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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT  
Year : 2013  |  Volume : 24  |  Issue : 6  |  Page : 1207-1209
Non-hemorrhagic dengue fever with rhabdomyolysis


Department of Nephrology, Medwin Hospital, Nampally, Hyderabad, AP, India

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Date of Web Publication13-Nov-2013
 

   Abstract 

Acute kidney injury occurs in 33-50% of patients with rhabdomyolysis and infections remain one of the major contributing factors. The incidence of rhabdomyolysis in non-hemorrhagic dengue virus infection is quite low and may go unnoticed, especially if the presentation is not florid. We report a case of a young male patient, sero-positive for dengue, with no hemorrhagic manifestations or hypotension, who developed rhabdomyolysis complicated by renal failure. The patient eventually needed dialysis support and later recovered fully. Clinicians need to be aware of the occurrence of rhabdomyolysis even in patients without the hemorrhagic manifestations of dengue viral infection and should employ early preventive strategies in such cases.

How to cite this article:
Jha R, Gude D, Chennamsetty S. Non-hemorrhagic dengue fever with rhabdomyolysis. Saudi J Kidney Dis Transpl 2013;24:1207-9

How to cite this URL:
Jha R, Gude D, Chennamsetty S. Non-hemorrhagic dengue fever with rhabdomyolysis. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2020 Sep 22];24:1207-9. Available from: http://www.sjkdt.org/text.asp?2013/24/6/1207/121296

   Introduction Top


Dengue fever has become one of the most important public health concerns regarding mosquito-borne diseases, with an incidence of over 50-100 million cases annually worldwide. [1] The spectrum of presentation may range from the asymptomatic or undifferentiated febrile illness to the more severe dengue hemorrhagic fever (DHF) and the dengue shock syndrome. [2]

The incidence of renal failure in the relatively innocuous non-hemorrhagic dengue fever is not well known. We intend to throw light on the occurrence of rhabdomyolysis in a dengue seropositive patient without evidence of DHF and the need to watch out for such atypical complications.


   Case Report Top


We report a 21-year-old male who presented with fever, arthralgia, and myalgia of 8 days duration. The patient gave a history of analgesic intake (ibuprofen and paracetamol for severe myalgia). He also complained of cola-colored urine and reduced urine output for 3 days prior to hospitalization. Vitals and physical examination were unremarkable except for swollen and tender lower limbs. Laboratory analysis showed the following: hemoglobin 11.1 g/dL, platelet count 78,000/mm 3 , total leukocyte count 11,000/mm 3 , blood urea 291 mg/dL, serum creatinine 10.2 mg/dL, serum potassium 5.4 mmol/L, serum calcium 6.8 mg/dL, phosphorous 6.5 mg/dL, uric acid 17.8 mg/dL, serum glutamate oxaloacetate transaminase 120 U/L, alkaline phosphatase 40 U/L, creatine phosphokinase (CPK) 71,500 U/L, and lactate dehydrogenase 270 U/L. Venous Doppler ruled out the presence of deep vein thrombosis. Ultrasonography showed normal-sized kidneys, with normal cortical area and no obstruction. Urinalysis showed pH of 6.2, blood 4 plus without red cell casts but with pigmented casts, and albumin 1 plus. Echocardiography and X-ray chest were normal. Serology for dengue was positive for both IgG and IgM [enzyme-linked immunosorbent assay (ELISA)]. A diagnosis of dengue fever with acute kidney injury (AKI) caused by pigment-induced acute tubular necrosis (oliguric) due to rhabdomyolysis was made; volume depletion was considered one of the contributing factors. Patient was not given forced alkaline diuresis as he had established oliguric AKI. He was initiated on thrice-weekly hemodialysis (a total of 12 sessions) with which he improved over the period of hospital stay (3 weeks) and was discharged in a satisfactory state. After 6 weeks of follow-up, his serum creatinine was 1.2 mg/dL and CPK was normal.


   Discussion Top


There is a high incidence of renal failure occurring in DHF, but the possibility of AKI in non-hemorrhagic dengue infection has not been well researched. An immune-mediated (immune complex deposition of IgG, IgM, or both, and C3) diffuse proliferative glomerular injury forms the pathological basis for AKI in dengue. [3] Myoglobin-related nephropathy (rhabdomyolysis) could be a second mechanism for AKI in such patients.

The incidence of AKI in rhabdomyolysis is high, although the varying definitions and clinical settings make it hard to exactly quantify the incidence. Among patients in the intensive care unit with evidence of rhabdomyolysis, the mortality may reach 59% in those with concomitant AKI while it is 22% in patients without AKI. [4] Severe rhabdomyolysis is usually complicated by AKI regardless of the cause, and the development of renal failure usually implies poor prognosis. Rhabdomyolysis of infectious etiology is mainly associated with influenza A and B, Coxsackie virus, Epstein-Barr virus, primary human immunodeficiency virus, Legionella, Streptococcus pyogenes, Staphylococcus aureus (pyomyositis), and Clostridium. [5] Rhabdomyolysis in dengue (especially non-hemorrhagic dengue virus syndrome) is relatively rare and underreported, although other atypical presentations like cardiomyopathy and myositis have been described.

