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Das akute Nierenversagen beim kritisch kranken Patienten auf der Intensivstation stellt eine schwerwiegende Komplikation dar, die unabhängig von der zugrunde liegenden Ursache eine erhebliche Morbidität und Letalität aufweist. Trotz modernster intensivmedizinischer Maßnahmen und Fortschritten in der Nierenersatztherapie ist die Letalität bei Patienten mit akutem Nierenversagen gegenüber Patienten ohne Nierenfunktionseinschränkung deutlich erhöht. Im folgenden Beitrag werden Inzidenz und Letalität des akuten Nierenversagens beleuchtet. Zudem werden der Zeitpunkt des Beginns der Nierenersatztherapie sowie die Auswahl des geeigneten Nierenersatzverfahrens und der geeigneten Therapiedosis diskutiert. Das akute Nierenversagen beim kritisch kranken Patienten auf der Intensivstation stellt eine schwerwiegende Komplikation dar, die unabhängig von der zugrunde liegenden Ursache eine erhebliche Morbidität und Letalität aufweist. Trotz modernster intensivmedizinischer Maßnahmen und Fortschritten in der Nierenersatztherapie ist die Letalität bei Patienten mit akutem Nierenversagen gegenüber Patienten ohne Nierenfunktionseinschränkung deutlich erhöht. Im folgenden Beitrag werden Inzidenz und Letalität des akuten Nierenversagens beleuchtet. Zudem werden der Zeitpunkt des Beginns der Nierenersatztherapie sowie die Auswahl des geeigneten Nierenersatzverfahrens und der geeigneten Therapiedosis diskutiert.

Real‐time contrast‐enhanced sonography (RT‐CES) can assess microvascular tissue perfusion using gas‐filled microbubbles. The study was performed to evaluate the feasibility of RT‐CES in detecting chronic allograft nephropathy (CAN) in comparison to color Doppler ultrasonography (CDUS). A total of 26 consecutive renal transplant recipients were prospectively studied using RT‐CES and conventional CDUS. Transplant tissue perfusion imaging was performed by low‐power imaging during i.v. administration of the sonocontrast Optison™. Renal tissue perfusion was assessed quantitatively using flash replenishment kinetics of microbubbles to estimate renal blood flow A *β (A = peak signal intensity, β= slope of signal intensity rise). In contrast to conventional CDUS resistance and pulsatility indices, renal blood flow estimated by CES was highly significant related to S‐creatinine (r =–0.62, p = 0.0004). Determination of renal blood flow by CES reached a higher sensitivity (91% vs. 82%, p < 0.05), specificity (82% vs. 64%, p < 0.05) and accuracy (85% vs. 73%, p < 0.05) for the diagnosis of CAN as compared to conventional CDUS resistance indices. Perfusion parameters derived from RT‐CES significantly improve the early detection of CAN compared to conventional CDUS. RT‐CES using low‐power real‐time perfusion imaging is a feasible method to evaluate microvascular perfusion in renal allograft recipients.

Real-time contrast-enhanced†sonography (RT-CES) can assess microvascular tissue perfusion using gas-filled microbubbles. The study was performed to evaluate the feasibility of RT-CES in detecting chronic allograft nephropathy (CAN) in comparison to color Doppler ultrasonography (CDUS). A total of 26 consecutive renal transplant recipients were prospectively studied using RT-CES and conventional CDUS. Transplant tissue perfusion imaging was performed by low-power imaging during i.v. administration of the sonocontrast Optison™. Renal tissue perfusion was assessed quantitatively using flash replenishment kinetics of microbubbles to estimate renal blood flow A *β (A = peak signal intensity, β= slope of signal intensity rise). In contrast to conventional CDUS resistance and pulsatility indices, renal blood flow estimated by CES was highly significant related to S-creatinine (r =–0.62, p = 0.0004). Determination of renal blood flow by CES reached a higher sensitivity (91% vs. 82%, p < 0.05), specificity (82% vs. 64%, p < 0.05) and accuracy (85% vs. 73%, p < 0.05) for the diagnosis of CAN as compared to conventional CDUS resistance indices. Perfusion parameters derived from RT-CES significantly improve the early detection of CAN compared to conventional CDUS. RT-CES using low-power real-time perfusion imaging is a feasible method to evaluate microvascular perfusion in renal allograft recipients.

We have previously demonstrated that Ang II enhances insulin sensitivity in humans and this is associated with a paradoxical increase in skeletal muscle blood flow. It is unclear whether these effects are mediated via subtype 1 receptors of Ang II, since these receptors are thougth to mediate vasoconstriction. We measured insulin-stimulated glucose uptake (euglycemic clamp) and leg muscle blood flow (plethysmography) in 9 healthy subjects (mean age 24 ± 2 y) on three occasions using a double blind placebo controlled study design. The subjects were allocated in random order to: (i) placebo premedication per os plus placebo infusion, (ii) placebo per os plus infusion of 5 ng Ang II/kg/min, and (iii) premedication with 300 mg of the angiotensin II-1-receptor antagonist irbesartan per os plus infusion of 5 ng Ang II/kg/min. In addition, GFR and effective renal plasma flow were assessed (inulin- and PAH-clearance). Insulin sensitivity (i.e. M-value) and muscle blood flow after infusion of Ang II (9.3 ± 1.8 mg/kg/min; 17.7 ± 2.2 ml/100g/min) were significantly higher (p < 0.05) than after placebo infusion (7.2 ± 1.6; 13.5 ± 1.8). In contrast, after irbesartan premedication they were not significantly different (7.5 ± 1.7; 14.3 ± 1.9) as compared with placebo infusion. Mean GFR and effective renal plasma flow were significantly lower (p < 0.05) and renal vascular resistance higher (p < 0.05) with Ang II infusion (107 ± 6 ml/min/1.73 m2; 461 ± 44 ml/min/1.73 m2; 126 ± 15 mmHg/ml/min) as compared with placebo infusion (120 ± 6; 672 ± 51; 74 ± 6). Irbesartan almost completely blocked the vasoconstrictive effect of Ang II on renal vasculature (118 ± 6; 650 ± 36; 76 ± 6). We conclude that under hyperinsulinemic euglycemic conditions Ang II has opposing effects on regional arterial blood flow, i.e. vasodilation in skeletal muscles but vasoconstriction of renal vasculature. Both effects are antagonized by blockade of subtype 1 Ang II receptors.