**1. Introduction**

The number of patients with diabetes mellitus is expanding, and diabetic kidney disease (DKD) is an important cause of diabetic microvascular complications that constitutes an independent risk factor of mortality and cardiovascular events [1].

The kidney is one of the most energy-demanding organs and, after the heart, has the second highest expression of proteins involved in mitochondrial function and oxygen consumption [2,3]. The kidney requires energy mainly for solute reabsorption, among other tasks including waste removal, maintenance of electrolyte and fluid balance and acid– base homeostasis [4]. The generation of an ion gradient across the plasma membrane by Na+/K+-ATPase is essential for solute reabsorption. Therefore, mitochondrial dysfunction is postulated to play a central role in the pathogenesis and progression of kidney diseases including DKD [5–7].

Since each component of the nephron has a distinct role and different energy requirement, the causes and phenotypes of mitochondrial dysfunction may differ among cell types in the kidney. In this review, we will discuss glucose-related and unrelated pathways of mitochondrial dysfunction contributing to DKD in terms of the categories as well as the causes.
