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==Differential Diagnosis==
==Differential Diagnosis==
Hyperkalemia is a laboratory finding that is a result of several conditions. These conditions must be differentiated as a cause of hyperkalemia. The following table summarize the differentiating features of causes of hyperkalemia.<ref name="pmid17331245">{{cite journal |vauthors=Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, Levin A |title=Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury |journal=Crit Care |volume=11 |issue=2 |pages=R31 |year=2007 |pmid=17331245 |pmc=2206446 |doi=10.1186/cc5713 |url=}}</ref><ref name="pmid12138150">{{cite journal |vauthors=Rodríguez Soriano J |title=Renal tubular acidosis: the clinical entity |journal=J. Am. Soc. Nephrol. |volume=13 |issue=8 |pages=2160–70 |year=2002 |pmid=12138150 |doi= |url=}}</ref><ref name="pmid15262664">{{cite journal |vauthors=Hsu CY, Vittinghoff E, Lin F, Shlipak MG |title=The incidence of end-stage renal disease is increasing faster than the prevalence of chronic renal insufficiency |journal=Ann. Intern. Med. |volume=141 |issue=2 |pages=95–101 |year=2004 |pmid=15262664 |doi= |url=}}</ref><ref name="pmid19564476">{{cite journal |vauthors=Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN |title=Hyperglycemic crises in adult patients with diabetes |journal=Diabetes Care |volume=32 |issue=7 |pages=1335–43 |year=2009 |pmid=19564476 |pmc=2699725 |doi=10.2337/dc09-9032 |url=}}</ref><ref name="pmid5013637">{{cite journal |vauthors=Arieff AI, Carroll HJ |title=Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases |journal=Medicine (Baltimore) |volume=51 |issue=2 |pages=73–94 |year=1972 |pmid=5013637 |doi= |url=}}</ref><ref name="pmid20823466">{{cite journal |vauthors=Speiser PW, Azziz R, Baskin LS, Ghizzoni L, Hensle TW, Merke DP, Meyer-Bahlburg HF, Miller WL, Montori VM, Oberfield SE, Ritzen M, White PC |title=Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline |journal=J. Clin. Endocrinol. Metab. |volume=95 |issue=9 |pages=4133–60 |year=2010 |pmid=20823466 |pmc=2936060 |doi=10.1210/jc.2009-2631 |url=}}</ref><ref name="pmid19955259">{{cite journal |vauthors=Hahner S, Loeffler M, Bleicken B, Drechsler C, Milovanovic D, Fassnacht M, Ventz M, Quinkler M, Allolio B |title=Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies |journal=Eur. J. Endocrinol. |volume=162 |issue=3 |pages=597–602 |year=2010 |pmid=19955259 |doi=10.1530/EJE-09-0884 |url=}}</ref><ref name="pmid18509186">{{cite journal |vauthors=Coiffier B, Altman A, Pui CH, Younes A, Cairo MS |title=Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review |journal=J. Clin. Oncol. |volume=26 |issue=16 |pages=2767–78 |year=2008 |pmid=18509186 |doi=10.1200/JCO.2007.15.0177 |url=}}</ref><ref name="pmid6282181">{{cite journal |vauthors=Knochel JP |title=Rhabdomyolysis and myoglobinuria |journal=Annu. Rev. Med. |volume=33 |issue= |pages=435–43 |year=1982 |pmid=6282181 |doi=10.1146/annurev.me.33.020182.002251 |url=}}</ref>
Hyperkalemia is a laboratory finding that is a result of several conditions. These conditions must be differentiated as a cause of hyperkalemia. The following table summarize the differentiating features of causes of hyperkalemia<br>
 
