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250]

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


renal failure (ARF) and sepsis. The develop-
Diabetic ketoacidosis (DKA) occurs in 10 to ment of ARF with rhabdomyolysis is a rare but
70% of children with type 1 diabetes mellitus potentially lethal disorder in children with
(DM1) and has a significant risk of mortality, DKA2 with an estimated mortality of about
mostly due to cerebral edema.1 Other potential 50%.3 The poor outcome of ARF associated
complications of DKA include hypokalemia, with DKA underlines the importance of early
hypophosphatemia, hypoglycemia, intracerebral recognition of ARF and early initiation of renal
and peripheral venous thrombosis, mucormy- replacement therapy.
Correspondence to: We describe our experience of treating a
child presenting with DKA and ARF as first
Dr. Janusz Feber manifestation of DM1.
Associate Professor of Pediatrics
Division of Nephrology Case Report
Department of Pediatrics
Children’s Hospital of Eastern Ontario A 12-year-old female presented to the Emer-
401 Smyth Road, Ottawa, gency Department with a history of polyuria
ON K1H 8L1, Canada and polydipsia for the last several weeks and
E-mail: jfeber@cheo.on.ca 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. quently admitted to the intensive care unit with
The initial physical examination showed se- diagnosis of severe diabetic ketoacidosis and
vere dehydration, Glasgow Coma Scale (GCS) acute oliguric renal failure. The patient was
of 8-9, pulse of 130/minutes, systolic blood resuscitated with IV fluids, Insulin and pota-
pressure below 70 mmHg, hyperventilation ssium chloride and a computer tomography
(respiratory rate 29/minutes), no edema of lo- scan of the brain were normal.
wer extremities, and oxygen saturation of 100% Blood pressure improved with addition of
at room air. vasopressors and addition of furosemide as IV
Family history was negative for renal disease, boluses and infusion improved the urine output
but one of her grandparents suffers from type to 1.5 mL/kg/h. However, her metabolic aci-
II diabetes mellitus, and her father has hypo- dosis persisted with arterial bicarbonate of 5
thyroidism. mmol/L and the arterial pH of 7.03. Level of
Past medical history revealed bronchial asthma consciousness improved (GCS 11-13) but her
controlled with salbutamol and inhaled steroids kidney function deteriorated Figure 1. Serum
as needed. Several weeks before admission, phosphate was persistently low at 0.9 mmol/L
our patient was diagnosed with a perineal abs- despite phosphate supplementation. Intact para-
cess and was treated with antibiotics. thyroid hormone level was 7.0 pmol/L (normal
Laboratory investigations revealed initial ar- range 1.6-9.3). Serum creatinine kinase was
terial gas with a pH of 6.77, bicarbonate of 5 2692 U/L (normal range 27-140) on day 2. At
mmol/L and base excess -30.5. Serum glucose that time the urine was positive for blood and
was 53.6 mmol/L, serum creatinine 315 µmol/L, protein (2+ to 3+), pH ranged from 5 to 6, spe-
urea 14.5 mmol/L, sodium 136 mmol/L, pota- cific gravity was 1.020 to 1.030, urine micros-
ssium 5.7 mmol/L, and chloride 198 mmol/L. copy revealed variable amount of red blood
Her urinalysis showed 3+ glucose, 3+ ketones, cells ranging from 2 to 50 per HPF. Renal
traces of blood and 1+ protein. Serum phos- ultrasound showed abnormal hyperechogeni-
phate was analyzed only 10 hours after admi- city and increased size of both kidneys with
ssion and was 0.3 mmol/L. Patient was subse- normal Doppler study.
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Severe acute renal failure in DKA 833

