eMedicine Specialties > Nephrology > Acid-Base, Fluid, and Electrolyte Disorders
Hyperchloremic Acidosis: Follow-up
Updated: Jul 30, 2009
Follow-up
Deterrence/Prevention
Avoiding drugs that can aggravate hyperchloremic acidose
- Drugs that increase GI bicarbonate loss include calcium chloride, magnesium sulfate, and cholestyramine.
- Drugs or toxins that can induce pRTA include streptozotocin, lead, mercury, arginine, valproic acid, gentamicin, ifosfamide, and outdated tetracycline
- Drugs or toxins that can cause dRTA include amphotericin B, toluene, nonsteroidal anti-inflammatory drugs, lithium,5 and cyclamate
Complications
- Underlying GI, renal, or autoimmune conditions
- Hereditary disorders
- Effects of agents used in treatment (eg, cardiac complications)
Patient Education
- Inform patients about the dietary issues related to the hyperchloremic acidoses.
- For excellent patient education resources, visit eMedicine's Endocrine System
Center, Kidneys and Urinary System Center, and Growth Hormone Deficiency Center. Also, see eMedicine's patient education article Low Potassium.
Miscellaneous
Medicolegal Pitfalls
- Failure to confirm the cause of the acidosis
- Failure to diagnose a primary condition
- Failure to inform patients about dietary issues related to their acidosis
- Failure to recognize and to inform the patient about possible adverse effects of agents used for treatment
More on Hyperchloremic Acidosis |
| Overview: Hyperchloremic Acidosis |
| Differential Diagnoses & Workup: Hyperchloremic Acidosis |
| Treatment & Medication: Hyperchloremic Acidosis |
Follow-up: Hyperchloremic Acidosis |
| References |
| Further Reading |
| « Previous Page |
References
Liborio AB, Daher EF, de Castro MC. Characterization of acid-base status in maintenance hemodialysis: physicochemical approach. J Artif Organs. 2008;11(3):156-9. [Medline].
Davenport A. Potential adverse effects of replacing high volume hemofiltration exchanges on electrolyte balance and acid-base status using the current commercially available replacement solutions in patients with acute renal failure. Int J Artif Organs. Jan 2008;31(1):3-5. [Medline].
Blake-Palmer KG, Karet FE. Cellular physiology of the renal H+ATPase. Curr Opin Nephrol Hypertens. Jun 24 2009;[Medline].
Basic DT, Hadzi-Djokic J, Ignjatovic I. The history of urinary diversion. Acta Chir Iugosl. 2007;54(4):9-17. [Medline].
Grünfeld JP, Rossier BC. Lithium nephrotoxicity revisited. Nat Rev Nephrol. May 2009;5(5):270-6. [Medline].
Batlle D, Kurtzman NA. Distal renal tubular acidosis: pathogenesis and classification. Am J Kidney Dis. May 1982;1(6):328-44. [Medline].
Burton DR. Metabolic acidosis. In: Clinical Physiology of Acid-Base and Electrolyte Disorders. 4th ed. New York, NY: McGraw-Hill; 1994:. 540-604.
DuBose TD Jr. Hyperkalemic hyperchloremic metabolic acidosis: pathophysiologic insights. Kidney Int. Feb 1997;51(2):591-602. [Medline].
Garella S, Salem MM. Clinical acid-base disorders. In: Oxford Textbook of Clinical Nephrology. 2nd ed. Oxford, UK: Oxford University Press; 1998:. 313-26.
Lash JP, Arruda JA. Laboratory evaluation of renal tubular acidosis. Clin Lab Med. Mar 1993;13(1):117-29. [Medline].
Rothstein M, Obialo C, Hruska KA. Renal tubular acidosis. Endocrinol Metab Clin North Am. Dec 1990;19(4):869-87. [Medline].
Walmsley RN, White GH. Normal "anion gap" (hyperchloremic) acidosis. Clin Chem. Feb 1985;31(2):309-13. [Medline].
Further Reading
Clinical guidelines:
Metabolic acidosis and growth in children. Caring for Australasians with Renal Impairment - Disease Specific Society. 2005 Dec. 3 pages. NGC:006105
Clinical trials:
Genetic Study of Nephrolithiasis in Gouty Diathesis
Keywords
hyperchloremic acidosis, acidosis, metabolic acidosis, renal acidosis, renal tubular, renal acidosis, metabolic acidosis anion gap, renal tubular acidosis, anion gap, AG acidosis, nonanion gap acidosis, normal anion gap acidosis, low plasma bicarbonate, low bicarbonate concentration, chronic metabolic acidosis, bicarbonate-wasting acidosis, hyperchloremic metabolic acidosis, proximal renal tubular acidosis, pRTA, distal renal tubular acidosis, dRTA, hypokalemic distal renal tubular acidosis, RTA type I, type I RTA, hyperkalemic distal renal tubular acidosis, RTA type IV, type IV RTA, classic distal tubular acidosis, uremic acidosis, gastrointestinal bicarbonate loss, bicarbonaturia, bicarbonate wasting, potassium wasting, hypokalemia
Follow-up: Hyperchloremic Acidosis