LDH release into perfusates of preserved kidneys

Area of Science:

• Nephrology
• Transplantation
• Biochemistry

Background:

• Hypothermic storage is crucial for organ preservation.
• Assessing ischemic injury in kidneys is vital for transplantation success.
• Lactate dehydrogenase (LDH) release is a potential biomarker for cellular damage.

Purpose of the Study:

• To evaluate lactate dehydrogenase (LDH) release as an indicator of ischemic injury in rabbit kidneys post-hypothermic storage.
• To compare the efficacy of different preservation solutions and additives in mitigating kidney damage.
• To investigate the impact of varying ischemia durations on LDH release.

Main Methods:

• Rabbit kidneys underwent warm and cold ischemia, followed by hypothermic storage in modified Collins solution.
• Venous effluent was collected in fractions, and total LDH activity was measured post-storage.
• LDH release was quantified to assess ischemic tissue damage and compare preservation strategies.

Main Results:

• Increased cold ischemia time significantly elevated LDH activity, confirming its role as an injury marker.
• No significant difference in tissue damage was observed between sodium-rich and potassium-rich perfusion fluids.
• Steroids, vitamins, and amino acids did not reduce estimated tissue damage.
• 5% DMSO significantly increased LDH release, while 5% glycerol decreased it compared to Collins solution alone.
• Higher concentrations of DMSO (up to 20%) led to severe tissue damage.

Conclusions:

• LDH release is a reliable index of ischemic injury in rabbit kidneys following hypothermic storage.
• The composition of perfusion fluid (sodium vs. potassium) did not significantly alter kidney damage.
• Cryoprotectants have varied effects; DMSO exacerbates injury, whereas glycerol offers some protection.
• Further research is needed to optimize cryoprotectant use in organ preservation.