Renal tubular acidosis differential diagnosis: Difference between revisions

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{{Renal tubular acidosis}}
[[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Renal_tubular_acidosis]]
{{CMG}} ; {{AE}} {{ADG}}
{{CMG}} ; {{AE}} {{ADG}}


==Overview==
==Overview==
Renal tubular acidosis must be differentiated form other diseases as most of them have a similar presentation of acidosis on [[Arterial blood gas|ABG]], [[dehydration]] ([[Nausea and vomiting|nausea]] and vomiting) and specific history pertaining to underlying etiology.
==Differentiating Renal tubular acidosis from other diseases==
==Differentiating Renal tubular acidosis from other diseases==
Renal tubular acidosis must be differentiated form other diseases causing metabolic acidosis such as ketoacidosis, sepsis,  
Renal tubular acidosis must be differentiated form other diseases as most of them have a similar presentation of acidosis on [[Arterial blood gas|ABG]], [[dehydration]] ([[Nausea and vomiting|nausea]] and vomiting) and specific history pertaining to underlying etiology. 
 
 
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==References==
==References==
{{reflist|2}}
{{reflist|2}}

Latest revision as of 21:08, 14 February 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Renal tubular acidosis must be differentiated form other diseases as most of them have a similar presentation of acidosis on ABG, dehydration (nausea and vomiting) and specific history pertaining to underlying etiology.

Differentiating Renal tubular acidosis from other diseases

Renal tubular acidosis must be differentiated form other diseases as most of them have a similar presentation of acidosis on ABG, dehydration (nausea and vomiting) and specific history pertaining to underlying etiology.


Category Disease Mechanism Clinical Paraclinical Gold standard diagnosis Other findings
Symptoms Signs Lab data
ABG CBC Chemistry Renal U/A
↑ acid

production

Loss of

bicarbonate

↓ renal acid

excretion

Fever N/V Diarrhea Dyspnea Toxic/ill BP Dehydration Level of consciousness HCO3− paCO2 O2 WBC Hb BS Cl− K+ Na+ Ketones Lactic acid Serum AG[1] Osmolar gap[2] Bun Cr Urine pH Urine AG Urine ketone
Ketoacidosis Diabetic ketoacidosis[3] + − − + + + + + ↓ + ↓ ↓ ↓ Nl to ↓ ↑ Nl to ↑ ↑↑ Nl ↑ ↓ ↑ ↑ ↑ ↑ Nl to ↑ Nl ↓ + + Clinical + hyperglycemia + ketosis
