Animal models to study cognitive impairment of chronic kidney disease.

Mild cognitive impairment (MCI) is common in people with chronic kidney disease (CKD), and its prevalence increases with progressive loss of kidney function. MCI is characterized by a decline in cognitive performance greater than expected for an individual age and education level but with minimal impairment of instrumental activities of daily living. Deterioration can affect one or several cognitive domains (attention, memory, executive functions, language, and perceptual motor or social cognition). Given the increasing prevalence of kidney disease, more and more people with CKD will also develop MCI causing an enormous disease burden for these individuals, their relatives, and society. However, the underlying pathomechanisms are poorly understood, and current therapies mostly aim at supporting patients in their daily lives. This illustrates the urgent need to elucidate the pathogenesis and potential therapeutic targets and test novel therapies in appropriate preclinical models. Here, we will outline the necessary criteria for experimental modeling of cognitive disorders in CKD. We discuss the use of mice, rats, and zebrafish as model systems and present valuable techniques through which kidney function and cognitive impairment can be assessed in this setting. Our objective is to enable researchers to overcome hurdles and accelerate preclinical research aimed at improving the therapy of people with CKD and MCI.

Cardioprotective effect of postconditioning against ischemia-reperfusion injury is lost in heart of 8-week diabetic rat.

Although ischemic preconditioning (IPC) and ischemic postconditioning (IPost) result in protection against ischemia-reperfusion (I/R) injury in healthy hearts, pathological conditions such as diabetes can modify the protective effects of IPC and IPost. There are a few studies concerning the effect of IPost only in diabetic hearts which have similar or decreased tolerance to I/R injury. In the present study we investigated the effects of IPost in diabetic hearts which had increased tolerance to I/R injury. Isolated hearts from control and diabetic rats were subjected to global ischemia (40 min) followed by reperfusion (40 min). IPost was induced by six cycles (10 s) of reperfusion and ischemia after the global ischemia. After I/R, cardiac recovery in diabetic hearts was better than that in control hearts. IPost did not produce any further protection in the diabetic hearts whereas it resulted in a significant recovery in the control hearts. Similarly, the decreased troponin I (TnI) levels of diabetic hearts did not change after IPost. However, IPost significantly lowered the increase in TnI levels of control hearts. In conclusion, these results show that IPost can not produce a further protection in the hearts of 8-week diabetic rats which have increased tolerance to I/R injury.