Abstract
Aims Proximal renal tubular dysfunction (PRTD) is an infrequent complication after nucleotide analogue therapy. We evaluated the outcomes of PRTD and nephrotoxicity after nucleotide analogue withdrawal in chronic hepatitis B (CHB). Methods A longitudinal follow-up study was performed in patients with PRTD after nucleotide analogue discontinuation. Serum and urine were collected at baseline and every 3 months for one year. The fractional excretion of phosphate (PO4), uric acid (UA), and potassium and tubular maximal reabsorption rate of PO4 to glomerular filtration rate (TmPO4/GFR) were calculated. Renal losses were defined based on the criteria of substance losses. Subclinical PRTD and overt PRTD were diagnosed when 2 and ≥3 criteria were identified. Results Eight subclinical and eight overt PRTD patients were enrolled. After nucleotide analogue withdrawal, there were overall improvements in GFR, serum PO4, and UA. Renal loss of PO4, UA, protein, and β2-microglobulin reduced over time. At one year, complete reversal of PRTD was seen in 13 patients (81.2%). Improvements in PRTD were seen in all but one patient. Conclusion One year after nucleotide analogue withdrawal, PRTD was resolved in most patients. Changes in TmPO4/GFR, urinary protein, and β2-microglobulin indicate that urinary biomarkers may represent an early sign of PRTD recovery.
Highlights
Over 240 million people worldwide are chronically infected with hepatitis B virus (HBV), which can lead to cirrhosis and hepatocellular carcinoma [1]
This paper presents a longitudinal follow-up study after nucleotide analogue was withdrawn in 16 chronic hepatitis B (CHB) patients who were affected by nucleotide analogue-related Proximal renal tubular dysfunction (PRTD), mostly by switching to ETV and LAM
Urinary β2microglobulin is known to be a specific marker of proximal renal tubular dysfunction, which has been studied in HIV patients who developed antiretroviral agents related to PRTD [28, 32,33,34]
Summary
Over 240 million people worldwide are chronically infected with hepatitis B virus (HBV), which can lead to cirrhosis and hepatocellular carcinoma [1]. The goal in chronic hepatitis B (CHB) treatment is to prevent the progression to end stage liver diseases and hepatocellular carcinoma. The ideal endpoint for the treatment of CHB is sustained off-therapy hepatitis B surface antigen loss [1,2,3]. If sustained off-therapy is not achievable, a long-term virological suppression with oral antiviral drugs is preferred [1, 3]. Long-term LAM therapy is associated with an emergence of LAM-resistant mutations, which require a modification in the treatment regimen by adding or switching nucleotide analogues including adefovir (ADV) or BioMed Research International tenofovir (TDF) [1]. Entecavir (ETV) and TDF are recommended as the preferred first-line oral antiviral therapy for CHB [1,2,3]
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