Begin typing your search above and press return to search.
Volume: 18 Issue: 1 January 2020 - Supplement - 1

FULL TEXT

Peculiarities of the Clinical Course of Chronic Viral Hepatitis C in the Background of End-Stage Chronic Renal Insufficiency

Objectives: We investigated the clinical, epidemiologic, and pathogenetic features of viral hepatitis C in hemodialysis departments.

Materials and Methods: This multicenter study included patients who were seen at the hemodialysis depart­ment in Tashkent, Uzbekistan and at regional departments located in the Republic of Uzbekistan. We examined 395 patients who were on hemodialysis from 3 to 15 years. A diagnosis of chronic viral hepatitis C was made on the basis of anamnesis, clinical laboratory data, and detection of immunoglobulin G antibodies for hepatitis C virus.

Results: From clinical and laboratory results analyzed in 395 patients, markers of infection with parenteral viral infections were shown in 181 patients (45.8%). Chronic viral hepatitis C had the highest incidence among infections, which was detected in 125 patients (31.6%). With regard to chronic renal failure, 11 patients (34%) with chronic viral hepatitis C had a transient form of chronic renal hepatic failure with development of adverse outcomes. Of patients with chronic viral hepatis C infection, 13 patients (40%) with hemorrhagic syndrome developed progressive anemia and 8 patients (25%) developed persistent polyserositis in the form of hydrothorax, ascites, and pericarditis. These developments reflect the aggravating effects of chronic viral hepatitis C on the course of chronic renal failure.

Conclusions: In our study that included patients seen at hemodialysis departments in Uzbekistan, chronic viral hepatitis C was greatly prevalent, although occurring mainly in a minimal form of the pathologic process. Chronic viral hepatitis C has an aggravating effect on the course of underlying diseases with development of adverse outcomes.


Key words : Chronic renal failure, Hemodialysis, Hepatitis C virus, Renal replacement therapy

Introduction

Recent scientific achievements have increased the understanding of the pathogenesis of chronic hepatitis C and its outcomes. This knowledge has affected methods for disease diagnosis, has led to realization of the main therapeutic directions in treatment, and has significantly improved prognosis.1 In recent years, the number of recorded cases of viral hepatitis B and C has changed significantly, with incidence of hepatitis C virus (HCV) sharply increased versus a decrease in the incidence of hepatitis B virus (HBV).2

Among the branches of medicine that are at high risk of spreading viral hepatitis are the departments of chronic hemodialysis, where frequent surgical interventions on vessels, a continuous treatment process, and frequent blood transfusion have caused a high risk of contracting viral hepatitis. Viral hepatitis can be a serious problem for many hemodialysis centers due to its high incidence in both patients and employees of these departments.3-5 The severe nature of its pathology in patients with chronic renal failure (CRF), which can have an aggravating effect of various intercurrent infections in underlying diseases and which can worsen prognoses, underlines the importance of this problem today.

A common transmission route for HBV and HCV leads to the formation of associated forms of the disease in patients with end-stage CRF. Presently, studies are not clear with regard to this problem and data are so far contradictory.6-8 Here, we investigated the clinical, epidemiologic, and pathogenetic features of HCV in our local hemodialysis departments.

Materials and Methods

In this multicenter study, we included patients from hemodialysis departments in Tashkent and other regional departments in the Republic of Uzbekistan. We examined 395 patients who had been undergoing hemodialysis from 3 to 15 years. Patients ranged from 17 to 65 years old, with 132 women (33.4%) and 263 men (66.6%). Among patients with end-stage CRF, chronic glomerulonephritis was diagnosed in 244 patients (61.7%), chronic pyelonephritis in 64 patients (16.2%), polycystic kidney disease in 18 patients (4.6%), urolithiasis in 4 patients (1%), nephrosclerosis associated with diabetes mellitus in 60 patients (15.2%), systemic lupus erythematosus in 3 patients (0.79%), and gout in 2 patients (0.51%).

