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LETTER TO EDITOR
Year : 2015  |  Volume : 2  |  Issue : 3  |  Page : 99-100

Acute Kidney Injury with Hyperuricemia: Is it All?


1 Department of Pulmonary Critical Care and Sleep Medicine, The Mission Hospital, Durgapur, West Bengal, India
2 Department of Pathology, The Mission Hospital, Durgapur, West Bengal, India

Date of Web Publication24-Jul-2015

Correspondence Address:
Dr. Animesh Ray
Department of Pulmonary Critical Care and Sleep Medicine, The Mission Hospital, Durgapur, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2225-1243.161443

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How to cite this article:
Ray A, Das S. Acute Kidney Injury with Hyperuricemia: Is it All?. J Integr Nephrol Androl 2015;2:99-100

How to cite this URL:
Ray A, Das S. Acute Kidney Injury with Hyperuricemia: Is it All?. J Integr Nephrol Androl [serial online] 2015 [cited 2019 Dec 9];2:99-100. Available from: http://www.journal-ina.com/text.asp?2015/2/3/99/161443

Dear Editor,

We had a 15-year-old male patient who presented to us with complaints of low-grade fever for 1-week along with vague arthralgia, myalgia, vomiting, loose motions, and decreased urine output for the same duration. The general and systemic examination was unremarkable except for mild pallor. Investigations revealed hemoglobin of 10.7 g/dL, total leukocyte count (TLC) of 9700/cmm (lymphocyte 76%, neutrophil 22%), platelet count 50,000/cmm, urea 126, creatinine 5.8, sodium 141, potassium 5.5, uric acid 16 mg/dL, and normal procalcitonin level. Urine examination showed pus cells (5-7/hpf) with scant albumin and culture was sterile. Ultrasound abdomen revealed normal sized kidney. A provisional diagnosis of acute kidney injury (AKI) secondary to probable viral illness was made, and the patient was treated with intravenous fluids, antibiotics, etc. In response to treatment the patient's urea, creatinine, and uric acid decreased (urea 22, creatinine 1.1 uric acid 6 mg/dL), but leukocytosis (TLC 1,67000/cmm with predominant lymphocytosis with no abnormal cells) developed and platelets decreased to 30000/cmm. A bone marrow aspiration biopsy was done, which revealed more than 30% blasts with the overall picture compatible with acute lymphoblastic leukemia (ALL) [Figure 1].
Figure 1: Bone marrow aspiration biopsy showing presence of significant lymphoblasts

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This case thus depicts an instance of ALL presenting as AKI. AKI was probably due to uric acid nephropathy. Following hydration and reduction of hyperuricemia the AKI resolved, but the hematological picture of ALL unraveled.

AKI has been described sparingly as a presenting feature of ALL. [1],[2]

The likely causes of kidney involvement in ALL are described in [Table 1].
Table 1: The possible causes of AKI in leukemia

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AKI can be associated with hyperuricemia but in these cases the uric acid level is usually <12 mg/dL (except for some cases of pre-renal failure where uric acid level may be higher as a result of proximal tubular re-absorption). Hence, in cases of AKI with significant hyperuricemia the possibility of acute leukemia has to be kept in mind.

AKI and hyperuricemia preceding the onset of ALL has been described very rarely. [3] Our patient had a similar kind of course of the disease.

In conclusion, we would like to reiterate that hyperuricemia in the presence of AKI in the appropriate setting should prompt the search for hematological malignancies like ALL. In such cases the full blown hematological picture of acute leukemia might be not be apparent initially.

 
  References Top

1.
Larsen G, Loghman-Adham M. Acute renal failure with hyperuricemia as initial presentation of leukemia in children. J Pediatr Hematol Oncol 1996;18:191-4.  Back to cited text no. 1
    
2.
Suh WM, Wainberg ZA, de Vos S, Cohen AH, Kurtz I, Nguyen MK. Acute lymphoblastic leukemia presenting as acute renal failure. Nat Clin Pract Nephrol 2007;3:106-10.  Back to cited text no. 2
    
3.
Appleyard WJ. Hyperuricaemia and renal failure preceding the onset of acute lymphoblastic leukaemia. Proc R Soc Med 1971;64:728.  Back to cited text no. 3
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1]



 

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