF ® brain shrinkage ® brain cell production of organic osmoslytes ® flux of fluid into brain cells ® normal brain volume. If hypernatremia is corrected too rapidly, the presence of the organic osmolytes can cause cerebral edema.
· Correct the underlying cause of hypernatremia (DDAVP for central DI; low Na+ diet & thiazide for nephrogenic DI; stop hypertonic fluids, treat hypercalcemia, control pyrexia, etc.).
· Choice of fluid for replacement:
- Hypernatremia with hypovolemia: isotonic normal saline to restore the volume deficit and treat the hyperosmolality. This should be followed by ½ normal saline (0.45%) to replace any remaining free water deficit.
- Hypernatremia with euvolemia: water drinking or D5W will result in excretion of excess sodium in the urine.
- Hypernatremia with hypervolemia: D5W to reduce hyperosmolality. Note that will expand the intravascular volume, and loop diuretics (furosemide 0.5-1 mg/kg) should be used to remove excess sodium.
· Correct the hypernatremia:
- Maximum rate of correction: 10 mmol/L/day
- Mode of correction: PO/NG tube (recommended) or IVF
- Equation for correction: To estimate the change in serum Na+ by 1liter of any IVF:
Change in serum Na+ per liter of fluid = (IVF[Na+] + IVF[K+]) – serum Na+
TBW(liters) + 1
Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med. 2000 May 18;342(20):1493-9
1. Causes:
· Inadequate intake
· GI losses: vomiting, diarrhea, laxative abuse, fistula, villous adenoma
· Renal losses: drugs (diuretics, gentamicin, amphotericin, carbenicillin), excess mineralocorticoids (Cushing’s, hyperaldosteronism,), congenital (Gilteman’s, Liddle’s), hyperglycemia (excessive diuresis); hypomagnesemia, alcoholism.
· Potassium shift into the cell: alkalosis (metabolic & respiratory), increased insulin, hypokalemic periodic paralysis, beta-agonists (nebulizers).
2. Symptoms/Signs:
3. ECG: T wave flattening, U waves, arrhythmias (e.g. PSVT, A-fib), and ST depression, pseudo–prolonged QT. Note—hypokalemia increases the likelihood of digitalis toxicity.
4. Diagnosis: greater than 30 mEq/day of urinary potassium loss with hypokalemia suggests a "renal leak". The diagnosis of hypokalemia is usually clear by history.
5. Treatment:
· Check creatinine first – supplement patients with renal insufficiency cautiously.
· Replete magnesium
· Supplement to keep near 4.0 mmol/L
· PO KCl causes GI upset: give max 40 mEq at a time, consider elixir form
· IV KCl should be given no faster than 10 mEq/hr through a peripheral IV or 20 mEq/hr through a central line.
· In the ICUs, you will save sleep by writing a sliding scale, only when renal function is normal (see Sliding Scales: Potassium)
Gennari FJ. Hypokalemia. N Engl J Med. 1998 Aug 13;339(7):451-8.
1. Causes:
· Spurious: hemolysis during phlebotomy, greatly increased platelets or WBC
· Excessive intake: ingestion, iatrogenic
· Insufficient loss: renal failure, type IV RTA, adrenal insufficiency or other hypomineralocorticoid state, drugs (spironolactone, ACE inhibitor, TMP-SMX, digitalis overdose)
· Cellular release of K+: acidosis, cell death (rhabdomyolysis, burns, tumor lysis), retroperitoneal hemorrhage
2. Symptoms/signs: muscle weakness, abdominal distension. Usually asymptomatic, which gives rise to the admonition – the first sign of hyperkalemia is asystole.
3. ECG: tall peaked T waves, PR prolongation followed by loss of P waves, QRS widening; V-fib.
4. Treatment:
· STAT ECG
· Verify with a repeat lab draw
· Immediate treatment (works in minutes): for ECG changes, stabilize myocardium with 1-2 amps of calcium gluconate (lasts 30-60 minutes)
· Temporary treatment (shift K into cells):
- 2 amps D50 plus 10 U regular insulin IV. Onset: 15-60 min. Duration 4-6 hours.
- ß2-agonists, e.g. Albuterol. Onset: 15-30 min. Duration: 2-4 hours.
- 2 amps NaHCO3: Onset: 15-30 min Duration: 1-2 hours. Best reserved for non-ESRD patients with severe hyperkalemia and acidosis; commonly used but probably least effective.
· Long-lasting elimination:
· Kayexalate: ion exchange resin. 30 g PO (repeat q2 hrs until BM) or retention enema
· Loop diuretic: increases renal potassium secretion. Duration: 0.5-2 hours. Dose: furosemide 40-160 mg IV ± NaHCO3 or normal saline
· Dialysis: note that per hour CVVHD corrects potassium more slowly than conventional hemodialysis
Halperin ML, Kamel KS. Potassium. Lancet. 1998 Jul 11;352(9122):135-40
1. Causes:
· Decreased intake: malnutrition (alcoholism), malabsorption, diarrhea, NG aspiration.
