Nephrol Dial Transplant Vol. 20 Suppl 1 © ERA–EDTA 2005; all rights reserved
Renal haemodynamic alterations in contrast medium-induced nephropathy and the benefit of hydration
Institute of Physiology, Humboldt University Berlin, Germany
Correspondence and offprint requests to: Professor Dr Pontus B. Persson, Institut für Vegetative Physiologie, Humboldt Universität, Berlin, Medizinische Fakultät (Charité), Tucholskystr. 2, D-10117 Berlin, Germany. Email: pontus.persson{at}charite.de
Though several suggestions have been put forward, the underlying mechanism of contrast medium-induced nephropathy (CIN) is not clear. Most probably, however, the culprit is a combination of various mechanisms working together to cause the development of CIN. The generally accepted main factors in the pathophysiology of CIN are the reduction in renal perfusion by contrast media (CM) combined with the toxic effects on the tubular cells. With regard to the literature, misconceptions are widespread when explaining the development of CIN, e.g. that osmolar challenge induces renal vasoconstriction due to the tubuloglomerular feedback mechanism (TGF). Although popular, this assumption is most probably false, since osmotic pressure is not the signal for the TGF. Much attention has been paid to reducing the osmolarity of CM further. In an effort to obtain iso-osmolar CM, dimers were formed. These CM have osmolarities in the near physiological range, but at the cost of increased viscosity. This seems to have adverse effects with regard to kidney haemodynamics. In contrast to the multifarious interpretations of CIN, it is generally accepted that hydration is effective in preventing CIN from occuring. There is no universally accepted explanation for the effect of hydration, but it may rely on enhancing renal medullary blood flow and reducing the viscosity of the fluid in the collecting duct.
Keywords: contrast medium-induced nephropathy; haemodynamics; hydration; tubuloglomerular feedback mechanism
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