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Saudi J Kidney Dis Transpl 2009;20(5):831-834

© 2009 Saudi Center for Organ Transplantation Saudi Journal
of Kidney Diseases
and Transplantation

Case Report

Severe Acute Renal Failure in a Patient with Diabetic Ketoacidosis

Jamila Al-Matrafi1,2, Jennifer Vethamuthu2, Janusz Feber2
1
King Khalid National Guard Hospital, Jeddah, Kingdom of Saudi Arabia
2
Division of Nephrology, Department of Pediatrics, Children’s Hospital of Eastern Ontario,
Ottawa, Canada

ABSTRACT. Acute renal failure (ARF) is a rare but potentially fatal complication of diabetic
ketoacidosis (DKA). Early recognition and aggressive treatment of ARF during DKA may im-
prove the prognosis of these patients. We present a case report of a 12 year old female admitted to
the hospital with severe DKA as the 1st manifestation of her diabetes mellitus. She presented with
severe metabolic acidosis, hypophosphatemia, and oliguric ARF. In addition, rhabdomyolysis was
noted during the course of DKA which probably contributed to the ARF. Management of DKA
and renal replacement therapy resulted in quick recovery of renal function. We suggest that early
initiation of renal replacement therapy for patients with DKA developing ARF may improve the
potentially poor outcome of patients with ARF associated with DKA.

Introduction cosis, rhabdomyolysis, acute pancreatitis, acute

Diabetic ketoacidosis (DKA) occurs in 10 to
70% of children with type 1 diabetes mellitus
(DM1) and has a significant risk of mortality,
mostly due to cerebral edema.1 Other potential
complications of DKA include hypokalemia,
hypophosphatemia, hypoglycemia, intracerebral
and peripheral venous thrombosis, mucormy-
Correspondence to:
Dr. Janusz Feber
Associate Professor of Pediatrics
Division of Nephrology
Department of Pediatrics
Children’s Hospital of Eastern Ontario
401 Smyth Road, Ottawa,
ON K1H 8L1, Canada
E-mail: jfeber@cheo.on.ca
renal failure (ARF) and sepsis. The develop-
ment of ARF with rhabdomyolysis is a rare but
potentially lethal disorder in children with
DKA2 with an estimated mortality of about
50%.3 The poor outcome of ARF associated
with DKA underlines the importance of early
recognition of ARF and early initiation of renal
replacement therapy.
We describe our experience of treating a
child presenting with DKA and ARF as first
manifestation of DM1.
Case Report
A 12-year-old female presented to the Emer-
gency Department with a history of polyuria
and polydipsia for the last several weeks and
now with decreased level of consciousness and
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832 Al-Matrafi J, Vethamuthu J, Feber J

Hemodialysis sessions
S-crea
S-phosphate

600 2.0

S-phosphate
1.5
S-crea

400

1.0
200
0.5

0 0.0
0 2 4 6 8 10 12 14 16 18 20 22
Days after admission

Figure 1. Evolution of serum creatinine (S-crea, left y axis) and serum phosphate (S-phosphate, right y
axis) in a patient with acute renal failure during diabetic ketoacidosis. Shaded dotted area depicts normal
range of S-crea, shaded lined area depicts normal range of S-phosphate