· Increased renal excretion: osmotic diuresis, hyperparathyroidism, drugs (loop diuretics, aminoglycosides, amphotericin, cisplatin), volume expansion, tubulointerstitial diseases.
· Others: diabetes mellitus, post-parathyroidectomy (hungry bone syndrome), respiratory alkalosis, pregnancy.
2. Signs:
· Tremor, fasciculations, ataxia, nystagmus, tetany, seizures
· Hypokalemia, hypocalcemia
· PR and QT prolongation
3. Treatment: supplement to keep 2.0 or greater except in renal failure patients. Oral preparations differ from one hospital to another. Note that oral preparations cause diarrhea in larger doses.
|
Formulation |
Dose per tablet |
Typical dose |
|
Mag complex |
300 mg elemental Mg |
1–2 tab qd |
|
Mag oxide |
420 mg (240 mg elemental Mg) |
1–2 tab qd |
|
Mag gluconate |
500 mg (27 mg elemental Mg) |
1–2 tab qd |
· For parenteral therapy, MgSO4 IV comes in amps, 1 amp = 1 g (8 mEq). Rate = 1 g/hour.
· In the ICU's, you can write a sliding scale, only when renal function is normal (see Sliding Scales: Magnesium).
Agus ZS. Hypomagnesemia. J Am Soc Nephrol. 1999 Jul;10(7):1616-22.
.
1. Causes:
· Insufficient excretion: Renal failure (avoid magnesium-containing laxatives in these patients).
· Excess intake: iatrogenic—overaggressive replacement, laxative use (with renal insufficiency), administration during treatment for preeclampsia/eclampsia.
2. Signs (rarely present until Mg > 4 mEq/L): areflexia, lethargy, weakness, paralysis, respiratory failure, hypotension, bradycardia, coma, cardiac arrest.
3. Treatment:
· Asymptomatic: hold magnesium supplementation.
· Symptomatic: 1 amp calcium gluconate IV over 10 minutes to antagonize Mg. Support ventilation and heart rate if necessary. Definitive therapy requires dialysis.
1. Correct for hypoalbuminemia: for every 1 mg/dL decrease in albumin, increase the Ca++ level by 0.8 mg/dL. If albumin is < 2, check ionized Ca++. Note that alkalosis augments Ca++ binding to albumin, decreasing the amount of ionized (effective) Ca++ and increasing severity of symptoms at a given level.
2. Signs: paresthesias, tetany (especially carpopedal spasm), lethargy, confusion, seizures, Trousseau’s sign (carpal spasm occurring after the occlusion of the brachial artery with a blood pressure cuff for 3 minutes), Chvostek’s sign (contraction of the facial muscle in response to tapping the facial nerve anterior to the ear), QT prolongation.
3. Causes:
· Insufficient GI absorption: hypoparathyroidism or pseudohypoparathyroidism (PTH resistance), vitamin D deficiency, renal failure (1,25(OH)2-vitamin D deficiency), critically ill patients, hypomagnesemia (inhibits PTH release and action).
· Intra-corporeal shifts: acute pancreatitis, rhabdomyolysis, tumor lysis syndrome, "hungry bones" s/p parathyroidectomy.
· Meds: e.g. loop diuretics
· HIPOCAL pneumonic
|
- |
H |
Hypoparathyroidism, hypo/hypermagnesemia |
|
- |
I |
Infection, especially gram negative sepsis |
|
- |
P |
Pancreatitis |
|
- |
O |
Overload (rapid intravascular volume expansion) |
|
- |
C |
Chronic renal failure-most common cause (or other vitamin D deficient states): decreased formation of active vitamin D; decreased intestinal Ca++ absorption. |
|
- |
A |
Absorption abnormalities: |
|
- |
L |
Loop diuretics occasionally cause enhanced renal excretion of Ca++ |
4. Treatment:
· PO: CaCO3 500-1000 mg TID between meals (to maximize absorption). Also consider vitamin D (give 1,25(OH)2-vit. D in patients with renal failure).
· IV: max 10 mEq/hour. CaCl2 has 14mEq/amp, Ca gluconate only 4.65 mEq/amp (one amp = one gram). Give 5-15 mEq at a time, more if necessary.
· Correct hypomagnesemia.
· Beware that treatment of concomitant metabolic acidosis may further reduce ionized calcium level because both hydrogen ions and calcium are bound to albumin. As acidosis is corrected, hydrogen ions dissociate from albumin, allowing calcium to bind to albumin and further reducing the ionized calcium level.
Bushinsky DA, Monk RD. Electrolyte quintet: Calcium. Lancet. 1998 Jul 25;352(9124):306-11.
