Hyperkalemia diagnostic study of choice
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon, M.D. [2] Syed Ahsan Hussain, M.D.[3]
Overview
Serum potassium is the gold standard test for the diagnosis of hyperkalemia. Pseudohyperkalemia needs to be ruled out whenever hyperkalemia is diagnosed. Pseudohyperkalemia is defined when serum potassium concentration exceeds that of plasma. Different etiologies of hyperkalemia can be assessed by using the diagnostic criteria.
Diagnostic Study of Choice
Study of choice
- There are two methods to determine serum potassium:
- Ion-specific electrode (ISE) potentiometry
- ISE potentiometry has two different subtypes: direct (undiluted) and indirect (diluted).
- Direct ISE measures plasma potassium directly from a whole-blood sample and it's not associated with pseudohyperkalemia.
- FES or indirect ISE requires sample dilution before assay and both are associated with pseudohyperkalemia.
Pseudohyperkalemia
- Pseudohyperkalemia is defined when serum potassium concentration exceeds that of plasma without any symptoms of hyperkalemia.
- It usually occurs when potassium moves out of cells during blood specimen collection or during centrifugation of the sample.
- Other causes are thrombocytosis, leukocytosis and erythrocytosis.
- To rule out pseudohyperkalemia we need to do the following :[3]
- Repeat the blood sample.
- Complete blood count to rule out thrombocytosis, erythrocytosis and leukocytosis.
- Measurement of plasma potassium and whole blood potassium.
Diagnostic results
Common Diagnostic Studies
The serum potassium must be performed when:
- The patient presented with cardiac arrhythmias, weakness, fatigue and known case of chronic kidney disease. The following investigations must be performed :
- Blood pressure(to look for hypoaldosteronism)
- Complete blood count
- Renal function tests
- Urine potassium,sodium and osmolality
- Metabolic profile(other electrolytes)
- ECG
- Bicarbonate level
- Serum glucose
- Serum calcium
Depending on the history and results of the above mentioned tests,other tests that can be performed for evaluating the cause of hyperkalemia [6][7]
- Digoxin level - If the patient is on a digitalis medication
- Arterial or venous blood gas
- Urinalysis
- Serum cortisol and aldosterone levels
- Serum uric acid and phosphorus assays
- Serum creatinine phosphokinase (CPK) measurements
- Urine myoglobin test
Sequence of diagnostic studies
- Serum potassium measurement.
- ECG-it denotes the urgency of the treatment
- Renal function test.
- Serum BUN and creatinine are measured
- Since creatinine levels are dependent on muscle mass so GFR measurement is preferred
- Urine potassium, sodium and osmolality measurement.
- Urine potassium measurement.
- Urine sodium < 20meq/L denotes decreased sodium delivery to the distal tubules which decreases potassium secretion.
- Urine osmolarity-measuring urine osmolarity is very important for accurate measurement of urine potassium as concenterated or dilute urine will alter the urine potassium concentration.
- Serum osmolarity
- High serum osmolarity (>295 mosm/kg) may result in extracellular shift of potassium [8][9]
- Blood gas analysis: [10]
- Decreased serum pH causes extracellular shift of potassium into the blood
- Transtubular potassium gradient [11][12]
- It calculates the ratio of amount potassium in the collecting duct of kidneys with the amount of potassium in the peritubular capillaries
- It indicates the activity of aldosterone on kidneys in regulation of potassium levels
- TTG calculation-( Urine K+ x Serum osmolarity)/(serum K+ x Urine osmolarity)
- TTG <3 suggests lack of aldosterone effect on collecting ducts causing decreased excretion of potassium
- TTG >7 suggest adequate effect of aldosterone in a case of hyperkalemia
- If TTG suggest aldosterone etiology then further testing done
- Aldosterone levels
- Renin levels [13]
Diagnostic criteria
| Potassium >5.1meq/L | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| ECG | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| If no changes,rule out pseudohyperkalemia | If changes present then start urgent treatment | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Urine sodium <25 meq/L | urine sodium >25 meq/L | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| ARF CKD Heart failure, Volume depletion | Decreased K+secretion(Urine K+<20meq/L | Transcellular shift(measure serum osmolarity and pH) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Low aldosterone(TTG<3) | Normal aldosterone(TTG>7) | Diabetic ketoacidosis, Metabolic acidosis | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Low renin | Normal renin | Tissue breakdown, Pseudohypoaldosternism type 1 and type 2, Type 1 RTA | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Interstital nephritis, Obstructive uropathies, Diabetic nephropathy, ACE inhibitors,Angiotensin 2 receptors | Primary hypoaldosteronism, Congenital adrenal hyperplasia, Aldosterone receptor antagonists, RTA type 4 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
References
- ↑ Lehnhardt A, Kemper MJ (2011). "Pathogenesis, diagnosis and management of hyperkalemia". Pediatr Nephrol. 26 (3): 377–84. doi:10.1007/s00467-010-1699-3. PMC 3061004. PMID 21181208.
