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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2018  |  Volume : 29  |  Issue : 4  |  Page : 1007-1009
Acute kidney injury and disseminated intravascular coagulation complicating hepatitis A

Department of Medicine, Dr. S. N. Medical College, Jodhpur, Rajasthan, India

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Date of Submission08-Jan-2018
Date of Acceptance14-Jan-2018
Date of Web Publication28-Aug-2018

How to cite this article:
Pahadiya HR, Lakhotia M, Gandhi R, Choudhary A. Acute kidney injury and disseminated intravascular coagulation complicating hepatitis A. Saudi J Kidney Dis Transpl 2018;29:1007-9

How to cite this URL:
Pahadiya HR, Lakhotia M, Gandhi R, Choudhary A. Acute kidney injury and disseminated intravascular coagulation complicating hepatitis A. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2020 Aug 9];29:1007-9. Available from: http://www.sjkdt.org/text.asp?2018/29/4/1007/239631
To the Editor,

A previously healthy 42-year-old nonalcoholic female with 3-day history of fever, yellowish discoloration of urine, and sclera presented with one-day history of altered sensorium and decreased urine output. She had no history of trauma, headache, chronic illness, or addictions. On examination, pulse rate was 124/min, blood pressure was 108/60 mm Hg, respiratory rate was 24 breaths/min, and temperature was 36.7°C. She was irritable, mildly dehydrated, and jaundiced. Further, the clinical examination was not contributory. Laboratory findings revealed anemia, thrombocytopenia, and renal and liver dysfunction with coagulopathy [Table 1]. IgM antihepatitis A antibodies were positive, while serology for malaria, HBV, HCV, HIV, and leptospirosis was negative. The chest X-ray, computed tomography scan of the head, and CSF examination were normal. Ultrasonography of the abdomen showed mild hepatomegaly with echogenic kidneys and preserved cortical echotexture. There were no gallstone and ascites. She was treated supportively. She did not respond to the treatment and expired on 2nd day of admission.

Table 1: Laboratory Investigations at presentation.

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Acute hepatitis A (AHA) is common in children and is usually asymptomatic or self-limiting. Recently, there is an upward shift in the average age of the first AHA. The risk of fulminant hepatitis increases with age, in preexisting liver disease or alcoholics. Persistent nausea, vomiting, coagulopathy, encephalopathy, and hepatic dysfunction point to severe disease.[1]

Acute kidney injury (AKI) is a rare complication of AHA. AKI has been reported most often as a complication of fulminant hepatitis whereas it is rarely associated with nonfulminating AHA.[2] Males, alcoholics, smokers, diabetics, and hypertensive are more prone for the development of AKI. Leukocytosis, prolonged PT, hypoalbuminemia, liver dysfunctions, and increased CRP are commonly found in patients of AKI with AHA.[2],[3]

The mechanism of AHA-induced AKI is still unclear for which various mechanisms have been put forward.[3]

  • Acute tubular necrosis
  • Acute tubulointerstitial nephritis
  • Endotoxemia
  • Immune complex-mediated glomerulonephritis
  • Hepatorenal syndrome

Acute tubular necrosis is the principal mechanism in AHA-associated AKI which is favored by high urinary sodium excretion. The AKI because of volume depletion state due to vomiting, diarrhea, fever, and poor oral intake reduces renal blood flow through the activation of the renin–angiotensin system.[2],[3] Hyper-bilirubinemia and bile salts also contribute in reducing renal blood flow by causing renal vasoconstriction.[4]

The immune complex-mediated mechanism is more common in HBV and HCV, as compared to the HAV infection. The common glomerulonephritis associated with AHA is membranous nephropathy, mesangial proliferative, and membranoproliferative glomerulo-nephritis. These patients usually have hematuria, hypertension, and proteinuria. Endo-toxemia can cause renal hypoperfusion which along with the cytopathic effect of the virus can cause AKI in fulminant hepatic failure.[2],[3]

Our patient had AHA complicated by disseminated intravascular coagulation (DIC) and AKI. The possible mechanism for AKI might be due to volume-depleted state, which was evident by clinical history and hypernatremia, along with hyperbilirubinemia-induced renal injury. The presence of DIC, accentuating renal injury can be thought as DIC could have caused fibrin-rich thrombi formation involving glomerular capillaries and arterioles and glo-merular endothelial and/or podocyte injury. The AKI and DIC complicating AHA infection are rarely reported.

Conflict of interest: None declared.

   References Top

Cuthbert JA. Hepatitis A: Old and new. Clin Microbiol Rev 2001;14:38-58.  Back to cited text no. 1
Lin CC, Chang CH, Lee SH, Chiang SS, Yang AH. Acute renal failure in non-fulminant hepatitis A. Nephrol Dial Transplant 1996;11:2061-6.  Back to cited text no. 2
Jung YJ, Kim W, Jeong JB, et al. Clinical features of acute renal failure associated with hepatitis A virus infection. J Viral Hepat 2010; 17:611-7.  Back to cited text no. 3
Green J, Beyar R, Bomzon L, Finberg JP, Better OS. Jaundice, the circulation and the kidney. Nephron 1984;37:145-52.  Back to cited text no. 4

Correspondence Address:
Dr. Hans Raj Pahadiya
Department of Medicine, Dr. S. N. Medical College, Jodhpur
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DOI: 10.4103/1319-2442.239631

PMID: 30152446

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