Decompression of inflammatory edema along with endothelial cell therapy expedites regeneration after renal ischemia-reperfusion injury.

Increased pressure due to postischemic edema aggravates renal ischemia-reperfusion injury (IRI). Prophylactic surgical decompression using microcapsulotomy improves kidney dysfunction after IRI. Supportive cell therapy in combination with microcapsulotomy might act synergistically protecting kidney function against IRI.

99mTc-MAG3 scintigraphy for the longitudinal follow-up of kidney function in a mouse model of renal ischemia-reperfusion injury.

Background: Experimental models are essential tools in the development and evaluation of novel treatment options, but the preclinical model of renal ischemia-reperfusion injury is limited to the retrieval of (very) early functional data, leaving the pivotal long-term outcome unknown. The present study applies technetium-99m-mercapto-acetyl-tri-glycine [99mTc-MAG3] scintigraphy for the longitudinal follow-up examination of long-term kidney function after renal ischemia-reperfusion injury.

Methods: Unilateral warm ischemia was induced in scid beige mice by vascular clamping of the kidney hilum for 40 min.

The intrinsic renal compartment syndrome: new perspectives in kidney transplantation.

Purpose: Inflammatory edema after ischemia-reperfusion may impair renal allograft function after kidney transplantation. This study examines the effect of edema-related pressure elevation on renal function and describes a simple method to relieve pressure within the renal compartment.

Methods: Subcapsular pressure at 6, 12, 24, 48 hr, and 18 days after a 45 min warm ischemia was determined in a murine model of renal ischemia-reperfusion injury.