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<br>
{| align=center
{| align=center
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|-
|-
| rowspan="3" align="center" style="background:#DCDCDC;"|Renal
| rowspan="3" align="center" style="background:#DCDCDC;"|Renal
|align="center" style="background:#DCDCDC;"|[[Acute kidney injury]]
|align="center" style="background:#DCDCDC;"|Acute kidney injury<ref name="pmid17331245">{{cite journal |vauthors=Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, Levin A |title=Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury |journal=Crit Care |volume=11 |issue=2 |pages=R31 |year=2007 |pmid=17331245 |pmc=2206446 |doi=10.1186/cc5713 |url=}}</ref>
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Nausea]], [[vomiting]], decreased [[urine output]], [[fatigue]], [[dyspnea]], [[edema]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Nausea]], [[vomiting]], decreased [[urine output]], [[fatigue]], [[dyspnea]], [[edema]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Tremor]], [[confusion]], [[edema]]  
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Tremor]], [[confusion]], [[edema]]  
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|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Recently developed symptoms
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Recently developed symptoms
|-
|-
|align="center" style="background:#DCDCDC;"|[[Chronic kidney disease]]
|align="center" style="background:#DCDCDC;"|Chronic kidney disease<ref name="pmid12138150">{{cite journal |vauthors=Rodríguez Soriano J |title=Renal tubular acidosis: the clinical entity |journal=J. Am. Soc. Nephrol. |volume=13 |issue=8 |pages=2160–70 |year=2002 |pmid=12138150 |doi= |url=}}</ref>
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Nausea]], [[vomiting]], decreased [[urine output]], [[fatigue]], [[dyspnea]], [[edema]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Nausea]], [[vomiting]], decreased [[urine output]], [[fatigue]], [[dyspnea]], [[edema]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Tremor]], [[confusion]], [[edema]]  
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Tremor]], [[confusion]], [[edema]]  
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|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Chronic underlying disease ([[Diabetes mellitus|DM]], [[Hypertension|HTN]]), duration of symptoms ≥ 3 months
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Chronic underlying disease ([[Diabetes mellitus|DM]], [[Hypertension|HTN]]), duration of symptoms ≥ 3 months
|-
|-
|align="center" style="background:#DCDCDC;"|[[Renal tubular acidosis|Renal tubular acidosis type-4]]
|align="center" style="background:#DCDCDC;"|[[Renal tubular acidosis|Renal tubular acidosis type-4]]<ref name="pmid15262664">{{cite journal |vauthors=Hsu CY, Vittinghoff E, Lin F, Shlipak MG |title=The incidence of end-stage renal disease is increasing faster than the prevalence of chronic renal insufficiency |journal=Ann. Intern. Med. |volume=141 |issue=2 |pages=95–101 |year=2004 |pmid=15262664 |doi= |url=}}</ref>
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Usually asyptomatic
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Usually asyptomatic
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Signs of underlying disease
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Signs of underlying disease
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|-
|-
| rowspan="4" align="center" style="background:#DCDCDC;"|Endocrine
| rowspan="4" align="center" style="background:#DCDCDC;"|Endocrine
|align="center" style="background:#DCDCDC;"|[[Diabetic ketoacidosis|DKA]]  
|align="center" style="background:#DCDCDC;"|[[Diabetic ketoacidosis|DKA]]<ref name="pmid19564476">{{cite journal |vauthors=Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN |title=Hyperglycemic crises in adult patients with diabetes |journal=Diabetes Care |volume=32 |issue=7 |pages=1335–43 |year=2009 |pmid=19564476 |pmc=2699725 |doi=10.2337/dc09-9032 |url=}}</ref>
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Change in mental status]], [[abdominal pain]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Change in mental status]], [[abdominal pain]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Decreased skin turgor, dry oral mucosa, [[tachycardia]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Decreased skin turgor, dry oral mucosa, [[tachycardia]]
