Shaheed Syed Nazrul Islam Medical College Journal

Volume 9, Issue 1, January 2024

Editorial

https://doi.org/10.69699/ssnimcj.2024.v9.i1.01

Dengue and Acute Kidney Injury

Dr. Abu Ayub Md. Nazmul Huda. MBBS, FCPS (Medicine), MD (Nephrology). Associate Professor and Head, Department of Nephrology, Shaheed Sayed Nazrul Islam Medical College, Kishoreganj. a2mnhuda71@gmail.com

Dengue is the most widespread and rapidly growing vector-borne disease.¹ An estimated 2.5 billion people in 129 countries live in endemic tropical and subtropical regions are at risk of contracting dengue, with 105 million people infected each year.² Dengue is a viral infection transmitted by arthropods, whose vector is the female mosquito of the genus Aedes, mainly Aedes aegypt.³ The infection is caused by an RNA virus of the Flaviviridae family, which has different serotypes: DEN-1, DEN-2, DEN-3 and DEN-4. This illness can range from subclinical illness to flu-like symptoms and, although less common, some patients develop the severe form of the disease, with severe bleeding, organ involvement and/or plasma leakage with reduced blood volume. One of the complications of dengue, associated with high morbidity and mortality rates, is acute kidney injury (AKI).⁴The pathophysiological mechanisms of kidney injury caused by dengue virus are still not fully understood, with gaps in understanding and, consequently, in the prevention and adequate management of this serious complication in patient with dengue. AKI, an abrupt decrease in the glomerular filtration rate, is one of the serious complications found in dengue. In recent decades, the incidence of AKI associated with dengue virus infection has increased significantly. Severe dengue affects 6.0-6.7% of patients diagnosed with dengue. Among hospitalized patients with severe dengue 3.3% to 4.8% develop AKI, of which 14.1% require dialysis.⁵ The need for dialysis can reach 70% in patients with dengue in intensive care units (ICU). AKI is associated with increased length of hospital stay and fatal cases of dengue. Independent risk factors for the development of AKI in patients with dengue are advanced age, male gender, obesity, hemorrhagic fever, rhabdomyolysis, multiple organ dysfunction, diabetes mellitus, concomitant bacterial infection, delay in hospital consultation and use of nephrotoxic drugs.⁶

Several hypotheses are considered as pathophysiology of kidney injury by the dengue virus including shock resulting from hypotension, direct injury caused by the virus, indirect mechanism via immune mechanism and rhabdomyolysis. The combination of two or more of these mechanisms has yet to be considered. Shock or hypotension is present in 16% to 100% of patients who develop dengue-induced AKI. Endothelial damage directly caused by the virus can also change vascular permeability, aggravating the hemodynamic instability. Various cytokines including TNFα, IL-6, IL-8, IL-10, IL-12, IL-17 in addition to activating the complement system and endothelial damage, results in increased vascular permeability with consequent hemoconcentration. Dengue virus appears to have broad cell tropism including hepatocyte, type II pneumocyte, and cardiac fibers, resident and circulating monocyte/macrophages and endothelial cells. A study of histopathological analysis after death from dengue showed microabscesses in kidneys. More recently evidence has emerged that dengue virus, when infecting the kidney tissue, may be associated with the development of glomerulopathies such as focal and segmental glomerulosclerosis. Glomerular deposits of IgG, IgM and C3 were found in patients with dengue induced renal failure.

Dengue patients who develop AKI need longer hospital stay and there is higher mortality among patients with severe dengue-induced AKI. The specific treatment for dengue-induced AKI is still limited and not very well established. Patient assessment in the case of warning signs of severe dengue fever together with blood volume assessment are important starting points for the prevention of AKI in dengue patients. Fluid administration should be optimized (preferably crystalloid) with infusion rates and controlled tonicities, to avoid osmolarity disorders, fluid overload and worsening of intravascular fluid extravasation. The maintenance of electrolyte balance should be prioritized, due to high prevalence of hyponatremia. There is no indication of steroid for AKI prevention in patients with dengue. Finally, renal replacement therapy may be necessary in some patients with AKI, especially in the presence of refractory uremia and hypercatabolism, metabolic acidosis, hyperkalemia and hypervolemia. Maintenance of blood volume, avoiding use of nephrotoxic drugs, clinical and laboratory monitoring for early identification of AKI to enable better management and avoid its complication is very important. Post-discharge follow-up is important because some patients of AKI can progress to CKD.

References

World Health Organization (WHO). Dengue bulletin. Geneva: WHO; WHO 2020: 1-12
Cattarino L, Rodriguez-Barraquer et al. Mapping global variation in dengue transmission intensity. Sci Transl Med. 2020; 12(528): 1-11
Khetarpal N, Khanna I. Dengue fever: causes, complications and vaccine strategies. J Immunol Res. 2016; 13(3) :68-78
Diptyanusa A, Phumratanaprapin W et a., Characteristics and associated factors of acute kidney injury among adult dengue patients. PLos One. 2019;14(1): 55-70
Daher E, Silva G et al, Acute kidney injury in a tropical country: a cohort study of 253 patients in an infectious disease intensive care unit. Rev Soc Bras Med Trop. 2014; 47(1):86-89

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