A later onset and milder forms of hypertension in patients with BEN during predialytic and dialytic clinical course most often explained by loss of sodium because of tubulopathy, which also occurs in other forms of interstitial nephritis, can be an additional explanation.31 Damage to juxtaglomerular cells and proximal tubules at the beginning of the disease probably leads to reduced synthesis of renin and angiotensin converting enzyme, which can contribute to normotension and, additionally, explain the later appearance of hypertension in BEN. The gene discussed is ACE; the disease is Balkan nephropathy.