A 29-year-old woman, a known case of chronic kidney disease (CKD) presented with history of fever from last 4 months. Her basic renal disease was unknown as she had presented with bilateral small kidneys. Fever was high grade, intermittent and was associated with poor appetite. She had no dysuria, cough or abdominal complaints. The examination was unremarkable except for left-sided axillary lymphadenopathy. There was no hepatosplenomegaly and breast examination was normal. Neurological examination was unremarkable. Her creatinine on admission was 6.9 mg/dl with an estimated glomerular filtration rate (eGFR) of 7 ml/min/1.73 m2.
She was evaluated for fever. Serological tests for malaria, dengue, and enteric fever were negative; urine cultures were sterile. Her hemoglobin, total leukocyte count and platelet counts were 8.5 g/dl, 5880/microl, and 1.5 lakhs/microl, respectively. The kidney function tests revealed serum urea of 223 mg/dl and serum creatinine of 6.90 mg/dl. The serum sodium and potassium levels were 136 mmol/l and 4.8 mmol/l, respectively. The liver function tests and thyroid function tests were normal. Blood cultures were sterile.
Ultrasound abdomen showed hepatosplenomegaly with irregular, shrunken kidneys. There was no hydroureteronephrosis. Computed tomography of chest and abdomen showed splenomegaly, retroperitoneal and axillary lymphadenopathy with no mediastinal lymphadenopathy. There was no consolidation, collapse or cavitating lesion.
Fine needle aspiration from the axillary lymph node was inconclusive. Endoscopic ultrasound-guided fine needle aspiration cytology of the retroperitoneal nodes showed reactive lymphoid cells with few histiocytes. Her tuberculosis gold quantiferon test was positive. In view of persistent fever, lymphadenopathy, hepatosplenomegaly and positive quantiferon gold test, she was empirically initiated on antitubercular therapy with four drugs (isoniazid [INH], rifampicin, pyrazinamide and ethambutol) with appropriate dose adjustments for her kidney function. She was also commenced on pyridoxine 40 mg once daily. Hemodialysis (HD) was initiated through left radiocephalic fistula. One-week after initiation of antitubercular therapy, she developed slurring of speech with unstable gait. On examination, she had pulse 100 beats/min, blood pressure was 150/90 mmHg with no postural drop. The oxygen saturations were 100% on room air, blood glucose levels, serum sodium, and calcium levels were normal. Central nervous system examination showed dysarthria with impaired finger-nose test on left side with past pointing. Her gait was ataxic with swaying on left side. She was unable to perform rapid alternating movements on left side. Motor examination done showed decreased tone with normal power and reflexes on left side. There were no neurological findings on the right side. Sensory examination was normal with negative Romberg's sign.
Magnetic resonance imaging (MRI) brain showed diffusion restriction in bilateral dentate nuclei with T2 fluid-attenuated inversion recovery hyperintensity with no evidence of hemorrhage [Figure 1]. There were no features suggestive of tuberculoma or abscess. As there was no other obvious explanation of the sudden development of cerebellar ataxia, a diagnosis of INH induced toxic encephalopathy was considered and INH was withdrawn. Two days after withdrawal of INH, patient's condition started to improve and had complete neurological recovery within a week. She was commenced on HD via a left radio-cephalic arteriovenous fistula. She was discharged on modified antitubercular therapy that included rifampicin at dose of 450 mg/day, pyrazinamide at dose of 500 mg twice daily and levofloxacin at dose of 250 mg/day. On follow-up after 3 weeks, she has remained afebrile with no neurodeficit.