A longitudinal study of kidney structure and function in adults

Dear Editor, I read the article by Kariyanna et al. [1] with great interest. The authors discussed a relatively neglected issue in clinical nephrology, namely interaction between kidney size and function. The authors drew some important conclusions which, inmy opinion, are difficult to accept due to limitations of the study. I will briefly discuss these limitations. Firstly, the authors used ultrasound to determine kidney size in an obese population, in which the sensitivity reduces dramatically (BMI 30.2 ± 4.9). Ultrasound was also performed by various technicians with different machines. Intraand inter-observer difference was not controlled in the study which claims that kidneys shrink at a rate of 0.072 cm per year. Ultrasound is not the gold standard as it was suggested by the authors to determine kidney size. In a comparative study, Ninan et al. [2] only compared ultrasoundwith abdominal plain X-ray, intravenous pyelogram, and renal angiogram but not with renal MRI or CT. To detect such subtle changes, standard MRI or CT scans should have been used or at least more measurements should have been performed with ultrasound (median follow-up is 3.7 years in the study). Secondly, the MDRD equation is not the perfect way to calculate the actual glomerular filtration rate. Twenty-fourhour urine collections, or inulin clearance ideally, would be better. Equations are especially prone to error in elderly and obese patients as applied in this study. Thirdly, it is not evident from the paper what the authors used as kidney size: the maximal longitudinal length of the bigger kidney or the mean of the two? We know size differences between the two kidneys as a variant of normal size can exist [3]. Some diseases such as stone disease, ischaemic nephropathy and obstructive nephropathy may further disproportionately affect the kidneys. Thus, a more exact analysis of kidney size should be offered. Lastly, a standard rate of atrophy for all aetiologic subclasses of chronic kidney disease seems unreasonable. Severity of the disease changes from patient to patient and various aetiologic subclasses progress at different rates. Thus, a constant atrophy irrespective of the aetiology may be a result of the retrospective study design and relatively small sample size. Al-Said et al. showed that even simple renal cysts may affect kidney size and function inversely [4,5]. However, in the current study, the authors did not mention the status of simple renal cysts in their patients. In conclusion, it is very difficult to ascertain from this that kidney atrophy occurs independently of the underlying aetiology of chronic kidney disease by such a data set.