of
admission in consequent to right upper pneumonitis caused by
Influenza-B virus. The dark urine with renal failure could
be due to hemoglobinuria or myoglobinuria.The authors have
assumed it to be due to rhabdomyolysis leading to
myoglobinuria based on striking elevation of serum creatine
kinase (CK), LDH.AST/ALT only. Screening of urine should be
done by Dipstick or Orthotoludine blue test which will be
indicative of hemoglobinuria, myoglobinuria, or hematuria.
Absence of RBC on urine microscopic examination will rule
out hematuria. Further urine analysis should be done by
electrophoresis or spectrophotometry to distinguish between
myoglobinuria and hemoglobinuria. It is not clear from this
case report whether blood examination for hemoglobin,
Reticulocyte count, Direct Coomb’s test were performed to
rule out hemoglobinuria.
Myoglobinuria can lead to acute renal
failure (ARF) by direct renal tubular damage or mechanical
blockage of tubular lumen [2]. Hemoglobinuria also can
behave in a similar way. After the development of ARF
patient’s serum creatinine level was 1.47 mg/ dL. Serum urea
nitrogen (BUN) was not studied at that time though both were
normal soon after admission. BUN and serum creatinine ratio
was important to know the type of ARF i.e. intrinsic
or prerenal. Urine routine analysis would also help in this
regard. The meagre degree of creatinine elevation raises
doubt about the possibility of rhabdomyolysis. Creatinine
level is considerably elevated out of proportion to BUN due
to excessive leak of creatine from damage of muscle cells.
Viral illness may cause dark urine due to
hemoglobinuria as well seen in G-6PD deficiency, autoimmune
haemolytic anaemia (AIHA) [3,4]. Hepatitis A virus has been
found to cause intravascular hemolysis in G-6PD deficiency
[5]. Severe hemoglobinuria in consequence to virus A with
normal G-6PD status has been observed due to AIHA [6].
So, it appears from the present case
report that the diagnostic possibility of Influenza-B virus
induced hemoglobinuria associated with viral myositis
leading to ARF caused by either G-6PD deficiency or AIHA
remains until necessary appropriate laboratory tests are
carried out.
1. Hung PL, Lin PC, Tseng PL.
Influenza-B Associated Rhabdomyolysis and Acute Renal
Failure. Indian Pediatr. 2013;50:595-6.
2. Beetham R. Biochemical
investigation of suspected rhabdomyolysis. Ann Clin
Biochem. 2000;37:581-7
3. Segel GB, Packman CH. Hemolytic
Anaemias Resulting from Extracellular Factors- Immune
Hemolytic Anaemias. In: Kilegman RM, Stanton BF,
Schor NF, St. Gene JW, Berhman RE, Editors. Nelson
Textbook of Pediatrics.19th ed. Philadelphia.
Elsevier; 2011. p. 1680-3.
4. Segel GB, Hackney LR.
Glucose-6-Phosphate Dehydrogenase deficiency and Related
deficiencies. In: Kilegman RM, Stanton BF, Schor
NF, St. Gene JW, Berhman RE, Editors. Nelson Textbook of
Pediatrics.19th ed. Philadelphia. Elsevier; 2011.
p. 1678-80.
5. Sarkar S, Prakash D, Marwah
RK.Acute intravascular hemolysis in G-6-P-D deficiency.
Ann Trop Padiatr. 1993;13:391-4.
6. Lyons DJ, Gilvarry JM, Fielding
JF. Severe hemolysis associated with hepatitis A and
normal glucose-6-phosphate dehydrogenase status. Gut.
1990;31:838-9.
Reply
We are thankful to the author for his
interest in our publication. Myoglobin is rapidly and
unpredictably eliminated by hepatic metabolism. Therefore,
tests for myoglobin in plasma or urine are not a sensitive
diagnostic procedure. Red discoloration of the urine when
erythrocytes cannot be detected by microscopy must be due to
hemoglobinuria or myoglobinuria. The urine microscopic
examination showed RBC 0-1/hpf should rule out hematuria.
The enzyme CK is ubiquitously present in
striated muscle. When muscle cells disintegrate, CK is
released into the bloodstream. Because overall degradation
and removal are slow, the concentration of CK remains
elevated much longer and in a more consistent manner than
that of myoglobin. Consequently, CK is more reliable than
myoglobin in assessing the presence and intensity of damage
to the muscles. The high level of CK was observed on this
case so rhabdomyolysis leading to myoglobinuria should be
highly suspected.
The serum creatinine level 3.46 mg/dL and
serum urea nitrogen (BUN) 74 mg/dL were studied on the next
day after acute renal failure happened. The ratio of BUN and
serum creatinine was at borderline for diagnosis of
intrinsic ARF. According to past history of this patient,
ARF caused by either G-6PD deficiency or AIHA were ruled
out.