Low prevalence of chronic kidney disease in Far-East Asian populations: impact of the ethnicity factor?

antiproteinuric treatment' [1]. We are pleased to answer both questions. First, it is believed that we forgot to mention a few papers. Before going into the details of the papers mentioned, we would like to stress the special hallmarks of our patient. She had infantile nephrotic syndrome, caused by nail-patella syndrome, as proven by mutation analysis, was treated exclusively with drugs interfering with the renin– angiotensin–aldosterone system and went into complete remission with a follow-up of more than 2 years. Indeed, we did not mention the patient reported by Sreedharan and Bockenhauer [2]. In fact, this infant, with congenital nephrotic syndrome of unidentified aetiology, did indeed go into complete remission with captopril alone, had a relapse when the drug was withheld and responded again, but the follow-up time was rather short. We did mention the patient described by Guez et al. [3], but this again was congenital nephrotic syndrome, this time with the Finnish type as a most likely diagnosis. But the treatment consisted of indomethacin and enalapril, and the remission was incomplete at the time of writing. There are at least two other papers that reported similar patients treated successfully with indomethacin and capto-pril [4,5]. The paper by Soliman et al. was, unfortunately, overlooked for the simple reason that it was not published yet when we wrote our paper [6]. This baby presented with infantile nephrotic syndrome; the biopsy showed focal segmental glomerulosclerosis—which by all means can hardly be considered an aetiologic category—but no mutation could be identified in the following genes: NPHS1, NPHS2, WT1 and PLCE1. The patient went into complete remission but with a multidrug regimen consisting of albumin infusions, furosemide, labetalol, amlodipine, vitamin E, captopril and enalapril. The follow-up was >1 year, and renal function was estimated to be within the normal range. Also, we wonder why the title of this paper ends with a question mark, 'is it renin–angiotensin blockade?' Second, the question was raised why we waited for 2 years before adding losartan to enalapril. From our short Case Report section, it is difficult to explain how well our patient was doing under enalapril therapy. In this early period of life, she was never really nephrotic, had no oedema and normal growth and development. Serum albumin was slightly below the lower limit of normality and serum cholesterol slightly above the normal figures for age. Moreover, she was normotensive with blood pressure figures around the …