All patients underwent clinical and laboratory examinations, including ultrasonographic exami­nations of the liver and kidneys. Patients underwent continuous conservative therapy and hemodialysis. The diagnosis of chronic HCV was based on an anamnesis, clinical and laboratory data, and the detection of anti-HCV immunoglobulin G in blood using enzyme-linked immunosorbent assay. RNA HCV genotypes and viral load were determined by polymerase chain reaction. To exclude mixed infections, all patients were tested for blood serum for HBsAg, anti-hepatitis D virus (HDV), and human immunodeficiency virus (HIV) infection by enzyme-linked immunosorbent assay. For analysis and processing of the obtained results, the generally accepted methods of variation statistics were used.

Results

Our analyses of the clinical and laboratory results of 395 patients showed parenteral viral infections in 181 patients (45.8%). In 214 patients (54.2%) with end-stage CRF, no infectious pathologies were detected. Data showed high detectability of markers of parenteral viral infections in patients with end-stage CRF both in Tashkent and in regional hemodialysis departments in Uzbekistan. Chronic HBV monoin­fection was shown in 23 patients (5.8%), chronic HCV infection in 125 patients (31.6%), and HIV infection in 5 patients (1.3%). We also observed mixed-type infections, with chronic HBV and HCV in 16 patients (4%), chronic HBV and HDV in 8 patients (2%), and chronic HCV and HIV in 4 patients (1%). As shown in Figure 1, the highest incidence rate of viral infections was HCV.

Clinical and laboratory results that aimed to determine the activity of the pathologic process in infected patients are presented in Figure 2. Patients with chronic HCV and HBV monoinfections predominantly had a minimally adverse form (87% and 95%, respectively). We observed that 68.8% of patients with mixed chronic HBV and HCV infections, 62.5% of patients with mixed chronic HBV and HDV, and 18% of patients with mixed chronic HCV and HIV infections had a moderate form of infection, as shown by the pathologic activity. No patients exhibited a pronounced form of activity of the pathologic process, which may be a feature of chronic HBV, HCV, and HDV in the presence of CRF (Figure 2).

Table 1 shows the clinical results of patients with chronic HCV and CRF. Patients with chronic HCV and end-stage CRF had symptoms of persistent weakness, nausea, and lack of appetite; these symptoms were significantly more prevalent (P < .05) than in patients with end-stage CRF without concomitant diseases. Patients with chronic HCV and CRF also had a significantly (P < .05) higher incidence of anemia, polyserositis in the form of ascites, pericarditis, and hydrothorax. Transient edematous syndrome was characteristic of patients with end-stage CRF without concomitant diseases, which, after adequate dialysis, was well correlated. However, persistent edema was not corrected by dialysis in 8 patients (25%) with chronic HCV and end-stage CRF, which was most likely because of protein synthesis dysfunction in the liver of these patients.

Of total patients with chronic HCV and end-stage CRF, 22 (69%) had hepatomegaly and 8 (25%) had splenomegaly; these results were comparable to results shown in patients with HCV infection alone and patients with CRF without coinfections. Patients with chronic HCV and end-stage CRF and patients with CRF without coinfections showed absence of yellowness of the skin, perhaps associated with the effects of constant detoxification with hemodialysis. Moreover, in those with chronic HCV and end-stage CRF, those with itching (P < .05) more often developed pruritus. Patients in this group had bilirubin and related results within reference levels. A high and significant (P < .05) incidence of anemia was shown in 29 patients (91%) with chronic HCV and end-stage CRF. Patients in this group also showed hypertension and cardiovascular failure, which indicated that chronic HCV has an ag­gravating effect on end-stage CRF.

When we evaluated the course of chronic HCV in the presence of end-stage CRF, 11 patients (34%) showed disease progression in the form of transient chronic renal hepatic failure with the development of adverse outcomes. Thirteen patients in this group with chronic HCV and end-stage CRF (40%) had hemor­rhagic syndrome and developed progressive anemia, and 8 (25%) developed persistent polyserositis in the form of hydrothorax, ascites, and pericarditis. These results reflect the aggravating effects of chronic HCV on end-stage CRF (Figure 3).