1. Causes: 90% due to hyperparathyroidism or malignancy. All etiologies are due to a combination of increased bone resorption, increased GI absorption, and decreased renal excretion:
· Primary hyperparathyroidism: mostly commonly due to adenoma; occasionally due to parathyroid hyperplasia; rarely due to parathyroid carcinoma.
· Malignancy:
- PTHrP-mediated (humoral): e.g. squamous cell lung carcinoma
- local osteolytic destruction (mediated by local cytokines): multiple myeloma some solid tumor metastases (e.g. breast cancer)
· Granulomatous disease: sarcoidosis, tuberculosis
· Thiazide diuretics
· Milk-alkali syndrome
· Vitamin D toxicity
· Paget’s disease
· Other endocrine: hyperthyroidism
· Immobilization (especially among younger adults)
· Familial hypocalciuric hypercalcemia
· Lithium
· ESRD: tertiary hyperparathyroidism, adynamic bone disease
2. Signs: “Stones, moans, groans, with psychic overtones”
· Renal: polyuria, nephrolithiasis, renal failure, ectopic calcification
· GI: anorexia, nausea, vomiting, constipation
· Neuro: weakness, fatigue, confusion, stupor, coma
· ECG: shortened QT interval
3. Initial evaluation: initial work-up may include calcium, phosphorous, albumin, ionized calcium, alkaline phosphatase, and PTH. Also consider vitamin D levels, PTHrP, SPEP, TSH, and imaging (CXR, bone scan, bone survey, CT scans, etc).
4. Treatment:
· IVF volume resuscitation and saline diuresis: at least 3-4 L in first 24 hours.
· IV lasix after volume repleted (urine Na and Cl > 90). Keep I =O.
· Pamidronate: 90 mg IV over 24hr (for Ca >13.5). Treatment of choice in hypercalcemia of malignancy. Side effects include decreased Mg and phos and low-grade temperature. Dose reduce with renal insufficiency.
· Calcitonin (salmon): 4-8 U SQ/IM q6-12hr. Works within hours, but weak effect (1-3 mg/dL) that wanes after 2-3 days.
· Glucocorticoids: decrease GI absorption, also may be anti-neoplastic
Ziegler R. Hypercalcemic crisis. J Am Soc Nephrol. 2001 Feb;12 Suppl 17:S3-9.
1. Causes:
· Decreased intake: malnutrition, malabsorption, vitamin D deficiency, phosphate binders, alcoholism.
· Shifts from serum into cells: respiratory alkalosis, refeeding, hyperalimentation, effects of insulin/glucagon/androgens.
· Increased urinary secretion: renal tubular defect, DKA.
2. Signs (generally seen only with total body depletion and serum PO4 < 1 mg/dL): weakness, rhabdomyolysis, respiratory compromise/failure, CHF, paresthesias, confusion, stupor, seizures, coma.
3. Therapy:
· PO: 1-2 tabs TID-QID:
- Neutraphos (250 mg tab = 75 mL solution) contains 8 mmol phos + 7 mEq Na + 7 mEq K.
- K-Phos (250 mg tab = 75 mL solution) contains 8 mmol phos + 14 mEq K
· IV: 15mmol Kphos (contains 22mEq K) or NaPhos (22mEq Na) over 2-6 hours
· Follow Ca, K, and Mg levels.
Weisinger JR, Bellorin-Font E. Magnesium and phosphorus. Lancet. 1998 Aug 1;352(9125):391-6
1. Causes:
· Increased intake (external/internal): overzealous PO4 replacement, excessive vitamin D, TPN, fleets enema/rhabdomyolysis, cell destruction (tumor lysis), metabolic acidosis (lactic- or ketoacidosis), respiratory acidosis (phosphate incorporation into cells is impaired).
· Decreased excretion: renal failure, hypoparathyroidism.
2. Signs: mostly asymptomatic; ectopic calcifications if Ca x PO4 product > 70. Hyperphosphatemia in chronic kidney disease leads to secondary hyperparathyroidism and renal osteodystrophy.
3. Treatment: bind phosphorous in the gut (give meds with meals to maximize binding). Avoid calcium-containing compounds if serum calcium is also high.
· CaCO3 (OsCal, TUMS): 500-1000 mg (or more) PO TID with meals
· Calcium acetate (PhosLo): 1-2 tabs (667 mg each) PO TID with meals
· Aluminum hydroxide (Amphogel): 600 mg PO TID with meals. Most effective, but can cause bone and CNS toxicity with long-term use
· Renagel: 2-4 capsules (either 403 mg or 806 mg cap dose) PO TID with meals. Weaker than amphogel but safe.
· Phosphorous is not as well hemodialyzed; convective clearance with CVVHD is better but the volume of distribution is large.
Weisinger JR, Bellorin-Font E. Magnesium and phosphorus. Lancet. 1998 Aug 1;352(9125):391-6