A 49-year-old Dutch male patient came to King Chulalongkorn Memorial Hospital (KCMH) with a complaint of low-grade fever and profuse sweating at night for 1 week. Three weeks earlier, he was diagnosed HIV infection when antiretroviral medications comprising of tenofovir, emtricitabine, and efavirenz were prescribed. He denied taking any over-the-counter drugs. The physical examination was unremarkable except for a body temperature of 38 C. He also had normotension (blood pressure 125/75 mmHg) without orthostatic hypotension or other signs of volume depletion. The chest X-ray showed miliary pulmonary nodules compatible with miliary tuberculosis which was later confirmed by positive polymerase-chain-reaction for Mycobacterium tuberculosis in his sputum. Disseminated tuberculosis was promptly diagnosed, and antituberculosis treatment (isoniazid, rifampicin, pyrazinamide, and ethambutol) was planned. However, he also had severe azotemia at admission (BUN 53.6 mmol/L, Cr 1,230 micromol/L) in contrast to his baseline values from one month earlier (Cr 115 micromol/L). At that time, there were no evidences of uremic symptoms or volume overload, and he still voided 500 mL of urine per day. Urinalysis revealed isosthenuria with bland urinary sediments (specific gravity 1.010, pH 5.0, albuminuria trace, glycose negative, WBC 0-1/hpf, and RBC 0-1/hpf). Renal ultrasonography demonstrated normal size and contour of both kidneys. Urine biomarker for renal tubular injury, neutrophil gelatinase-associated lipocalin (NGAL), was markedly elevated (7,891 ng/mL). Acute kidney injury was diagnosed and likely caused by nephrotoxic acute tubular necrosis (ATN) even though a renal biopsy had not been done. In the absence of other offending drugs or conditions, tenofovir was suspected to be a causal drug for ATN resulting in an adjustment of the antiretroviral regimen (abacavir, lamivudine, and raltegravir).
In the absence of uremic symptom or volume overload, PD was, nevertheless, initiated due to high level of nitrogen catabolites. The flexible double-cuffed PD catheter was inserted on day 4 of admission, and automated PD (Homechoice cycler ; Baxter) using a total dialysate (Dianeal ; Baxter) volume of 10 L (initial fill volume of 700 mL, 14 cycles, 20 hours) was promptly started on the same day of the catheter insertion. PD dose was gradually increased to achieve the total dialysate volume of 20 L per day in the next few days. The delivered dose of PD by total weekly Kt/V and total weekly creatinine clearance (CCr) were 3.23 and 97.84 L/week, respectively. After a week of automated PD, nitrogen catabolites decreased gradually (BUN 27.8 mmol/L, Cr 840 micromol/L). At one month, his urine volume had increased to 1 L per day, but measured renal CCr was still at 4 mL/min/1.73 m2 which reflected inadequate recovery of renal function. He was discharged on day 31 of admission with continuation of automated PD at a total dialysate volume of 10 L per day. At follow-up visit, the patient showed gradually improvement in renal function and the dose of PD was tapered accordingly. Eventually, PD could be discontinued at 4 months after the onset of AKI. The patient attained stable serum Cr of 124 micromol/L and measured CCr of 29 mL/min/1.73 m2 afterwards.