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. Author manuscript; available in PMC: 2013 Jun 1.
Published in final edited form as: Aliment Pharmacol Ther. 2012 Apr 16;35(11):1317–1325. doi: 10.1111/j.1365-2036.2012.05093.x

Table 1.

Clinical features of seven patients with renal tubular dysfunction

Pt No. Age Sex Results at the start of therapy Therapy Years on therapy Results at diagnosis of RTD New Medication Last results recorded Follow-up after switch (years)
Phos Uric acid Cr Urine protein Urine glucose Phos Uric acid Cr Urine protein Urine glucose Phos Uric acid Cr Urine protein Urine glucose
1 56 M 3.1 6.5 1.3 None None Adv/Lam 2.1 2.1 2.9 2.0 1+ None Entecavir 3.0 5.1 1.3 None None 6.3
2 40 M 3.1 4.5 0.9 None None Adv/Lam 4.9 1.7 2.5 1.4 Trace None Entecavir 2.1 2.7 0.9 None None 1.0
3 62 M 4.0 3.6 1.0 None None Ten 3.9 2.3 2.4 1.8 Trace None Entecavir 3.1 3.2 1.2 None None 1.0
4 66 M 3.2 5.8 1.1 None None Adv → Ten* 7.7 2.1 3.6 1.7 1+ None Entecavir 2.7 3.7 1.4 None None 1.0
5 76 F 3.5 5.3 0.6 None None Adv/Lam 3.4 1.9 1.5 1.3 2+ None Entecavir 3.1 3.9 0.7 None None 2.0
6 33 M 3.5 5.7 1.1 None None Adv/Lam 6.5 2.0 2.3 1.4 Trace None Not switched 2.7 2.7 1.4 1+ None
7 71 M 3.7 5.3 0.8 None None Adv/Lam 8.4 2.0 1.8 1.6 Trace None Entecavir 3.7 4.2 1.2 Trace None 1.0

Adv, adefovir; Cr, creatinine; Phos, phosphate; RTD, renal tubular dysfunction; Ten, tenofovir.

*

This patient was on adefovir for 4 years before switching to tenofovir due to inadequate virological response. At the time of switching therapies, his phosphate, uric acid and creatinine were 2.9, 5.6 and 1.3, respectively, and had no proteinuria or glucosuria. RTD was diagnosed 3.7 years after switch to tenofovir.

On phosphate replacement.