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Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Tumor lysis syndrome differential diagnosis

Introduction

Overview

Overview

Tumor lysis syndrome must be differentiated from other diseases that cause hyperuricemia, hyperkalemia, and hyperphosphatemia, such as acute kidney injury. The common conditions are hereditary hyperuricemia, Insulin resistance, Hypertension, Obesity, Gout, Alcoholism and renal insufficiency. Patients taking ACE inhibitor, NSAIDs and Antibiotics such as trimethoprim are more prone to hyperkalemia. Hyperphosphatemia is usually seen in Acute kidney injury, Hypoparathyroidism, vitamin D supplementation and also in sarcoidos.

Differentiating tumor lysis syndrome from other Diseases

Differentiating tumor lysis syndrome from other Diseases

Tumor lysis syndrome must be differentiated from other diseases that cause electrolytes disturbance.[1]

  • Transcellular phosphate shifts:

Differentiating tumor lysis syndrome based on hyperkalemia:

Organ system Conditions Distinguishing features Additional findings
Symptoms Signs Labs
Tissue break down Tumor lysis syndrome[3] Fever, weight loss, symptoms related to underlying malignancy Altered mental status, lymphadenopathy, muscle weakness Hyperkalemia, hyperphosphatemia, hypocalcemia History of underlying malignancy
Rhabdomyolysis[4] Myalgia, fatigue Altered mental status, hypotension Hyperkalemia, increased muscle enzymes (CK, aldolase) History of seizure, drug overdose, or trauma
Renal Acute kidney injury[5] Nausea, vomiting, decreased urine output, fatigue, dyspnea, edema Tremor, confusion, edema Hyperkalemia, increased BUN and Cr, metabolic acidosis Recently developed symptoms
Chronic kidney disease[6] 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[7] Usually asyptomatic Signs of underlying disease Hyperkalemia, normal anion gap metabolic acidosis, urine PH< 5.5 History of diabetes mellitus
Endocrine DKA[8] 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[9] 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)[10][11] 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
References

References

  1. ↑ Wilson FP, Berns JS (2014). “Tumor lysis syndrome: new challenges and recent advances”. Adv Chronic Kidney Dis. 21 (1): 18–26. doi:10.1053/j.ackd.2013.07.001. PMC 4017246. PMID 24359983.
  2. ↑ 2.0 2.1 2.2 Wikipedia.https://en.wikipedia.org/wiki/Hyperuricemia
  3. ↑ 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.
  4. ↑ Knochel JP (1982). “Rhabdomyolysis and myoglobinuria”. Annu. Rev. Med. 33: 435–43. doi:10.1146/annurev.me.33.020182.002251. PMID 6282181.
  5. ↑ 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.
  6. ↑ Rodríguez Soriano J (2002). “Renal tubular acidosis: the clinical entity”. J. Am. Soc. Nephrol. 13 (8): 2160–70. PMID 12138150.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohamad Alkateb, MBBCh [2]