  • Labs might show elevated K+ even in K+ depletion due to extravasation of intracellular K+ in exchanged with extracellular H+
Starvation[4] + − − − + − − + ↓ + ↓ ↓ ↓ Nl Nl Nl Nl to ↓ Nl ↓ ↓ ↑ Nl ↑ Nl Nl Nl Nl + − Clinical manifestation
Alcoholic ketoacidosis (Ethanol)[5] + − − − + ± − + ↓ ↑ + Agitated ↓ ↓ ↓ Nl to ↑ Nl to ↑ ↓ Nl ↑ Nl ↓ ↓ ↑↑ ↑ ↑ ↑↑ ↑ Nl ↓ + + Clinical manifestation + ketosis
Systemic Sepsis[6] + − − + + − + + ↓ ↑ + ↓ ↓ ↓ Nl to ↓ ↑ Nl Nl Nl ↑ ↓ Nl Nl to ↑ Nl Nl ↑ ↑ Nl − − Clinical manifestation and lab finding
  • Not applicable
Ischemia[7] + − − − + − + + ↓ + − ↓ ↓ ↑ Nl to ↓ Nl to ↑ Nl Nl Nl ↑ ↓ Nl Nl to ↑ Nl Nl Nl to ↑ Nl to ↑ Nl − − Clinical manifestation and lab finding
  • Not applicable
Lactic acidosis[8] + − − ± + − − + ↓ ↑ ± Agitated ↓ ↓ ↓ Nl to ↑ ↓ Nl Nl Nl Nl Nl ↑ ↑ ↑ Nl or ↑ Nl ↓ − − Clinical manifestation and lab finding
  • Not applicable
Renal Uremia[9] − − + + + − − + ↓ ↑ ± ↓ ↓ ↓ Nl to ↓ ↑ ↓ Nl Nl ↑ ↑ Nl Nl ↑ ↑ ↑ ↑ ↓ + − Clinical manifestation and lab finding
Renal failure[10] − − + − + − − + ↓ + ↓ ↓ ↓ Nl to ↓ ↑ ↓ Nl ↑ ↑ ↓ Nl Nl ↑ ↑ ↑ ↑ ↓ − − Renal function test
  • Not applicable
Renal tubular acidosis[11] Type I[12] − − + ± ± − − − ↓ ↑ − − ↓ ↓ Nl Nl Nl Nl ↑ ↓ ↓ Nl Nl Nl Nl ↑ ↑ ↑ + − Clinical manifestation and lab finding
Type II − + − ± ± − − − ↓ ↑ − − ↓ ↓ Nl Nl Nl Nl ↑ ↓ Nl Nl Nl Nl Nl Nl Nl Nl − − Clinical manifestation and lab finding
  • Not applicable
Type IV − − + ± ± ± − − ↓ − − ↓ ↓ Nl Nl Nl Nl ↑ ↑ Nl Nl Nl Nl Nl Nl Nl Nl + − Clinical manifestation and lab finding
Heart Heart failure[13] + + − − ± − + + ↓ ↑ + − ↓ ↓ ↑ ↓ Nl Nl Nl Nl ↓ ↓ Nl Nl Nl Nl Nl to ↑ Nl to ↑ Nl − − Clinical manifestation+ echocardiogram
Myocardial infarction[14] + − − − + − + + ↓ ↑ − ↓ ↓ ↓ ↑ Nl to ↓ Nl to ↑ Nl Nl Nl ↑ ↓ Nl ↑ Nl Nl Nl to ↑ Nl to ↑ Nl − − Clinical manifestation + ECG
  • Not applicable
GI Diarrhea[15] − + − ± + + − + ↓ + May be lethargic ↓ ↓ Nl Nl ↓ ↓ ↑ ↑ Nl Nl Nl Nl Nl ↑ Nl Nl − − Stool exam
  • Not applicable
Hyperalimentation[16] + + − − − + − − Nl − − ↓ ↓ Nl Nl ↓ Nl ↑ ↑ Nl Nl Nl Nl Nl Nl Nl Nl − − Clinical manifestation
  • Not applicable
Liver failure[17] − + − − + + − + ↓ + Confused ↓ ↓ Nl Nl ↓ ↓ ↑ ↑ ↓ ↓ Nl Nl Nl Nl Nl Nl Nl − − Liver biopsy
  • Not applicable
Endocrine Hyperparathyroidism[18] − + + − + − − − Nl + Confused ↓ ↓ Nl Nl Nl Nl Nl Nl Nl Nl Nl Nl Nl Nl to ↑ Nl Nl − − PTH level
  • Not applicable
Addison's disease[19] − + − − + + − − ↓ + Irritable ↓ ↓ Nl Nl Nl ↓ Nl ↑ ↓ Nl Nl Nl Nl Nl Nl Nl − − Hormone level