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|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Rapidly developing [[polyuria]], [[polydipsia]], and [[weight loss]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Rapidly developing [[polyuria]], [[polydipsia]], and [[weight loss]]
|-
|-
|align="center" style="background:#DCDCDC;"|[[Hyperosmolar hyperglycemic state|HHS]]
|align="center" style="background:#DCDCDC;"|[[Hyperosmolar hyperglycemic state|HHS]]<ref name="pmid5013637">{{cite journal |vauthors=Arieff AI, Carroll HJ |title=Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases |journal=Medicine (Baltimore) |volume=51 |issue=2 |pages=73–94 |year=1972 |pmid=5013637 |doi= |url=}}</ref>
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Change in mental status]], [[abdominal pain]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Change in mental status]], [[abdominal pain]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Decreased skin turgor, dry oral mucosa, [[tachycardia]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Decreased skin turgor, dry oral mucosa, [[tachycardia]]
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|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Polyuria]], [[polydipsia]], and [[weight loss]] develop more insidious
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Polyuria]], [[polydipsia]], and [[weight loss]] develop more insidious
|-
|-
|align="center" style="background:#DCDCDC;"|[[Congenital adrenal hyperplasia]] (CAH)
|align="center" style="background:#DCDCDC;"|[[Congenital adrenal hyperplasia]] (CAH)<ref name="pmid20823466">{{cite journal |vauthors=Speiser PW, Azziz R, Baskin LS, Ghizzoni L, Hensle TW, Merke DP, Meyer-Bahlburg HF, Miller WL, Montori VM, Oberfield SE, Ritzen M, White PC |title=Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline |journal=J. Clin. Endocrinol. Metab. |volume=95 |issue=9 |pages=4133–60 |year=2010 |pmid=20823466 |pmc=2936060 |doi=10.1210/jc.2009-2631 |url=}}</ref><ref name="pmid19955259">{{cite journal |vauthors=Hahner S, Loeffler M, Bleicken B, Drechsler C, Milovanovic D, Fassnacht M, Ventz M, Quinkler M, Allolio B |title=Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies |journal=Eur. J. Endocrinol. |volume=162 |issue=3 |pages=597–602 |year=2010 |pmid=19955259 |doi=10.1530/EJE-09-0884 |url=}}</ref>
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Poor feeding]], [[failure to thrive]], [[precocious puberty]], short statue, [[hirsutism]], [[weight loss]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Poor feeding]], [[failure to thrive]], [[precocious puberty]], short statue, [[hirsutism]], [[weight loss]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Ambiguous genitalia]], [[hypotension]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Ambiguous genitalia]], [[hypotension]]
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|-
|-
| rowspan="2" align="center" style="background:#DCDCDC;"|Tissue break down
| rowspan="2" align="center" style="background:#DCDCDC;"|Tissue break down
|align="center" style="background:#DCDCDC;"|[[Tumor lysis syndrome]]
|align="center" style="background:#DCDCDC;"|[[Tumor lysis syndrome]]<ref name="pmid18509186">{{cite journal |vauthors=Coiffier B, Altman A, Pui CH, Younes A, Cairo MS |title=Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review |journal=J. Clin. Oncol. |volume=26 |issue=16 |pages=2767–78 |year=2008 |pmid=18509186 |doi=10.1200/JCO.2007.15.0177 |url=}}</ref>
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Fever]], [[weight loss]], symptoms related to underlying malignancy
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Fever]], [[weight loss]], symptoms related to underlying malignancy
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Altered mental status]], [[lymphadenopathy]], [[muscle weakness]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Altered mental status]], [[lymphadenopathy]], [[muscle weakness]]
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|style="padding: 5px 5px; background: #F5F5F5;" align="center" |History of underlying malignancy
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |History of underlying malignancy
|-
|-
|align="center" style="background:#DCDCDC;"|[[Rhabdomyolysis]]
|align="center" style="background:#DCDCDC;"|[[Rhabdomyolysis]]<ref name="pmid6282181">{{cite journal |vauthors=Knochel JP |title=Rhabdomyolysis and myoglobinuria |journal=Annu. Rev. Med. |volume=33 |issue= |pages=435–43 |year=1982 |pmid=6282181 |doi=10.1146/annurev.me.33.020182.002251 |url=}}</ref>
 
