NDT Plus Advance Access originally published online on February 26, 2008
NDT Plus 2008 1(2):127; doi:10.1093/ndtplus/sfm044
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Renal ultrasound in acute kidney injury: long-term findings
1 Department of Nephrology, Ramón y Cajal University Hospital, Madrid
2 Department of Nephrology, Hospital Nuestra Senora de Sonsoles, Avila, Spain
Sir,
We recently reported the long-term outcome of 187 patients surviving an acute kidney injury episode (AKI) [1]. The ultrasonographic pattern of the kidney in late follow-up after AKI has never been analysed. Since 1991, one nephrologist (MR) has performed all renal sonographies in our department [2]. We present here the long-term sonographic findings in 39 AKI patients (out of 82 still alive during follow-up) who agreed to undergo a renal sonography.
Characteristics between patients who agreed to undergo the renal sonography (n = 39) and those who did not (n = 42) were compared and no statistically significant differences were found. In the group analysed there were 26 males and 13 females (60 ± 13 years old with a mean follow-up after AKI of 11.7 ± 3.7 years). Causes of AKI as defined elsewhere [1] were nephrotoxic (n = 17), sepsis (n = 5), medical (n = 6) and surgical (n = 11). The mean glomerular filtration rate (GFR) was 85.5 ± 33.0 ml/min/1.73 m2 (range 22–157). The GFR was <60 ml/min/1.73 m2 in seven patients.
Renal sonography was performed using abdominal 2D ultrasound equipment with a 3.5 MHz convex transducer (ALOKA 620-SSD, Japan). The following parameters were measured: diameters (longitudinal, transverse and postero-anterior), two poles cortex and meso-kidney. All kidneys were examined for lithiasis, cysts or scars. The presence of one or two simple polar cysts in patients older than 45 years was considered normal.
Echography was normal in 35 patients (89.7%). Mean renal diameters and renal cortex thickness were measured in both kidneys. Results are shown in Tables 1 and 2. Eight patients presented two simple polar renal cysts and one an uncomplicated lithiasis.
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Sonography was abnormal in four patients. Findings consisted of thin and shrunken renal cortex in all of them. Renal function was normal in two (SCr 1.1 and 1.2 mg/dl) and impaired in the other two (SCr 3.6 and 2.2 mg/dl). They were all male. Aetiology of AKI was: nephrotoxicity (n = 3) and sepsis (n = 1).
The renal sonographic findings observed at the time of the ATN episode have been described [3]. However, long-term kidney sonographic studies in AKI have not been carried out previously. With the involvement of the tubulo-interstitial structures, we could expect a higher incidence of ultrasonographic changes in the long-term evolution of these patients. However, 
11 years after the AKI episode, we found neither major changes in normal morphology of the kidneys nor a higher incidence of cysts than those observed in the normal population [3–4].
Conflict of interest statement. None declared.
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- Liano F, Felipe C, Tenorio MT, et al. Long-term outcome of acute tubular necrosis: a contribution to its natural history. Kidney Int (2007) 71(7):679–686.[CrossRef][Medline]
- Rivera M, Ortuno J. Ultrasonography in nephrology. Am J Kidney Dis (1998) 32(4):703.[Medline]
- O'Neill WCH. Sonographic evaluation of renal failure. Am J Kidney Dis (2000) 35(6):1021–1038.[Web of Science][Medline]
- Brandt TD, Neiman HL, Dragowski MJ, et al. Ultrasound assessment of normal renal dimensions. J Ultrasound Med (1982) 1(2):49–52.[Abstract]
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