On day 4 after admission serum creatinine due to lower urinary excretion of phosphate in
increased to 620 µmol/L, urea was 34.3 mmol/L the course of DKA.8 Hypophosphatemia-induced
and persistent severe metabolic acidosis and decrease in DPG may also affect the oxygen
oliguria warranted initiation of hemodialysis, dissociation curve which results in impaired
Figure 1. Her metabolic profile improved and oxygen delivery and eventually respiratory fai-
urine output started to increased to 2.2 mL/kg/ lure. In addition, haemolytic anemia may occur
hour on day 11 and she required only 8 hemo- from hypophosphatemia-induced rigidity of the
dialysis sessions. red cell membrane.8
Patients hemoglobin progressively decreased It is therefore very important to detect changes
from 135 to 87 g/L (normal range 120-160 g/L) in serum phosphate levels early on in DKA in
on hemodialysis therapy in the absence of order to prevent the above mentioned compli-
hemolysis (LDH was 574 U/L, normal range cations. However, symptoms of even severe
300-700 U/L) and no obvious blood losses. hypophosphatemia may mimic symptoms of
Darbepoeitin 40 micrograms subcutaneously the underlying disease and therefore may not
once per week and iron supplementation were be recognized in a critically ill patient.8 This
initiated resulting in normalization of hemo- was the case in our patient, where we did not
globin after 6 weeks. recognize severe hypophosphatemia imme-
The patient was discharged in stable condi- diately on admission, but 10 hours later. Even
tion and cystatin C GFR at follow-up was 110 after intermittent phosphate supplementation,
mL/min/1.73 m2 suggesting good recovery of serum phosphate level did not normalize, and
the kidney function, however, she had persis- severe metabolic acidosis persisted despite im-
tent hypertension and microalbuminuria. provement/normalization of blood glucose level
with insulin therapy. The persistence of meta-
Discussion bolic acidosis and hypophosphatemia with tran-
sient rhabdomyolysis probably contributed to
The patient described in this case report had the ongoing renal injury due to hypotension.
severe acute oliguric acute renal failure with Phosphate replacement is essential in DKA10
hypophosphatemia, persistent acidosis and rhab- however, it may be difficult and is considered
domyolysis associated with diabetic ketoaci- controversial by others in diabetic ketoacido-
dosis. Acute renal failure is an uncommon com- sis11. Our patient developed hyperphosphatemia
plication of DKA in children2 and rarely re- even after several days of discontinuation of
quires renal replacement therapy.4 phosphate supplements despite several hemo-
The etiology of ARF associated with DKA is dialysis sessions (see Figure 1). It was pro-
probably multifactorial, most likely due to bably due to the re-equilibration between the
hypovolemia and hypotension.2 Prolonged pro- intracellular and extracellular space.
found ketoacidosis and insulin infusions can Hypophosphatemia resulted in rhabdomyolysis
lead to severe hypophosphatemia,5-7 mainly as in our patient. This was reported by others12,13
a result of intracellular phosphate shifting.8 In but it rarely causes significant acute renal failure.
addition, urinary phosphate excretion is initially Although acute renal failure rarely develops
increased in response to an acidemia-induced in DKA patients, it may be severe and po-
inhibition of phosphate proximal tubular reab- tentially life threatening.2 Our patient had se-
sorption.9 veral indications of hemodialysis including
Consequently, prolonged hypophosphatemia oliguria, intractable metabolic acidosis, fluid
may lead to cardiomyopathy and rhabdomyo- overload and hypertension. Hypophosphatemia
lysis secondary to decreased intracellular con- also easily corrected when metabolic acidosis
centration of ATP and 2,3 diphosphoglycerate was corrected.
(DPG).8 Hypophosphatemia also contributes to In conclusion, our patient presented with se-
the metabolic acidosis, which cannot be com- vere oliguric acute renal failure, hypophospha-
pensated by the renal production of ammonia temia and rhabdomyolysis associated with dia-
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834 Al-Matrafi J, Vethamuthu J, Feber J

betic ketoacidosis as her initial presentation of betic patients. Metabolism 1979;28(3):191-4.


diabetes mellitus. Early institution of renal re- 6. Kebler R, McDonald FD, Cadnapaphornchai P.
placement therapy may be considered not only Dynamic changes in serum phosphorus levels
to treat usual features of acute renal failure like in diabetic ketoacidosis. Am J Med 1985;79
(5):571-6.
uremia and fluid retention but also helps in
7. Becker DJ, Brown DR, Steranka BH, Drash
correcting metabolic abnormalities like hypo- AL. Phosphate replacement during treatment
phosphatemia and metabolic acidosis. of diabetic ketosis. Effects on calcium and
phosphorus homeostasis. Am J Dis Child
Acknowledgment 1983;137(3):241-6.
8. Liu PY, Jeng CY. Severe hypophosphatemia in
We thank Stephanie Barnes, administrative a patient with diabetic ketoacidosis and acute
assistant to the Nephrology Division, for her respiratory failure. J Chin Med Assoc 2004;67
help with the preparation of the manuscript. (7):355-9.
9. Busch A, Waldegger S, Herzer T, et al.
Electrophysiological analysis of Na+/Pi
References
cotransport mediated by a transporter cloned
from rat kidney and expressed in Xenopus
1. Rosenbloom AL. Hyperglycemic crises and their oocytes. Proc Natl Acad Sci U S A 1994;91
complications in children. J Pediatr Endocrinol (17):8205-8.
Metab 2007;20(1):5-18. 10. Kitabchi AE, Umpierrez GE, Murphy MB, et
2. Murdoch IA, Pryor D, Haycock GB, Cameron al. Hyperglycemic crises in diabetes. Diabetes
SJ. Acute renal failure complicating diabetic Care 2004;27 Suppl 1:S94-102.
ketoacidosis. Acta Paediatr 1993;82(5):498- 11. Amanzadeh J, Reilly RF, Jr. Hypophosphatemia:
500. an evidence-based approach to its clinical
3. Woodrow G, Brownjohn AM, Turney JH. Acute consequences and management. Nat Clin Pract
renal failure in patients with type 1 diabetes Nephrol 2006;2(3):136-48.
mellitus. Postgrad Med J 1994;70(821):192-4. 12. Casteels K, Beckers D, Wouters C, Van Geet
4. Kawata H, Inui D, Ohto J, et al. The use of C. Rhabdomyolysis in diabetic ketoacidosis.
continuous hemodiafiltration in a patient with Pediatr Diabetes 2003;4(1):29-31.
diabetic ketoacidosis. J Anesth 2006;20(2): 13. Singhal PC, Abramovici M, Venkatesan J.
129-31. Rhabdomyolysis in the hyperosmolal state. Am
5. Riley MS, Schade DS, Eaton RP. Effects of J Med 1990;88(1):9-12.
insulin infusion on plasma phosphate in dia-