What laboratory findings would be expected in a patient with impaired renal function, undergoing aggressive chemotherapy for high-grade lymphoma, with a recent increase in creatinine level from a baseline of 1.0 milligram per deciliter (mg/dL) to 2.1 mg/dL, presenting with symptoms of malaise, nausea, anorexia, and lethargy?

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From the Guidelines

The patient's laboratory findings are most likely consistent with acute kidney injury (AKI) stage 2, as evidenced by a creatinine rise of 100-199% from baseline within 7 days, according to the KDIGO guidelines 1. The expected abnormal laboratory findings in this patient would include elevated uric acid, hyperkalemia, hyperphosphatemia, hypocalcemia, and elevated lactate dehydrogenase (LDH). These abnormalities are consistent with tumor lysis syndrome (TLS), a metabolic emergency that occurs when large numbers of cancer cells are rapidly destroyed, releasing their intracellular contents into the bloodstream. This patient has several risk factors for TLS: high-grade lymphoma (a highly proliferative malignancy), recent aggressive chemotherapy, and acute kidney injury (elevated creatinine from baseline 1.0 to 2.1 mg/dL). The kidney injury likely results from uric acid crystal formation in the renal tubules, impairing the kidney's ability to clear these metabolites. The patient's symptoms of malaise, nausea, anorexia, and lethargy are nonspecific but consistent with both the metabolic derangements of TLS and uremia from acute kidney injury. According to the ACR Appropriateness Criteria for renal failure, AKI is defined as an increase in creatinine by 0.3 mg/dL within 48 hours or an increase in serum creatinine to 1.5 times baseline (within prior 7 days) or urine volume 0.5 mL/kg/hr for 6 hours 1. Prompt recognition and treatment of TLS with aggressive hydration, allopurinol or rasburicase, and correction of electrolyte abnormalities is essential to prevent further kidney damage and potentially life-threatening cardiac arrhythmias from electrolyte disturbances. Key laboratory findings to monitor in this patient include:

  • Serum creatinine and blood urea nitrogen to assess renal function
  • Electrolyte panel to monitor for hyperkalemia, hyperphosphatemia, and hypocalcemia
  • Uric acid level to assess for TLS
  • Lactate dehydrogenase (LDH) to assess for tissue damage
  • Complete blood count and differential to assess for anemia and other hematologic abnormalities.

From the Research

Laboratory Findings in Impaired Renal Function

The patient's recent increase in creatinine level from 1.0 mg/dL to 2.1 mg/dL, along with symptoms of malaise, nausea, anorexia, and lethargy, suggests acute kidney injury (AKI) 2, 3, 4, 5. The expected laboratory findings in this patient would include:

  • Elevated serum creatinine levels, indicating a decline in kidney function 2, 3, 4, 5
  • Increased blood urea nitrogen (BUN) levels, which can be affected by various renal and nonrenal factors 6
  • Electrolyte imbalances, such as hyperkalemia, hypokalemia, hyperphosphatemia, or hypophosphatemia, due to the kidney's impaired ability to regulate electrolyte levels 2, 4
  • Acid-base disturbances, such as metabolic acidosis, which can occur in AKI due to the kidney's reduced ability to excrete hydrogen ions 2, 4
  • Biomarkers of kidney injury, such as interleukin-18, neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1, which may be elevated in the urine before the increase in serum creatinine 6

Underlying Causes of AKI

The patient's underlying causes of AKI may include:

  • Prerenal causes, such as dehydration or decreased blood flow to the kidneys 3, 5
  • Intrinsic renal causes, such as acute tubular necrosis caused by ischemia or nephrotoxicity 5
  • Postrenal causes, such as urinary tract obstruction 3, 5
  • Nephrotoxicity caused by aggressive chemotherapy 5

Clinical Evaluation and Management

The patient's clinical evaluation and management would involve:

  • A thorough history and physical examination to categorize the underlying cause of AKI 3
  • Laboratory work-up, including measurements of serum creatinine, BUN, and electrolyte levels 2, 3, 6
  • Medication adjustment and identification and reversal of underlying causes 3
  • Referral to appropriate specialty care, such as nephrology, for further evaluation and management 3

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Pathophysiology and Clinical Work-Up of Acute Kidney Injury.

Contributions to nephrology, 2016

Research

Acute Kidney Injury.

Primary care, 2020

Research

Acute kidney injury.

Lancet (London, England), 2019

Research

Acute Kidney Injury: Medical Causes and Pathogenesis.

Journal of clinical medicine, 2023

Research

Biomarkers of acute kidney injury.

Advances in chronic kidney disease, 2008

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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