Objective To investigate the role of the PINK1/ Parkin mitochondrial autophagy pathway in myocardial injury of chronic kidney disease, and the mechanism of Shenshuai recipe in the treatment of 5/6 nephrectomy CKD myocardial injury in rats. Methods Overall, 48 nephrectomized rats were randomly divided into six groups: sham then sacrificed. Heart tissue was collected, stained with HE, and observed under a light microscope. Autophagosomes and autophagic lysosomes were observed by transmission electron microscopy. PINK1, Parkin, P62, and LC3B mRNA levels were measured by RT?PCR. PINK1, Parkin, P62, and LC3B protein levels in nephrectomized rats were measured by Western Blot. Results Compared with the sham?operated group, CK?MB and hs?cTnI were significantly increased in the model group (P<0.01). Compared with the model group, benazepril group, low, medium, and high dose Shenshuai recipe groups were significantly decreased (P< 0.05). Compared with the sham operated group, myocardial tissue in the model group after nephrectomy was obviously disordered and displayed interstitial hyperplasia, vascular wall thickening, and glassy changes. There were no obvious abnormalities in Benazepril and low, medium, and high dose Shenshuai Recipe groups. Compared with the model group, the numbers of autophagosomes and autophagic lysosomes were increased significantly in low, middle, and high dose Shenshuai recipe groups(P< 0.01). Compared with the sham operated group, PINK1, Parkin, P62, and LC3B mRNA levels were significantly decreased in the model group(P< 0.05). Compared with the model group, PINK1, Parkin, P62, and LC3B mRNA levels were significantly increased in benazepril and high, medium, and low dose Shenshuai recipe groups(P< 0.05). Compared with the sham operated group, PINK1, Parkin, P62, and LC3B protein levels were significantly decreased in the model group (P< 0.01). Compared with the model group, PINK1, Parkin, P62, and LC3B protein levels were significantly increased in Benazepril and low?, medium?, and high?dose Shenshuai recipe groups (P< 0.01). Conclusions The PINK1/ Parkin mitochondrial autophagy pathway in myocardial cells of rats with myocardial injury caused by 5/6 nephrectomy was inhibited. Shenshuai recipe enhanced mitochondrial autophagy by activating the PINK1/ Parkin mitochondrial autophagy pathway, and played a protective role in myocardial cells. Among the groups, the highest dose of Shenshuai recipe had the most significant effects on mitochondrial autophagy intensity.