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& 2010 International Society of Nephrology
Kidney International (2010) 77, 261–262; doi:10.1038/ki.2009.437
The Case | A woman with severe metabolic acidosis
Yu-Ming Chang1, Yeong-Woei Chiew1 and Chwei-Shiun Yang1
1
Division of Nephrology, Department of Medicine, Cathay General Hospital, Taipei Medical University, Taipei, Taiwan, ROC
Correspondence: Chwei-Shiun Yang, Division of Nephrology, Department of Medicine, Cathay General Hospital, No. 280, Section 4, Ren-Ai
Road, Taipei Da An 106, Taiwan, ROC. E-mail: [email protected]
Table 1 | Laboratory findings on arrival
Our case
Blood urea nitrogen (mg/dl)
Creatinine (mg/dl)
Sodium (mmol/l)
Potassium (mmol/l)
Chloride (mmol/l)
Serum glucose (mg/dl)
Serum osmolality (mmol/kg)
Serum osmolar gap (mmol/l)
pH
PaO2 (mm Hg)
PaCO2 (mm Hg)
Bicarbonate (mmol/l)
Base excess (mmol/l)
SaO2 (%)
Serum anion gap (mmol/l)
Lactate (mmol/l)
Ketone body
A 86-year-old woman was brought to the emergency room
with tachypnea, mental confusion, and cerebral ataxia. She
had history of chronic renal failure and perforated peptic
ulcer, and had undergone oversew perforation, and gastrojejunostomy for subsequent intestinal obstruction 1 year ago.
She had regularly taken Biofermin supplements (containing
Lactobacillus acidophilus) and mulberry juice mixed with
sugar and honey during the previous 3 days. She denied
taking any toxins. On examination she was malnourished.
103
3.4
143
4.4
118
137
339
8.6
7.22
188.6
9.6
3.9
23.7
99.1
21.1
2.6
Negative
Reference value
6–20
0.5–1.5
135–145
3.5–5.0
98–110
70–110
275–295
0–15
7.35–7.45
80–105
35–45
22–26
3.3 to 2.3
95–100
10–12
0.7–2.1
Negative
Her blood pressure was 180/96 mm Hg, respiratory rate
42/min, and body temperature 36.8 1C. An abdominal X-ray
showed distended intestinal loops. A computed tomography
scan of the brain was normal. The pertinent laboratory findings
on arrival are shown in Table 1.
Emergent hemodialysis was performed due to severe
metabolic acidosis refractory to intravenous sodium bicarbonate.
Her tachypnea and neurological symptoms dramatically
improved after hemodialysis.
What is the cause of her acidosis?
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Kidney International (2010) 77, 261–262
261
make your diagnosis
Y-M Chang et al.: D-lactic acidosis
The Diagnosis | High anion gap metabolic acidosis
from D-lactic acid
Glucose
Pyruvate
ADP
Pyruvate
dehydrogenase
ATP
Acetyl-CoA
O2
CO2+H2O
D-2-hydroxy
acid
dehydrogenase
D-Lactate
Overgrowth of acid
resistant Gram-positive
anerobes (such as
Lactobacillus, the major
D-lactate producer)
Organic acids
production
High carbohydrate
loading
Glucose
fermentation
in the colon
Short or bypass
small intestine
Figure 1 | The pathogenesis of D-lactic acidosis.
This patient had high anion gap metabolic acidosis. Ketoacidosis
and lactic acidosis were excluded by negative blood ketones and
normal L-lactate levels. Intoxication (such as that from methanol,
ethylene glycol, or salicylate ingestion) was unlikely due to lack
of history and normal serum osmolar gap. Severe metabolic
acidosis was out of proportion to the degree of renal failure.
Therefore, the blood was screened for other possible acids.
D-Lactate is normally undetectable, and in this patient
the measured concentration was elevated at 6.8 mmol/l
(o0.1 mmol/l in normal individual).
D-Lactic acidosis was first reported in a male with short
bowel syndrome in 1979.1 Since then this entity has been
reported in patients with jejunoileal bypass, small bowel
resection, and other causes of short bowel syndrome or
malabsorption syndrome. The clinical manifestation is
characterized by episodes of encephalopathy and metabolic
acidosis. The encephalopathy was thought to be due to not
only D-lactate but also other unidentified co-products by
colon flora.2 The development of D-lactic acidosis was shown
as Figure 1. In this case, a large amount of carbohydrate
intake, combined with gastrojejunal bypass, diminished
colonic motility, and an additional diet supplement containing lactobacilli enhanced the production of D-lactic acid.3
Impaired renal function further reduced its excretion.
262
Humans have a capacity to metabolize D-lactate to pyruvate
by the enzyme D-2-hydroxy acid dehydrogenase.
D-Lactic acidosis should be strongly considered in the
patient with short bowel or other malabsorption syndrome,
high anion gap metabolic acidosis, negative ketones, and
normal serum concentration of L-lactate. Neurologic symptoms
and signs are also clues. Definite diagnosis required direct
measurement of D-lactic acid. The standard assay for lactate
uses L-lactate dehydrogenase, which will not detect D-lactate.
Treatment includes withholding enteral carbohydrate, intravenous bicarbonate solution, and rehydration. Oral antimicrobial
agents against acid-resistant lactobacilli, such as metronidazole,
neomycin, or vancomycin, may be useful. Hemodialysis could be
an effective treatment for severe D-lactic acidosis.
ACKNOWLEDGMENTS
We thank Professor Shih-Hua Lin, Division of Nephrology, Tri-Service
General Hospital Taipei, Taiwan, for measuring the D-lactate
concentration.
REFERENCES
1.
2.
3.
Oh MS, Phelps KR, Traube M et al. Dh-Lactic acidosis in a man with the
short bowel syndrome. N Engl J Med 1979; 301: 249–252.
Halperin MI, Kamel KS. D-lactic acidosis: turning sugar into acids in the
gastrointestinal tract. Kidney Int 1996; 49: 1–8.
Ku WH, Lau DCY, Huen KF. Probiotics provoked D-lactic acidosis in short bowel
syndrome: case report and literature review. HK J Paediatr 2006; 11: 246–254.
Kidney International (2010) 77, 261–262