- ↑ Crop MJ, Hoorn EJ, Lindemans J, Zietse R (2007). "Hypokalaemia and subsequent hyperkalaemia in hospitalized patients". Nephrol Dial Transplant. 22 (12): 3471–7. doi:10.1093/ndt/gfm471. PMID 17848395.
- ↑ Šálek T (2018). "Pseudohyperkalemia - Potassium released from cells due to clotting and centrifugation - a case report". Biochem Med (Zagreb). 28 (1): 011002. doi:10.11613/BM.2018.011002. PMC 5806620. PMID 29472808.
- ↑ Montford JR, Linas S (2017). "How Dangerous Is Hyperkalemia?". J Am Soc Nephrol. 28 (11): 3155–3165. doi:10.1681/ASN.2016121344. PMC 5661285. PMID 28778861.
- ↑ Boddy K, King PC, Hume R, Weyers E (1972). "The relation of total body potassium to height, weight, and age in normal adults". J Clin Pathol. 25 (6): 512–7. PMC 477368. PMID 4625433.
- ↑ Adrogué HJ, Madias NE (1981). "Changes in plasma potassium concentration during acute acid-base disturbances". Am J Med. 71 (3): 456–67. PMID 7025622.
- ↑ Allon M (1995). "Hyperkalemia in end-stage renal disease: mechanisms and management". J Am Soc Nephrol. 6 (4): 1134–42. PMID 8589279.
- ↑ Viberti GC (1978). "Glucose-induced hyperkalaemia: A hazard for diabetics?". Lancet. 1 (8066): 690–1. PMID 76227.
- ↑ Adrogué HJ, Lederer ED, Suki WN, Eknoyan G (1986). "Determinants of plasma potassium levels in diabetic ketoacidosis". Medicine (Baltimore). 65 (3): 163–72. PMID 3084904.
- ↑ SCRIBNER BH, FREMONT-SMITH K, BURNELL JM (1955). "The effect of acute respiratory acidosis on the internal equilibrium of potassium". J Clin Invest. 34 (8): 1276–85. doi:10.1172/JCI103174. PMC 438696. PMID 13242660.
- ↑ Choi MJ, Ziyadeh FN (2008). "The utility of the transtubular potassium gradient in the evaluation of hyperkalemia". J Am Soc Nephrol. 19 (3): 424–6. doi:10.1681/ASN.2007091017. PMID 18216310.
- ↑ Ethier JH, Kamel KS, Magner PO, Lemann J, Halperin ML (1990). "The transtubular potassium concentration in patients with hypokalemia and hyperkalemia". Am J Kidney Dis. 15 (4): 309–15. PMID 2321642.
- ↑ Conte G, Dal Canton A, Imperatore P, De Nicola L, Gigliotti G, Pisanti N; et al. (1990). "Acute increase in plasma osmolality as a cause of hyperkalemia in patients with renal failure". Kidney Int. 38 (2): 301–7. PMID 2402122.