This is the first study that shows a significant correlation between renal allograft perfusion, as assessed with ASL perfusion measurements, and the fraction of pseudodiffusion derived from biexponential diffusion-weighted imaging measurements.
CCR5 deficiency does not influence hypertensive renal and cardiac end-organ damage. Cells that infiltrate by expression of CCR5 are either not pathogenic or CCR5-positive leukocytes can migrate via alternative chemokine receptors. Beneficial effects of CCR5 antagonists in hypertension are most likely due to unspecific effects of the antagonists. Possibly, other chemokine receptors in concert with CCR5 are important for hypertensive injury.
Atherosclerotic renal artery stenosis stimulates the renin-angiotensin system and thereby causes secondary hypertension. Furthermore, adrenal disorders that lead to abnormal aldosterone secretion, i.e., primary hyperaldosteronism, often result in secondary hypertension. Though the simultaneous occurrence of two potential causes of secondary hypertension is rare, it has to be considered for differential diagnosis and therapy. The presumed pathophysiological relevance should guide the order of therapeutic measures.
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