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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR  
Year : 2021  |  Volume : 32  |  Issue : 2  |  Page : 592-594
Acute kidney injury in a patient treated with tenofovir alafenamide fumarate for Hepatitis B virus infection


1 Department of Nephrology, Sri Ramachandra Institute of Higher Education and Research (SRIHER), Chennai, India
2 Department of Nephrology, SRM Medical College and Research Center, Kattankulathur, Tamilnadu, India
3 Department of Hepatology, Global Hospitals, Hyderabad, India

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Date of Web Publication11-Jan-2022
 

How to cite this article:
Deiva A, Jayaprakash V, Jose N, Chandan Kumar K N, Jayakumar M. Acute kidney injury in a patient treated with tenofovir alafenamide fumarate for Hepatitis B virus infection. Saudi J Kidney Dis Transpl 2021;32:592-4

How to cite this URL:
Deiva A, Jayaprakash V, Jose N, Chandan Kumar K N, Jayakumar M. Acute kidney injury in a patient treated with tenofovir alafenamide fumarate for Hepatitis B virus infection. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 Jan 28];32:592-4. Available from: https://www.sjkdt.org/text.asp?2021/32/2/592/335480


To the Editor,

Tenofovir alafenamide fumarate (TAF) is an orally bioavailable prodrug of tenofovir (TFV), a nucleotide analog that inhibits reverse transcription of human immunodeficiency virus (HIV) and hepatitis B virus (HBV).[1] TAF was designed to have greater plasma stability than tenofovir disoproxil fumarate (TDF) allowing delivery of the active metabolite tenofovir diphosphate to hepatocytes more efficiently than TDF, which must be dosed at relatively high levels to achieve a therapeutic concentration in hepatic cells.[2] Due to high systemic exposure of TFV, the long-term use of TDF has been associated with bone and renal toxicity.[3] Since TAF is considered non-nephrotoxic, it is prescribed for HIV and HBV treatment in patients with renal failure.

A 50-year-old man presented to emergency with acute kidney injury (AKI) in May 2019. He was a diabetic patient with morbid obesity and on admission, he was incidentally detected to have HBV infection. During workup for etiology of AKI, computed tomography (CT) of the abdomen was performed, which revealed features of bilateral acute pyelonephritis. There was no pelvicalyceal system dilatation and he was initiated on intravenous antibiotics. Double J stenting was not done. He required two sessions of hemodialysis in the initial few days of admission. His symptoms and azotemia improved with parenteral antibiotics. He was initiated on TAF for the treatment of HBV infection taking in view of recovering AKI in consultation with a hepatologist. His discharge medications included TAF 25 mg, oral antibiotics, and insulin. After discharge, the follow-up serum creatinine was 1.2 mg/dL.

Four weeks after discharge from hospital, he was readmitted with severe low backache and was diagnosed to be suffering from spondylodiscitis D10-D11. Workup for the etiology of bone lesion (bacterial vs. tuberculous vs. myeloma) was initiated. In the meantime, his renal parameters started worsening gradually during this hospital admission. The peak creatinine was 4.6 mg/dL. He did not require renal replacement therapy. He was investigated for the causes of acute worsening of renal failure such as sepsis and hypovolemia. Complete hemogram and CT imaging of kidneys were normal. Urine culture did not grow any organism. Having ruled out the possible common causes of AKI, it was suspected that TAF could be the factor that has contributed to his renal failure. TAF was stopped and in about 72 h of stopping it, serum creatinine levels started declining. In about two weeks’ time, it became normal [Figure 1]. The spondylodiscitis was managed conservatively with bed rest and immobilization. Myeloma workup was negative. Empirical anti-tuberculous treatment (ATT) was started. His serum creatinine was 1.2 mg/dL at the time of discharge. He is currently on continuation phase of ATT and has started mobilization exercises. He is underregular follow-up and his last serum creatinine was 1 mg/dL (December 2019).
Figure 1: Serum creatinine levels (in mg/dL).

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Renal safety profile of TAF is sparsely reported in the literature. Agarwal et al demonstrated the superiority of TAF over TDF with regard to bone and renal parameters in a study of 96 weeks of double-blind treatment for HBV infection. Serologic responses were similar for TAF compared with TDF and the significant differences in declines in estimated glomerular filtration rate, smaller changes in biomarkers of proximal tubular function support that TAF has lesser impact on renal function than TDF.[4]

Recently, a case of Fanconi syndrome and nephrogenic diabetes insipidus on initiating TAF as part of HIV treatment has been reported by Zhao et al.[5] Contrary to the claims that TAF is non-nephrotoxic, renal failure secondary to TAF is possible and should be always be considered. TAF may be initiated preferably to TDF in patients with renal dysfunction, but periodic monitoring of renal function is warranted. This is probably the first case report of TAF-induced AKI from Asia. The temporal association of renal function improving dramatically after stopping TAF confirms the diagnosis in this patient. Similar case reports and experiences from other centers will throw more light on TAF-related nephrotoxicity.

The authors obtained all appropriate consent forms from the patient for the publication of the case.

Conflict of interest: None declared.



 
   References Top

1.
DeClercq E. Tenofovir alafenamide (TAF) as the successor of tenofovir disoproxil fumarate (TDF). BiochemPharmacol2016;119:1-7.  Back to cited text no. 1
    
2.
Murakami E, Wang T, Park Y, et al. Implications of efficient hepatic delivery by tenofovir alafenamide (GS-7340) for hepatitis B virus therapy. Antimicrob Agents Chemother 2015;59:3563-9.  Back to cited text no. 2
    
3.
Maggi P, Montinaro V, Leone A, et al. Bone and kidney toxicity induced by nucleotide analogues in patients affected by HBV-related chronic hepatitis: A longitudinal study. J Antimicrob Chemother 2015;70:1150-4.  Back to cited text no. 3
    
4.
Agarwal K, Brunetto M, Seto WK, et al. 96 weeks treatment of tenofovir alafenamide vs. tenofovir disoproxil fumarate for hepatitis B virus infection. J Hepatol 2018;68:672-81.  Back to cited text no. 4
    
5.
Zhao X, Sanchez CR, Gampa A, Rodby RA. Tenofovir alefanamide-induced nephrotoxicity: A rare case of fanconi syndrome and nephrogenic insipidus instigated by the ‘Non- Nephrotoxic’ Tenofovir-Containing Haart. Am J Kidney Dis 2018;71:600.  Back to cited text no. 5
    

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Correspondence Address:
V Jayaprakash
Department of Nephrology, SRM Medical College and Research Center, Kattankulathur, Tamilnadu
India
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DOI: 10.4103/1319-2442.335480

PMID: 35017362

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