Urine YKL-40 is associated with progressive acute kidney injury or death in hospitalized patients

Acute renal failure, now referred to as acute kidney injury (AKI), complicates 5–10% of general hospital admissions and is associated with increased morbidity and mortality and prolonged hospitalizations. The definition of AKI varies, but it is usually defined as an increase in serum creatinine concentration of 25–50% above the baseline, a decline in estimated glomerular filtration rate (eGFR) of 25–50%, or the need for renal replacement therapy. It is now recognized that changes in GFR are delayed manifestations of renal injury, and the development of urinary biomarkers may help to identify AKI earlier in the course of injury. The major causes of AKI in hospitalized patients include prerenal causes (~40%), postrenal causes (~5–10%), and intrinsic diseases affecting blood vessels, glomeruli, or tubules. Of the intrinsic causes, tubular disorders (acute tubular necrosis and acute interstitial nephritis) are the most common etiologies, accounting for 40–50% of all causes of AKI. Acute glomerulonephritis and vascular disorders are rare etiologies of AKI in hospitalized patients (〈5%).

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Admission plasma uromodulin and the risk of acute kidney injury in hospitalized patients with cirrhosis: a pilot study

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00158.2019 ◽

2019 ◽

Vol 317 (4) ◽

pp. G447-G452

Author(s):

Kavish R. Patidar ◽

Pranav S. Garimella ◽

Etienne Macedo ◽

James E. Slaven ◽

Marwan S. Ghabril ◽

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Keyword(s):

Acute Kidney Injury ◽

Kidney Injury ◽

Predictive Biomarker ◽

Hospitalized Patients ◽

Susceptible Population ◽

Baseline Creatinine ◽

Low Levels ◽

Time Of Admission ◽

Hospital Acquired

Acute kidney injury (AKI) is a common complication in hospitalized patients with cirrhosis. Uromodulin, a protein uniquely produced by the kidney and released both in the urine and circulation, has been shown to regulate AKI and is linked to tubular reserve. Although low levels of urine uromodulin are associated with AKI after cardiac surgery, it is unclear whether circulating uromodulin can stratify the risk of AKI, particularly in a susceptible population such as hospitalized patients with cirrhosis. Thus, we investigated whether plasma uromodulin measured at the time of admission is associated with subsequent hospital-acquired AKI (defined by a rise in serum creatinine >0.3mg/dL within 48 h or ≥ 1.5 times baseline) in patients with cirrhosis. A total of 98 patients [mean age 54 yr, Model for Endstage Liver Disease Sodium (MELD-Na) score 19, and baseline creatinine of 0.95 mg/dL] were included, of which 13% ( n = 13) developed AKI. Median uromodulin levels were significantly lower in patients who developed AKI compared with patients who did not (9.30 vs. 13.35 ng/mL, P = 0.02). After adjusting for age, sex, diabetes, hypertension, albumin, and MELD-Na score as covariates on multivariable logistic regression, uromodulin was independently associated with AKI [odd ratios of 1.19 (95% confidence interval 1.02, 1.37; P = 0.02)]. Lower uromodulin levels on admission are associated with increased odds of subsequent AKI in hospitalized patients with cirrhosis. Further studies are needed to better understand the role of uromodulin in the pathogenesis and as a predictive biomarker of AKI in this population. NEW & NOTEWORTHY In this study, we found that admission plasma uromodulin levels are significantly lower in patients who developed subsequent acute kidney injury (AKI) during their hospital stay compared with patients who did not. Additionally, uromodulin is independently associated with AKI development after adjusting for clinically relevant parameters such as age, sex, diabetes, hypertension, severity of cirrhosis, and kidney function. To our knowledge, this is the first study linking plasma uromodulin with AKI development in patients with cirrhosis.

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