Acute kidney injury (AKI) is a common clinical syndrome that is characterized by abnormal renal function and structure. The Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference in 2019 reviewed the stages of AKI and the definitions of AKI-related terminologies, and discussed the advances in the last decade. Along with serum creatinine level and urine output, more accurate novel biomarkers for predicting AKI are being applied for the early detection of renal dysfunction. A literature search was conducted in PubMed, Scopus, Medline, and ClinicalTrials.gov using the terms AKI and biomarker, combined with diagnosis, management, or prognosis. Because of the large volume of data (160 articles) published between 2005 and 2022, representative literature was chosen. A number of studies have demonstrated that new biomarkers are more sensitive in detecting AKI in certain populations than serum creatinine and urine output according to the recommendations from the Acute Disease Quality Initiative Consensus Conference. To be specific, there is a persistently unresolved need for earlier detection of patients with AKI before AKI progresses to a need for renal replacement therapy. Biomarker-guided management may help to identify a high-risk group of patients in progression to severe AKI, and decide the initiation time to renal replacement therapy and optimal follow-up period. However, limitations such as biased data to certain studied populations and absence of cutoff values need to be solved for worldwide clinical use of biomarkers in the future. Here, we provide a comprehensive review of biomarker-based AKI diagnosis and management and highlight recent developments.
Bladder augmentation using the gastrointestinal tract is an enlargement surgery designed to lower bladder pressure in patients with low bladder compliance. But, metabolic acidosis develops in some patients who have had bladder augmentation using the gastrointestinal tract due to the part of the intestine that absorbs urinary components including hydrogen ions and chlorides, and exchanges sodium for bicarbonate. We experienced a rare case of metabolic acidosis in a kidney transplantation who underwent bladder augmentation and both nephrectomy due to myelomeningocele. A 33-year-old male born with myelomeningocele and neurogenic bladder. He started hemodialysis due to severe hydronephrosis and recurrent cystitis. But inpatient treatment was repeated for recurrent cystitis undergoing clean intermittent self-catheterization. In the end, both nephrectomies were performed and bladder augmentation when he was 28 years old. A 20 cm distal ileal segment was isolated proximal to the ileo-cecal valve. The bladder dome was incised and ileo-bladder anastomosis was performed. He received a cadaveric donor kidney transplantation when he was 33 years old. His postoperative course was stable, but severe metabolic acidosis developed on postoperative day 15. At that time, the serum creatine 1.71 mg/dL and urine output was maintained at 3,000 cc/day. Arterial blood gas demonstrated hyperchloremic metabolic acidosis with pH 7.28, bicarbonate 14 mmol/L. Normal serum AG of 9 mEq/L and CRP (<0.5 mg/dL) may rule out the initial diagnosis of urosepsis, high urine AG of 22 mEq/L has a narrow differential diagnosis that include renal tubular acidosis (RTA). However, urine pH 7.0 and serum K of 4.6 mmol/L may rule out the RTA. We started intravenous sodium bicarbonate supplementation and the metabolic acidosis improved. On his most recent outpatient visit, he had no further metabolic acidosis without complications. In this report, we introduce a rare case with transient severe hyperchloremic metabolic acidosis in a kidney transplantation who underwent bladder augmentation using distal ileum.
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