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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 5  |  Page : 831-834
Severe acute renal failure in a patient with diabetic ketoacidosis


1 King Khalid National Guard Hospital, Jeddah, Kingdom of Saudi Arabia, Department of Pediatrics, Division of Nephrology, Children's Hospital of Eastern Ontario, Ottawa, Canada, Canada
2 Department of Pediatrics, Division of Nephrology, Children's Hospital of Eastern Ontario, Ottawa, Canada

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Date of Web Publication2-Sep-2009
 

   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 im­prove 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 1s t 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.

How to cite this article:
Al-Matrafi J, Vethamuthu J, Feber J. Severe acute renal failure in a patient with diabetic ketoacidosis. Saudi J Kidney Dis Transpl 2009;20:831-4

How to cite this URL:
Al-Matrafi J, Vethamuthu J, Feber J. Severe acute renal failure in a patient with diabetic ketoacidosis. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2017 Mar 30];20:831-4. Available from: http://www.sjkdt.org/text.asp?2009/20/5/831/55371

   Introduction Top


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, mucormy­cosis, rhabdomyolysis, acute pancreatitis, acute renal failure (ARF) and sepsis. The develop­ment of ARF with rhabdomyolysis is a rare but potentially lethal disorder in children with DKA [2] 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 Top


A 12-year-old female presented to the Emer­gency Department with a history of polyuria and polydipsia for the last several weeks and now with decreased level of consciousness and decreased urine output.

The initial physical examination showed se­vere 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 lo­wer 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 hypo­thyroidism.

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 abs­cess and was treated with antibiotics.

Laboratory investigations revealed initial ar­terial 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, pota­ssium 5.7 mmol/L, and chloride 198 mmol/L. Her urinalysis showed 3+ glucose, 3+ ketones, traces of blood and 1+ protein. Serum phos­phate was analyzed only 10 hours after admi­ssion and was 0.3 mmol/L. Patient was subse­quently 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 pota­ssium 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 aci­dosis 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 para­thyroid 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, spe­cific gravity was 1.020 to 1.030, urine micros­copy revealed variable amount of red blood cells ranging from 2 to 50 per HPF. Renal ultrasound showed abnormal hyperechogeni­city and increased size of both kidneys with normal Doppler study.

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 hemo­dialysis 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 hemo­globin after 6 weeks.

The patient was discharged in stable condi­tion and cystatin C GFR at follow-up was 110 mL/min/1.73 m 2 suggesting good recovery of the kidney function, however, she had persis­tent hypertension and microalbuminuria.


   Discussion Top


The patient described in this case report had severe acute oliguric acute renal failure with hypophosphatemia, persistent acidosis and rhab­domyolysis associated with diabetic ketoaci­dosis. Acute renal failure is an uncommon com­plication of DKA in children [2] and rarely re­quires renal replacement therapy. [4]

The etiology of ARF associated with DKA is probably multifactorial, most likely due to hypovolemia and hypotension. [2] Prolonged pro­found ketoacidosis and insulin infusions can lead to severe hypophosphatemia, [5],[6],[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 reab­sorption. [9]

Consequently, prolonged hypophosphatemia may lead to cardiomyopathy and rhabdomyo­lysis secondary to decreased intracellular con­centration of ATP and 2,3 diphosphoglycerate (DPG). [8] Hypophosphatemia also contributes to the metabolic acidosis, which cannot be com­pensated by the renal production of ammonia 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 fai­lure. 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 compli­cations. 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 imme­diately on admission, but 10 hours later. Even after intermittent phosphate supplementation, serum phosphate level did not normalize, and severe metabolic acidosis persisted despite im­provement/normalization of blood glucose level with insulin therapy. The persistence of meta­bolic acidosis and hypophosphatemia with tran­sient rhabdomyolysis probably contributed to the ongoing renal injury due to hypotension.