 
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Myalgia]], [[fatigue]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Myalgia]], [[fatigue]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Altered mental status]], [[hypotension]]
|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Altered mental status]], [[hypotension]]

Revision as of 14:53, 16 July 2018



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

Overview

Hyperkalemia is a laboratory finding that is a result of several conditions. These conditions must be differentiated as a cause of hyperkalemia. The following table summarize the differentiating features of causes of hyperkalemia.

Differential Diagnosis

Hyperkalemia is a laboratory finding that is a result of several conditions. These conditions must be differentiated as a cause of hyperkalemia. The following table summarize the differentiating features of causes of hyperkalemia

Organ system Conditions Distinguishing features Additional findings
Symptoms Signs Labs
Renal Acute kidney injury[1] Nausea, vomiting, decreased urine output, fatigue, dyspnea, edema Tremor, confusion, edema Hyperkalemia, increased BUN and Cr, metabolic acidosis Recently developed symptoms
Chronic kidney disease[2] Nausea, vomiting, decreased urine output, fatigue, dyspnea, edema Tremor, confusion, edema Hyperkalemia, increased BUN and Cr, metabolic acidosis, hypocalcemia, hyperphosphatemia Chronic underlying disease (DM, HTN), duration of symptoms ≥ 3 months
Renal tubular acidosis type-4[3] Usually asyptomatic Signs of underlying disease Hyperkalemia, normal anion gap metabolic acidosis, urine PH< 5.5 History of diabetes mellitus
Endocrine DKA[4] Change in mental status, abdominal pain Decreased skin turgor, dry oral mucosa, tachycardia Hyperglycemia, increased anion gap metabolic acidosis, ketonemia Rapidly developing polyuria, polydipsia, and weight loss
HHS[5] Change in mental status, abdominal pain Decreased skin turgor, dry oral mucosa, tachycardia Severe hyperglycemia, normal anion gap, increased serum osmolality Polyuria, polydipsia, and weight loss develop more insidious
Congenital adrenal hyperplasia (CAH)[6][7] Poor feeding, failure to thrive, precocious puberty, short statue, hirsutism, weight loss Ambiguous genitalia, hypotension Hyperkalemia, increased 17 hydroxyprogestrone, hyponatremia Salt wasting
Addison's disease Skin hyperpigmentation, fatigue, salt craving, nausea and vomiting, amenorrhea, depression Hyperpigmentation, hypotension, pubic and axillary hair loss Hyperkalemia, decreased serum cortisol level Diagnosis by cosyntropin test
Tissue break down Tumor lysis syndrome[8] Fever, weight loss, symptoms related to underlying malignancy Altered mental status, lymphadenopathy, muscle weakness Hyperkalemia, hyperphosphatemia, hypocalcemia History of underlying malignancy
Rhabdomyolysis[9]


Myalgia, fatigue Altered mental status, hypotension Hyperkalemia, increased muscle enzymes (CK, aldolase) History of seizure, drug overdose, or trauma

References

  1. Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, Levin A (2007). "Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury". Crit Care. 11 (2): R31. doi:10.1186/cc5713. PMC 2206446. PMID 17331245.
  2. Rodríguez Soriano J (2002). "Renal tubular acidosis: the clinical entity". J. Am. Soc. Nephrol. 13 (8): 2160–70. PMID 12138150.
  3. Hsu CY, Vittinghoff E, Lin F, Shlipak MG (2004). "The incidence of end-stage renal disease is increasing faster than the prevalence of chronic renal insufficiency". Ann. Intern. Med. 141 (2): 95–101. PMID 15262664.
  4. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN (2009). "Hyperglycemic crises in adult patients with diabetes". Diabetes Care. 32 (7): 1335–43. doi:10.2337/dc09-9032. PMC 2699725. PMID 19564476.
  5. Arieff AI, Carroll HJ (1972). "Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases". Medicine (Baltimore). 51 (2): 73–94. PMID 5013637.
  6. Speiser PW, Azziz R, Baskin LS, Ghizzoni L, Hensle TW, Merke DP, Meyer-Bahlburg HF, Miller WL, Montori VM, Oberfield SE, Ritzen M, White PC (2010). "Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline". J. Clin. Endocrinol. Metab. 95 (9): 4133–60. doi:10.1210/jc.2009-2631. PMC 2936060. PMID 20823466.
  7. Hahner S, Loeffler M, Bleicken B, Drechsler C, Milovanovic D, Fassnacht M, Ventz M, Quinkler M, Allolio B (2010). "Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies". Eur. J. Endocrinol. 162 (3): 597–602. doi:10.1530/EJE-09-0884. PMID 19955259.
  8. Coiffier B, Altman A, Pui CH, Younes A, Cairo MS (2008). "Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review". J. Clin. Oncol. 26 (16): 2767–78. doi:10.1200/JCO.2007.15.0177. PMID 18509186.
  9. Knochel JP (1982). "Rhabdomyolysis and myoglobinuria". Annu. Rev. Med. 33: 435–43. doi:10.1146/annurev.me.33.020182.002251. PMID 6282181.


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