Coronavirus disease 2019: acute Fanconi syndrome precedes acute kidney injury

被引:45
|
作者
Kormann, Raphael [1 ]
Jacquot, Audrey [2 ]
Alla, Asma [1 ]
Corbel, Alice [1 ]
Koszutski, Matthieu [2 ]
Voirin, Paul [1 ,3 ]
Parrilla, Matthieu Garcia [4 ]
Bevilacqua, Sybille [3 ]
Schvoerer, Evelyne [5 ]
Gueant, Jean-Louis [6 ]
Namour, Fares [4 ,6 ]
Levy, Bruno [2 ,7 ]
Frimat, Luc [1 ,8 ]
Oussalah, Abderrahim [4 ,6 ]
机构
[1] Univ Lorraine, Dept Nephrol, CHRU Nancy, Vandoeuvre Les Nancy, France
[2] Univ Lorraine, Dept Intens Care Med, CHRU Nancy, Vandoeuvre Les Nancy, France
[3] Univ Lorraine, Dept Infect & Trop Dis, CHRU Nancy, Vandoeuvre Les Nancy, France
[4] Univ Lorraine, Dept Mol Med, CHRU Nancy, Div Biochem Mol Biol Nutr & Metab, Vandoeuvre Les Nancy, France
[5] Univ Lorraine, Dept Microbiol, CHRU Nancy, Div Virol, Vandoeuvre Les Nancy, France
[6] Univ Lorraine, INSERM, UMRS 1256 NGERE Nutr Genet Environm Risk Exposure, Nancy, France
[7] Univ Lorraine, INSERM, U1116, Nancy, France
[8] Univ Lorraine, INSERM, CIC EC CIE6, Nancy, France
关键词
acute kidney injury; acute proximal tubule injury; COVID-19; Fanconi syndrome; hypophosphataemia; SARS-CoV-2; RENAL TUBULAR REABSORPTION; PHOSPHATE; SCORE;
D O I
10.1093/ckj/sfaa109
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Background. Recent data have shown that severe acute respiratory syndrome coronavirus 2 can infect renal proximal tubular cells via Angiotensin Converting Enzyme 2 (ACE2). Our objective was to determine whether Fanconi syndrome is a frequent clinical feature in coronavirus disease 2019 (COVID-19) patients. Methods. A retrospective cohort of 42 laboratory-confirmed COVID-19 patients without history of kidney disease hospitalized in University Hospital of Nancy was investigated. Patients were admitted to the intensive care unit (ICU) (n = 28) or the Medical department (n = 14) and were screened at least once for four markers of proximal tubulopathy. Results. The mean (standard deviation) follow-up was 19.7 (612.2) days. Of the patients, 75% (30/40) showed at least two proximal tubule abnormalities (incomplete Fanconi syndrome). The main disorders were proteinuria (88%, n = 35), renal phosphate leak defined by renal phosphate threshold/glomerular filtration rate (TmPi/GFR) <0.77 (55%, n = 22), hyperuricosuria (43%, n = 17) and normoglycaemic glycosuria (30%, n = 12). At the time of the first renal evaluation, ICU patients presented more frequent (96 versus 62%, P = 0.0095) and more severe (8446343 versus 3506221 mg/g, P = 0.0001) proteinuria, and a trend for an increased number of proximal tubule abnormalities (P = 0.038). During follow-up, they presented a lower nadir of serum phosphate [median (interquartile range) 0.68 (0.43-0.76) versus 0.77 (0.66-1.07) mmol/L, P = 0.044] and Acute kidney Injury (AKI) during the hospitalization (P = 0.045). Fanconi syndrome preceded severe AKI KDIGO Stages 2 and 3 in 88% (7/8) of patients. Proximal tubular abnormalities (such as proteinuria, TmPi/GFR and glycosuria in five, two and two patients, respectively) were not detected anymore in recovering patients before hospital discharge. Conclusion. Incomplete Fanconi syndrome is highly frequent in COVID-19 patients and precedes AKI or disappears during the recovery phase.
引用
收藏
页码:362 / 370
页数:9
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