Phosphate replacement is essential in DKA [10] however, it may be difficult and is considered controversial by others in diabetic ketoacido­sis [11] . Our patient developed hyperphosphatemia even after several days of discontinuation of phosphate supplements despite several hemo­dialysis sessions (see [Figure 1]). It was pro­bably due to the re-equilibration between the intracellular and extracellular space.

Hypophosphatemia resulted in rhabdomyolysis in our patient. This was reported by others [12],[13] but it rarely causes significant acute renal failure.

Although acute renal failure rarely develops in DKA patients, it may be severe and po­tentially life threatening. [2] Our patient had se­veral 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 se­vere oliguric acute renal failure, hypophospha­temia and rhabdomyolysis associated with diabetic ketoacidosis as her initial presentation of diabetes mellitus. Early institution of renal re­placement 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 hypophosphatemia and metabolic acidosis.


   Acknowledgment Top


We thank Stephanie Barnes, administrative assistant to the Nephrology Division, for her help with the preparation of the manuscript.

 
   References Top

1.Rosenbloom AL. Hyperglycemic crises and their complications in children. J Pediatr Endocrinol Metab 2007;20(1):5-18.  Back to cited text no. 1    
2.Murdoch IA, Pryor D, Haycock GB, Cameron SJ. Acute renal failure complicating diabetic ketoacidosis. Acta Paediatr 1993;82(5):498­500.  Back to cited text no. 2    
3.Woodrow G, Brownjohn AM, Turney JH. Acute renal failure in patients with type 1 diabetes mellitus. Postgrad Med J 1994;70(821):192-4.  Back to cited text no. 3    
4.Kawata H, Inui D, Ohto J, et al. The use of continuous hemodiafiltration in a patient with diabetic ketoacidosis. J Anesth 2006;20(2): 129-31.  Back to cited text no. 4    
5.Riley MS, Schade DS, Eaton RP. Effects of insulin infusion on plasma phosphate in dia­betic patients. Metabolism 1979;28(3):191-4.  Back to cited text no. 5    
6.Kebler R, McDonald FD, Cadnapaphornchai P. Dynamic changes in serum phosphorus levels in diabetic ketoacidosis. Am J Med 1985;79 (5):571-6.  Back to cited text no. 6    
7.Becker DJ, Brown DR, Steranka BH, Drash AL. Phosphate replacement during treatment of diabetic ketosis. Effects on calcium and phosphorus homeostasis. Am J Dis Child 1983;137(3):241-6.  Back to cited text no. 7    
8.Liu PY, Jeng CY. Severe hypophosphatemia in a patient with diabetic ketoacidosis and acute respiratory failure. J Chin Med Assoc 2004;67 (7):355-9.  Back to cited text no. 8    
9.Busch A, Waldegger S, Herzer T, et al. Electrophysiological analysis of Na+/Pi cotransport mediated by a transporter cloned from rat kidney and expressed in Xenopus oocytes. Proc Natl Acad Sci U S A 1994;91 (17):8205-8.  Back to cited text no. 9    
10.Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in diabetes. Diabetes Care 2004;27 Suppl 1:S94-102.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Amanzadeh J, Reilly RF, Jr. Hypophosphatemia: an evidence-based approach to its clinical consequences and management. Nat Clin Pract Nephrol 2006;2(3):136-48.  Back to cited text no. 11    
12.Casteels K, Beckers D, Wouters C, Van Geet C. Rhabdomyolysis in diabetic ketoacidosis. Pediatr Diabetes 2003;4(1):29-31.  Back to cited text no. 12    
13.Singhal PC, Abramovici M, Venkatesan J. Rhabdomyolysis in the hyperosmolal state. Am J Med 1990;88(1):9-12.  Back to cited text no. 13    

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Correspondence Address:
Janusz Feber
Department of Pediatrics, Division of Nephrology, Children's Hospital of Eastern Ontario, 401 Smyth Road, Ottawa, ON K1H 8L1
Canada
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PMID: 19736483

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    Abstract
    Introduction
    Case Report
    Discussion
    Acknowledgment
    References
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