decreased urine output.
The initial physical examination showed se-
vere dehydration, Glasgow Coma Scale (GCS)
of 8-9, pulse of 130/minutes, systolic blood
pressure below 70 mmHg, hyperventilation
(respiratory rate 29/minutes), no edema of lo-
wer extremities, and oxygen saturation of 100%
at room air.
Family history was negative for renal disease,
but one of her grandparents suffers from type
II diabetes mellitus, and her father has hypo-
thyroidism.
Past medical history revealed bronchial asthma
controlled with salbutamol and inhaled steroids
as needed. Several weeks before admission,
our patient was diagnosed with a perineal abs-
cess and was treated with antibiotics.
Laboratory investigations revealed initial ar-
terial gas with a pH of 6.77, bicarbonate of 5
mmol/L and base excess -30.5. Serum glucose
was 53.6 mmol/L, serum creatinine 315 µmol/L,
urea 14.5 mmol/L, sodium 136 mmol/L, pota-
ssium 5.7 mmol/L, and chloride 198 mmol/L.
Her urinalysis showed 3+ glucose, 3+ ketones,
traces of blood and 1+ protein. Serum phos-
phate was analyzed only 10 hours after admi-
ssion and was 0.3 mmol/L. Patient was subse-
quently admitted to the intensive care unit with
diagnosis of severe diabetic ketoacidosis and
acute oliguric renal failure. The patient was
resuscitated with IV fluids, Insulin and pota-
ssium chloride and a computer tomography
scan of the brain were normal.
Blood pressure improved with addition of
vasopressors and addition of furosemide as IV
boluses and infusion improved the urine output
to 1.5 mL/kg/h. However, her metabolic aci-
dosis persisted with arterial bicarbonate of 5
mmol/L and the arterial pH of 7.03. Level of
consciousness improved (GCS 11-13) but her
kidney function deteriorated Figure 1. Serum
phosphate was persistently low at 0.9 mmol/L
despite phosphate supplementation. Intact para-
thyroid hormone level was 7.0 pmol/L (normal
range 1.6-9.3). Serum creatinine kinase was
2692 U/L (normal range 27-140) on day 2. At
that time the urine was positive for blood and
protein (2+ to 3+), pH ranged from 5 to 6, spe-
cific gravity was 1.020 to 1.030, urine micros-
copy revealed variable amount of red blood
cells ranging from 2 to 50 per HPF. Renal
ultrasound showed abnormal hyperechogeni-
city and increased size of both kidneys with
normal Doppler study.
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Severe acute renal failure in DKA
On day 4 after admission serum creatinine
increased to 620 µmol/L, urea was 34.3 mmol/L
and persistent severe metabolic acidosis and
oliguria warranted initiation of hemodialysis,
Figure 1. Her metabolic profile improved and
urine output started to increased to 2.2 mL/kg/
hour on day 11 and she required only 8 hemo-
dialysis sessions.
Patients hemoglobin progressively decreased
from 135 to 87 g/L (normal range 120-160 g/L)
on hemodialysis therapy in the absence of
hemolysis (LDH was 574 U/L, normal range
300-700 U/L) and no obvious blood losses.
Darbepoeitin 40 micrograms subcutaneously
once per week and iron supplementation were
initiated resulting in normalization of hemo-
globin after 6 weeks.
The patient was discharged in stable condi-
tion and cystatin C GFR at follow-up was 110
mL/min/1.73 m2 suggesting good recovery of
the kidney function, however, she had persis-
tent hypertension and microalbuminuria.
Discussion
The patient described in this case report had
severe acute oliguric acute renal failure with
hypophosphatemia, persistent acidosis and rhab-
domyolysis associated with diabetic ketoaci-
dosis. Acute renal failure is an uncommon com-
plication of DKA in children2 and rarely re-
quires renal replacement therapy.4
The etiology of ARF associated with DKA is
probably multifactorial, most likely due to
hypovolemia and hypotension.2 Prolonged pro-
found ketoacidosis and insulin infusions can
lead to severe hypophosphatemia,5-7 mainly as
a result of intracellular phosphate shifting.8 In
addition, urinary phosphate excretion is initially
increased in response to an acidemia-induced
inhibition of phosphate proximal tubular reab-
sorption.9
Consequently, prolonged hypophosphatemia
may lead to cardiomyopathy and rhabdomyo-
lysis secondary to decreased intracellular con-
centration of ATP and 2,3 diphosphoglycerate
(DPG).8 Hypophosphatemia also contributes to
the metabolic acidosis, which cannot be com-
pensated by the renal production of ammonia
833
due to lower urinary excretion of phosphate in
the course of DKA.8 Hypophosphatemia-induced
decrease in DPG may also affect the oxygen
dissociation curve which results in impaired
oxygen delivery and eventually respiratory fai-
lure. In addition, haemolytic anemia may occur
from hypophosphatemia-induced rigidity of the
red cell membrane.8
It is therefore very important to detect changes
in serum phosphate levels early on in DKA in
order to prevent the above mentioned compli-
cations. However, symptoms of even severe
hypophosphatemia may mimic symptoms of
the underlying disease and therefore may not
be recognized in a critically ill patient.8 This
was the case in our patient, where we did not
recognize severe hypophosphatemia imme-
diately on admission, but 10 hours later. Even
after intermittent phosphate supplementation,
serum phosphate level did not normalize, and
severe metabolic acidosis persisted despite im-
provement/normalization of blood glucose level
with insulin therapy. The persistence of meta-
bolic acidosis and hypophosphatemia with tran-
sient rhabdomyolysis probably contributed to
the ongoing renal injury due to hypotension.
Phosphate replacement is essential in DKA10
however, it may be difficult and is considered
controversial by others in diabetic ketoacido-
sis11. Our patient developed hyperphosphatemia
even after several days of discontinuation of
phosphate supplements despite several hemo-
dialysis sessions (see Figure 1). It was pro-
bably due to the re-equilibration between the
intracellular and extracellular space.
Hypophosphatemia resulted in rhabdomyolysis
in our patient. This was reported by others12,13
but it rarely causes significant acute renal failure.
Although acute renal failure rarely develops
in DKA patients, it may be severe and po-
tentially life threatening.2 Our patient had se-
veral indications of hemodialysis including
oliguria, intractable metabolic acidosis, fluid
overload and hypertension. Hypophosphatemia
also easily corrected when metabolic acidosis
was corrected.
In conclusion, our patient presented with se-
vere oliguric acute renal failure, hypophospha-
temia and rhabdomyolysis associated with dia-
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834
betic ketoacidosis as her initial presentation of
diabetes mellitus. Early institution of renal re-
placement therapy may be considered not only
to treat usual features of acute renal failure like
uremia and fluid retention but also helps in
correcting metabolic abnormalities like hypo-
phosphatemia and metabolic acidosis.
Acknowledgment
We thank Stephanie Barnes, administrative
assistant to the Nephrology Division, for her
help with the preparation of the manuscript.
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