Extreme Type B Lactic Acidosis with Hyperphosphatemia: A Multifactorial Storm

Introduction: Lactic acidosis can result from hypoperfusion and shock (type A) or impaired clearance/increased production of lactate despite normal perfusion (type B). Hyperphosphatemia can occur from reduced clearance and transcellular shift. Case Description: A 40-year-old male with a history of alcohol use disorder, pancreatitis, cirrhosis, and type 2 diabetes presented with 2 days of nausea/vomiting. He had been binge-drinking for 10 days and without food intake for 5 days. On initial evaluation, he was tachycardic, hypertensive, afebrile, and saturating >95% on room air. He had dry mucous membranes with normal mentation. The Table reveals his marked metabolic derangements and the significant improvement after receiving IV fluids, insulin infusion, thiamine, folate, and K repletion. Discussion: This case reveals severe lactic acidosis without shock or intoxication. Thiamine deficiency and an elevated NADH/NAD+ ratio from ethanol metabolism shifted pyruvate metabolism to lactate production. Additionally, AKI and cirrhosis impaired lactate clearance. A coexisting severe metabolic alkalosis from vomiting, evidenced by a serum HCO3 of 59 mmol/L when corrected for the lactate level, further worsened the condition through increased phosphofructokinase activity, left shift of the oxygen–hemoglobin dissociation curve, and redistribution of lactate to the extracellular space. The ketoacidosis aggravated the lactic acidosis through increased glycolytic substrate and inhibition of pyruvate dehydrogenase by acetyl-CoA accumulation. Severe hyperphosphatemia was the result of AKI and transcellular shift from organic acidosis and relative insulin deficiency. Here we present a unique case that demonstrates multiple converging pathophysiologic mechanisms leading to extreme type B lactic acidosis and massive hyperphosphatemia.Figure. Pathophysiology of the lactic acidosis and hyperphosphatemia in this case Table. Lab data for the first day of the hospitalization - Na (135-145 mmol/L) K (3.6-5.0 mmol/L) Cl (98-109 mmol/L) HCO3 (22-31 mmol/L) Glucose (65-200 mg/dL) Anion gap (6-16mmol/L) Cr (0.67-1.17 mg/dL) Phosphorus (2.4-4.5mg/dL) Lactate (0.5-2.2mmol/L) Etoh On admission 131 ↓ 2.9 ↓ <60 ↓ 8 ↓ 784 ↑ incalculable 2.39 ↑ 22.9 ↑ 51.2 ↑ <10 18 hour 134 ↓ 3.6 84 ↓ 39 ↑ 133 ↑ 11 1.43 ↑ 3.4 1.6 n/a

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Journal of the American Society of Nephrology
Published
2025-10-01
DOI
https://doi.org/10.1681/asn.2025cvxn0ntd
Primary Topic
Metabolism and Genetic Disorders
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article
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article

Extreme Type B Lactic Acidosis with Hyperphosphatemia: A Multifactorial Storm

Emine Bilge Çaparali, Kamalanathan K. Sambandam
Journal of the American Society of Nephrology
Metabolism and Genetic Disorders
article

Extreme Type B Lactic Acidosis with Hyperphosphatemia: A Multifactorial Storm

Emine Bilge Çaparali, Kamalanathan K. Sambandam
article en

Abstract

Introduction: Lactic acidosis can result from hypoperfusion and shock (type A) or impaired clearance/increased production of lactate despite normal perfusion (type B). Hyperphosphatemia can occur from reduced clearance and transcellular shift. Case Description: A 40-year-old male with a history of alcohol use disorder, pancreatitis, cirrhosis, and type 2 diabetes presented with 2 days of nausea/vomiting. He had been binge-drinking for 10 days and without food intake for 5 days. On initial evaluation, he was tachycardic, hypertensive, afebrile, and saturating >95% on room air. He had dry mucous membranes with normal mentation. The Table reveals his marked metabolic derangements and the significant improvement after receiving IV fluids, insulin infusion, thiamine, folate, and K repletion. Discussion: This case reveals severe lactic acidosis without shock or intoxication. Thiamine deficiency and an elevated NADH/NAD+ ratio from ethanol metabolism shifted pyruvate metabolism to lactate production. Additionally, AKI and cirrhosis impaired lactate clearance. A coexisting severe metabolic alkalosis from vomiting, evidenced by a serum HCO3 of 59 mmol/L when corrected for the lactate level, further worsened the condition through increased phosphofructokinase activity, left shift of the oxygen–hemoglobin dissociation curve, and redistribution of lactate to the extracellular space. The ketoacidosis aggravated the lactic acidosis through increased glycolytic substrate and inhibition of pyruvate dehydrogenase by acetyl-CoA accumulation. Severe hyperphosphatemia was the result of AKI and transcellular shift from organic acidosis and relative insulin deficiency. Here we present a unique case that demonstrates multiple converging pathophysiologic mechanisms leading to extreme type B lactic acidosis and massive hyperphosphatemia.Figure. Pathophysiology of the lactic acidosis and hyperphosphatemia in this case Table. Lab data for the first day of the hospitalization - Na (135-145 mmol/L) K (3.6-5.0 mmol/L) Cl (98-109 mmol/L) HCO3 (22-31 mmol/L) Glucose (65-200 mg/dL) Anion gap (6-16mmol/L) Cr (0.67-1.17 mg/dL) Phosphorus (2.4-4.5mg/dL) Lactate (0.5-2.2mmol/L) Etoh On admission 131 ↓ 2.9 ↓ <60 ↓ 8 ↓ 784 ↑ incalculable 2.39 ↑ 22.9 ↑ 51.2 ↑ <10 18 hour 134 ↓ 3.6 84 ↓ 39 ↑ 133 ↑ 11 1.43 ↑ 3.4 1.6 n/a

Journal of the American Society of NephrologyVol. 36(10S)
The University of Texas Southwestern Medical Center (US)
Openalex Percentile: Top 66%
Metabolism and Genetic Disorders
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