Discussion

Among patients who were receiving hemodialysis, chronic HCV had the highest prevalence among viral infections; however, most patients had a minimal form of activity in the pathologic process. This low-symptom course of chronic HCV in patients with end-stage CRF may be because these patients are regularly treated with hemodialysis and thus viruses and their waste products are regularly removed from the bloodstream, leading to decreased levels of viremia.9 On the other hand, patients on hemodialysis have low levels of immunity.8-10 We suggest that low immunity increases the incidence of chronic hepatitis, since HCV, HBV, and HDV are immune-mediated viral infections, and the severities of these are correlated with the degree of host immune response. Further detailed studies of the clinical and laboratory manifestations of viral hepatitis in patients with end-stage CRF are needed, as well as investigations on additional tests of viral infection activity and additional antiviral therapies.

Conclusions

In patients on hemodialysis in Tashkent and in other regions in the Republic of Uzbekistan, the incidence of chronic HCV prevails. In patients with end-stage CRF, HCV mainly proceeds in a minimal form of the pathologic process. Chronic HCV can have an aggravating effect on the course of the underlying disease with the development of adverse outcomes.


References:

  1. Kuznetsov NI, Romanova ES, Startseva GY. Modern principles of anti-viral therapy for hepatitis C. Russian Fam Doctor. 2018;22(3):23-27. doi: 10.17816/RFD2018323-27.
    CrossRef
  2. Arisheva OS, Moiseev SV, Kotenko ON. Daclatasvir and asunaprevir combination in hemodialysis patients with chronic hepatitis C . Clin Pharmacol Ther. 2016;25(3):5-10.
  3. Akimkin VG, Semenenko TA, Nikitina GY, et al. Epidemiology and prevention of viral hepatitis B and C in medical institutions. Bionika. 2013;216.
  4. Milovanova SY, Milovanov YS, Kozlovskaya LV, et al. Prevention and treatment of viral hepatitis B and C in patients with program hemodialysis. Hepatologic Forum. 2009;4:19-26.
  5. Yarosh LV, Semenenko TA, Nikitina GY, et al. Prevalence of the hepatitis B and C viruses markers in the hemodialysis departments. Nephrol Dialysis. 2013;15(4):293-298.
  6. Gumilevskaya OP, Gumilevsky BY. Infectious complications of renal replacement therapy. Med Bull. 2011;6(6):27-33. http://www.volgmed.ru/uploads/journals/articles/1348049010-drugs-bulletin-2011-4-1531.pdf.
  7. Ivashkin VT. The immune system and liver damage in chronic hepatitis B and C. Russian J Gastroenterol Hepatol Colloproctol. 2009;6:4-9.
  8. Fabrizi F, Verdesca S, Messa P, Martin P. Hepatitis C virus infection increases the risk of developing chronic kidney disease: A systemic review and meta-analysis. Dig Dis Sci. 2015;60(12):3801-3813. doi: 10.1007/s10620-015-3801-y.
    CrossRef - PubMed
  9. Dobronravov VA, Dunaeva NV. Kidney damage and chronic viral hepatitis C. Nephrology. 2008;12(4):9-19.
    CrossRef
  10. Fabrizzi F, Messa P. Transmission of hepatitis C virus dialysis units: a systematic review of reports on outbreaks. Int J Artif Organs. 2015;38(9):471-480. doi: 10.5301%2Fijao.5000437.
    CrossRef - PubMEd


Volume : 18
Issue : 1
Pages : 47 - 50
DOI : 10.6002/ect.TOND-TDTD2019.O23


PDF VIEW [147] KB.

From the 1Scientific Research Institute of Epidemiology, Microbiology and Infectious Diseases, Tashkent, Uzbekistan; the 2Republican Scientific Center for Emergency Medical Aid, Tashkent, Uzbekistan; and the 3Republican Specialized Scientific-Practical Medical Center for Nephrology and Kidney Transplantation, Tashkent, Uzbekistan
Acknowledgements: The authors have no sources of funding for this study and have no conflicts of interest to declare.
Corresponding author: Firuza A. Aripkhodjayeva, Scientific Research Institute of Epidemiology, Microbiology and Infectious Diseases, Uchtepa District, Zakovat street, house 2, Tashkent 100133, Uzbekistan
Phone: +99 890 327 11 31
E-mail: firuza_axborovna@mail.ru