Tenofovir indcued reversible nephrogenic diabetes insipidus without fanconi syndrome in a patient with hepatitis b

Abstract

Background In patients with Hepatitis B Virus, there are approximately 10 cases of Tenofovir related Fanconi Syndrome but no report of nephrogenic diabetes insipidus.

Case Report A 54 year old female with hepatitis B virus on tenofovir for 1 year presented with polyuria and acute urinary retnetion. There was no history of diabetes, thyroid, kidney and intracranial pathology. The patient had acute transverse meyelitis that was treated successfully with steroid and plasmapharesis, however polyuria (10 L/day) persisted beyond an accepted time frame. As HBV‐PCR was negative, tenofovir was ceased. Her full blood count, inflammatory makers, blood sugar, thyroid, kidney and liver function tests were normal. Urine didn’t show haematuria or protienuria. Renal imaging showed no evidence of obstructive uropathy or chronic kidney disease. MRI brain excluded any intracranial lesions.Primary polydipsia was excluded as urine osmolality was not elevated >500 mosmol/kg during 8 h water deprivation and the patient responded to DDAVP significantly. Submaximal response to DDAVP at 30% excluded complete nephrogenic DI and complete central DI. Normal ADH result and resolution of polyuria after cessation of an offending drug suggested both complete and partial central DI was unlikely. A submaximal rise in urine osmolality (358 mmol/kg) with DDAVP producing elevation of urine osmolality of approximately 30% suggested a diagnosis of partial nephrogenic DI. Polyuria resolved 6 weeks after tenofvoir therapy alone was discontinued.

Conclusion Patients receiving tenofovir must be monitored closely even several months after initiation of treatment as the drug can cause nephrogenic DI. Combinging plasma ADH assay with water deprivation testing can lead to greater accuracy in differentiating the different forms of DI.