Radiocontrast-induced acute kidney injury.

Nephron Physiol. 2008;109(4):p61-72

Authors: McCullough PA

Many radiographic studies and procedures use iodinated contrast media and consequently pose the risk of contrast-induced acute kidney injury (AKI). This is an important complication, which accounts for a significant number of cases of hospital-acquired renal failure associated increased hospital length of stay and increased mortality. Sustained reductions in renal blood flow, hypoxic injury, direct cellular toxicity by the contrast media, and superimposed organ injury are all believed to play a role in this form of AKI. Avoidance of dehydration and multimodality prevention measures may reduce rates of this problem in patients at risk. Contrast-induced AKI is likely to remain a significant challenge for specialists in the future since the patient population is aging, chronic kidney disease and diabetes are coming more common, and use of iodinated contrast is growing.

PMID: 18802377 [PubMed - indexed for MEDLINE]

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Acute kidney injury: new concepts. Hepatorenal syndrome: the role of vasopressors.

Nephron Physiol. 2008;109(4):p73-9

Authors: Moreau R, Lebrec D

Type 1 hepatorenal syndrome (HRS) is prerenal failure specific to decompensated cirrhosis. In patients with HRS, there is marked splanchnic/systemic vasodilation resulting in arterial hypotension, arterial baroreceptor unloading, overstimulation of the sympathetic nervous and renin-angiotensin systems. This reflex neurohumoral hyperactivity via endogenous vasoconstrictors/vasopressors such as angiotensin II and noradrenaline induces arterial vasoconstriction in different extrasplanchnic vascular beds (including preglomerular arteries in the kidneys). Decreased arterial pressure (i.e. low renal perfusion pressure) and preglomerular vasoconstriction are thought to play a major role in the decline of the glomerular filtration rate (GFR). Nonrandomized studies in patients with HRS have shown that the administration of a splanchnic vasoconstrictor (vasopressin analogue or alpha(1)-adrenoceptor agonist), usually combined with intravenous albumin, causes increases in arterial pressure, arterial baroreceptor uploading, decreased neurohumoral activity, decreased renal vascular resistance, and increased GFR. Randomized clinical trials have shown that treatment with a combination of the vasopressin analogue terlipressin and intravenous albumin improves renal function in patients with type 1 HRS. Vasopressor therapy with terlipressin plus intravenous albumin is the medical treatment of choice for type 1 HRS.

PMID: 18802378 [PubMed - indexed for MEDLINE]

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