The hallmark of rhabdomyolysis is the elevation of muscle enzymes, most notably serum CPK (skeletal muscle fraction-MM) with levels exceeding 100,000 IU/L. [6] Myoglobin, the postulated true pathogenic factor in rhabdomyolysis-induced AKI, is also elevated significantly. The rise in serum myoglobin levels may precede that of the serum CPK levels and can be a valuable pointer to rhabdomyolysis when coupled with the clinical scenario. However, the rapid and unpredictable metabolism of myoglobin precludes its sensitivity, and hence, it is not routinely measured directly in urine or plasma. The increased concentration of myoglobin along the renal tubules from intra-renal vasoconstriction, direct and ischemic tubule injury, and tubular obstruction (pigment casts) has probably contributed to the renal failure in this case. [5] The other common causes of rhabdomyolysis (trauma, exertion, drugs/toxins, metabolic and electrolyte disorders) were excluded in our patient.

Direct viral invasion of the muscle fibers and generation of toxin are the two hypothesized mechanisms fundamentally responsible for the deleterious effects on the muscles. [7] Electron microscopic findings suggesting virus-like particles support the former hypothesis. [8] Davis et al postulated that the release of myotoxic cytokines, particularly tumor necrosis factor (TNF), could be the more likely cause of myositis and rhabdomyolysis. Gagnon et al confirmed the increased production of TNF in response to the dengue virus. [9] Muscle biopsy studies in dengue patients had shown a spectrum of findings ranging from inflammatory infiltrate (peri-vascular mononuclear infiltrate and lipid accumulation) to foci of myonecrosis. [10]

In dengue infections with renal failure, a complicated clinical course with higher mortality rate has been observed. [11] Our case highlights the need for high index of clinical suspicion of renal failure even in non-hemorrhagic dengue fever and timely preventive strategies in such cases (hydration and avoidance of nonsteroidal anti-inflammatory drugs) that help curb the need for dialysis and the associated economic burden, especially in developing countries.


   Acknowledgment Top


We thank our colleagues Drs B. Srinivasa Rao, Girish Narayen, and Surya Narayan Mandal and the staff of the Department of Nephrology for their invaluable support.

 
   References Top

1.Gibbons RV, Vaughn DW. Dengue: An escalating problem. BMJ 2002;324:1563-6.  Back to cited text no. 1
    
2.Lall R, Dhanda V. Dengue hemorrhagic fever and dengue shock syndrome in India. Natl Med J India 1996;9:20-3.  Back to cited text no. 2
    
3.Lima EQ, Gorayeb FS, Zanon JR, Nogueira ML, Ramalho HJ, Burdmann EA. Dengue hemorrhagic fever-induced acute kidney injury without hypotension, haemolysis or rhabdomyolysis. Nephrol Dial Transplant 2007;22:3322-6.  Back to cited text no. 3
    
4.De Meijer AR, Fikkers BG, deKeijzer MH, van Engelen BG, Drenth JP. Serum creatinine kinase as predictor of clinical course in rhabdomyo-lysis: A 5-year intensive care survey. Intensive Care Med 2003;29:1121-5.  Back to cited text no. 4
    
5.Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009; 361:62-72.  Back to cited text no. 5
    
6.Miller ML. Rhabdomyolysis. In: Rose BD, ed. UpToDate. Waltham, Mass: UpToDate; 2005.  Back to cited text no. 6
    
7.Seibold S, Merkel F, Weber M, Marx M. Rhabdomyolysis and acute renal failure in an adult with measles virus infection. Nephrol Dial Transplant 1998;13:1829-31.  Back to cited text no. 7
    
8.Greco TP, Askenase PW, Kashgarian M. Post-viral myositis: Myxovirus like structures in affected muscle. Ann Intern Med 1977;86:193-4.  Back to cited text no. 8
    
9.Gagnon SJ, Mori M, Kurane I, et al. Cytokine gene expression and protein production in peripheral blood mononuclear cells of children with acute dengue virus infections. J Med Virol 2002;67:41-6.  Back to cited text no. 9
    
10.Malheiros SM, Oliveira AS, Schmidt B, Lima JG, Gabbai AA. Dengue: Muscle biopsy findings in 15 patients. Arquivos de Neuro-Psiquiatria 1993;51:159-64.  Back to cited text no. 10
    
11.Kuo MC, Lu PL, Chang JM, et al. Impact of renal failure on the outcome of dengue viral infection. Clin J Am Soc Nephrol 2008;3:1350-6.  Back to cited text no. 11
    

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Correspondence Address:
Ratan Jha
Department of Nephrology, Medwin Hospital, Chirag Ali lane, Nampally, Hyderabad, AP 500001
India
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DOI: 10.4103/1319-2442.121296

PMID: 24231486

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    Abstract
   Introduction
   Case Report
   Discussion
   Acknowledgment
    References
 

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