Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
The Iranian model of kidney transplantation, whereby donors are paid by a government-sponsored agency, has eliminated the waiting list completely. Elsewhere, black markets for kidneys encourage exploitation of the poor and harm both donors and recipients. As the buying and selling of organs increases relentlessly despite legislation, this author argues that failure to regulate these practices could be considered unethical.
Seven single gene mutations are known to cause hypertension, generally by affecting electrolyte transport in the distal nephron, or synthesis or activity of mineralocorticoid hormones. These relatively uncommon disorders should be considered when young patients with a family history of high blood pressure present with severe or refractory hypertension. This article guides clinicians through identification of these defects, their associated laboratory findings, and recommended treatments.
This short article is an introduction to the histology of damage to transplanted kidneys caused by active BK virus infection. Aimed at trainee pathologists and nephrologists wishing to enhance their understanding of the histological basis of the diseases they manage, this beautifully illustrated paper describes the key features, differential diagnosis and clinical implications of this increasingly frequent complication.
Are polymorphisms of the G protein-coupled receptor kinase GRK4 the key to developing new tools for the diagnosis and management of essential hypertension? Here, Felder and Jose explore the therapeutic potential of manipulating this protein, which regulates the activity of the dopamine-1 receptor. The role of GRK4 is set in the context of the contributions of the dopaminergic and renin–angiotensin systems to the pathogenesis of hypertension.