References

  1. ↑ Brubaker RH, Meseeha M. High Anion Gap Metabolic Acidosis. [Updated 2017 Oct 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448090/
  2. ↑ Kraut JA, Xing SX (September 2011). "Approach to the evaluation of a patient with an increased serum osmolal gap and high-anion-gap metabolic acidosis". Am. J. Kidney Dis. 58 (3): 480–4. doi:10.1053/j.ajkd.2011.05.018. PMID 21794966.
  3. ↑ Wolfsdorf, Joseph I; Allgrove, Jeremy; Craig, Maria E; Edge, Julie; Glaser, Nicole; Jain, Vandana; Lee, Warren WR; Mungai, Lucy NW; Rosenbloom, Arlan L; Sperling, Mark A; Hanas, Ragnar (2014). "Diabetic ketoacidosis and hyperglycemic hyperosmolar state". Pediatric Diabetes. 15 (S20): 154–179. doi:10.1111/pedi.12165. ISSN 1399-543X.
  4. ↑ Mostert M, Bonavia A (October 2016). "Starvation Ketoacidosis as a Cause of Unexplained Metabolic Acidosis in the Perioperative Period". Am J Case Rep. 17: 755–758. PMC 5070574. PMID 27752032.
  5. ↑ Howard RD, Bokhari S. PMID 28613672. Vancouver style error: initials (help); Missing or empty |title= (help)
  6. ↑ Ganesh K, Sharma RN, Varghese J, Pillai MG (2016). "A profile of metabolic acidosis in patients with sepsis in an Intensive Care Unit setting". Int J Crit Illn Inj Sci. 6 (4): 178–181. doi:10.4103/2229-5151.195417. PMC 5225760. PMID 28149822.
  7. ↑ Kimmoun, Antoine; Novy, Emmanuel; Auchet, Thomas; Ducrocq, Nicolas; Levy, Bruno (2015). "Hemodynamic consequences of severe lactic acidosis in shock states: from bench to bedside". Critical Care. 19 (1). doi:10.1186/s13054-015-0896-7. ISSN 1364-8535.
  8. ↑ Kraut, Jeffrey A.; Ingelfinger, Julie R.; Madias, Nicolaos E. (2014). "Lactic Acidosis". New England Journal of Medicine. 371 (24): 2309–2319. doi:10.1056/NEJMra1309483. ISSN 0028-4793.
  9. ↑ Brown, Denver; Melamed, Michal L. (2018). "New Frontiers in Treating Uremic Metabolic Acidosis". Clinical Journal of the American Society of Nephrology. 13 (1): 4–5. doi:10.2215/CJN.11771017. ISSN 1555-9041.
  10. ↑ Kraut, Jeffrey A.; Madias, Nicolaos E. (2016). "Metabolic Acidosis of CKD: An Update". American Journal of Kidney Diseases. 67 (2): 307–317. doi:10.1053/j.ajkd.2015.08.028. ISSN 0272-6386.
  11. ↑ Gil-Peña, Helena; Mejía, Natalia; Santos, Fernando (2014). "Renal Tubular Acidosis". The Journal of Pediatrics. 164 (4): 691–698.e1. doi:10.1016/j.jpeds.2013.10.085. ISSN 0022-3476.
  12. ↑ Hemstreet, Brian A (2004). "Antimicrobial-Associated Renal Tubular Acidosis". Annals of Pharmacotherapy. 38 (6): 1031–1038. doi:10.1345/aph.1D573. ISSN 1060-0280.
  13. ↑ Park, Jin Joo; Choi, Dong-Ju; Yoon, Chang-Hwan; Oh, Il-Young; Lee, Ju Hyun; Ahn, Soyeon; Yoo, Byung-Su; Kang, Seok-Min; Kim, Jae-Joong; Baek, Sang-Hong; Cho, Myeong-Chan; Jeon, Eun-Seok; Chae, Shung Chull; Ryu, Kyu-Hyung; Oh, Byung-Hee (2015). "The prognostic value of arterial blood gas analysis in high-risk acute heart failure patients: an analysis of the Korean Heart Failure (KorHF) registry". European Journal of Heart Failure. 17 (6): 601–611. doi:10.1002/ejhf.276. ISSN 1388-9842.
  14. ↑ Mann, Sarah; Bajulaiye, Akinyemi; Sturgeon, Kathleen; Sabri, Abdelkarim; Muthukumaran, Geetha; Libonati, Joseph R. (2014). "Effects of acute angiotensin II on ischemia reperfusion injury following myocardial infarction". Journal of the Renin-Angiotensin-Aldosterone System. 16 (1): 13–22. doi:10.1177/1470320314554963. ISSN 1470-3203.
  15. ↑ Guerrant, R. L.; Van Gilder, T.; Steiner, T. S.; Thielman, N. M.; Slutsker, L.; Tauxe, R. V.; Hennessy, T.; Griffin, P. M.; DuPont, H.; Bradley Sack, R.; Tarr, P.; Neill, M.; Nachamkin, I.; Reller, L. B.; Osterholm, M. T.; Bennish, M. L.; Pickering, L. K. (2001). "Practice Guidelines for the Management of Infectious Diarrhea". Clinical Infectious Diseases. 32 (3): 331–351. doi:10.1086/318514. ISSN 1058-4838.
  16. ↑ Erlingsson, Styrbjörn; Herard, Sebastian; Dahlqvist Leinhard, Olof; Lindström, Torbjörb; Länne, Toste; Borga, Magnus; Nystrom, Fredrik H. (2009). "Men develop more intraabdominal obesity and signs of the metabolic syndrome after hyperalimentation than women". Metabolism. 58 (7): 995–1001. doi:10.1016/j.metabol.2009.02.028. ISSN 0026-0495.
  17. ↑ Lange, Christian M.; Bojunga, Jörg; Hofmann, Wolf Peter; Wunder, Katrin; Mihm, Ulrike; Zeuzem, Stefan; Sarrazin, Christoph (2009). "Severe lactic acidosis during treatment of chronic hepatitis B with entecavir in patients with impaired liver function". Hepatology. 50 (6): 2001–2006. doi:10.1002/hep.23346. ISSN 0270-9139.
  18. ↑ Bilezikian, John P.; Potts, John T.; Fuleihan, Ghada El-Hajj; Kleerekoper, Michael; Neer, Robert; Peacock, Munro; Rastad, Jonas; Silverberg, Shonni J.; Udelsman, Robert; Wells, Samuel A. (2002). "Summary Statement from a Workshop on Asymptomatic Primary Hyperparathyroidism: A Perspective for the 21st Century". The Journal of Clinical Endocrinology & Metabolism. 87 (12): 5353–5361. doi:10.1210/jc.2002-021370. ISSN 0021-972X.
  19. ↑ Ten, Svetlana; New, Maria; Maclaren, Noel (2001). "Addison's Disease 2001". The Journal of Clinical Endocrinology & Metabolism. 86 (7): 2909–2922. doi:10.1210/jcem.86.7.7636. ISSN 0021-972X.
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