MO325: Renal Glycosuria in Acute Kidney Injury Predicts the Diagnosis of Acute Interstitial Nephritis

Abstract

Abstract BACKGROUND AND AIMS Acute interstitial nephritis (AIN) is one of the most frequent causes of acute kidney injury (AKI). Interstitial inflammation can lead to tubular epithelial infiltration producing tubular dysfunction, which could be clinically detected by glycosuria (with or without Fanconi syndrome), leukocyturia, microscopic haematuria or tubular proteinuria. The aim of this study was to determine the predictive value of renal glycosuria in AKI for the diagnosis of AIN. METHOD We conducted a retrospective study of kidney biopsies performed at out centre between May 1998 and December 2021, and included patients whose kidney biopsy was performed while presenting with AKI. We excluded patients with other indications for kidney biopsy, patients with diabetes mellitus and patients who presented a serum glucose level of > 120 mg/dL at presentation. We registered demographic, clinical and laboratory variables at presentation of AKI, and compared patients with a final diagnosis of AIN to patients with other causes of AKI. RESULTS The study included 211 patients; 39 patients (18.5%) with a diagnosis of AIN and 172 patients (81.5%) with other diagnoses for AKI. Eight patients with AIN presented with renal glycosuria (20.5%) compared with seven patients with other causes of AKI (4.1%) (P < .001). Patients with AIN presented less frequently haematuria (46.2% versus 86%; P < .001), lower albuminuria [86 (35–151) mg/g versus 694 (136–1414) mg/g; P < .001], proteinuria [0.43 (0.22–0.92) g/24 h versus 1.43 (0.76–2.97) g/24 h; P < .001], serum glucose (89.5 ± 12 versus 94.7 ± 12.5 mg/dL; P = .019) and uric acid (6.5 ± 2.5 versus 7.8 ± 2.3 mg/dL; P = .003), and more frequently metabolic acidosis (68.6% versus 33.3%; P < .001) and eosinophilia (17.9% versus 5.2%; P = .007) than in patients with other causes of AKI. There were no differences in age, sex, extrarenal manifestations, serum creatinine, potassium or phosphorus levels at presentation. The presence of at least traces (≥50 mg/dL) of glycosuria had a specificity of 96.5% (92.6–98.7) for the diagnosis of AIN, with a positive predictive value of 57.1% (32.9–78.3) and a negative predictive value of 84.3% (82%–86.3%). The positive likelihood ratio was 5.9 (2.2–16) and the negative likelihood ratio was 0.82 (0.7–0.97). The presence of > 100 mg/dL of glycosuria had a specificity of 99.4% for the diagnosis of AIN, with a positive predictive value of 75% (24.3–96.6) and a positive likelihood ratio of 13.2 (1.4–123.8). CONCLUSION AIN can lead to proximal tubular dysfunction, which can be clinically expressed as renal glycosuria. The presence of renal glycosuria in patients with AKI guides towards the diagnosis of AIN, with an excellent specificity when glycosuria > 100 mg/dL.