Ultrastructural Study of Ciliary Fragmentation in Renal Tubules During Ischemia-Reperfusion Injury

Abstract Primary cilia on renal tubular cells are critical for kidney function. This study investigated how acute kidney injury affects cilia length, specifically focusing on their shortening during ischemia-reperfusion injury. Using Sprague–Dawley rats, renal pedicles were clamped for 30 min followed by six hours of reperfusion. Kidney tissues were analyzed using confocal laser scanning microscopy and scanning electron microscopy. Acetylated α-tubulin and specific markers such as aquaporin 1 and H + -ATPase were used to identify proximal tubules and collecting ducts. Under normal conditions, renal tubular cells exhibited long primary cilia. Following injury, significant shortening of primary cilia was observed in both proximal tubules and collecting ducts. Intermingled microvilli in proximal tubules complicated ultrastructural observation. However, the collecting duct exhibited distinct responses. While intercalated cells detached into the lumen, principal cells remained attached to the basal lamina. Electron microscopy confirmed the shortening of cilia in principal cells, often accompanied by bulging regions of varying sizes, observed at either the tip or middle, and appearing as single or multiple structures. These findings demonstrate that acute ischaemic injury induces ciliary fragmentation in collecting duct principal cells. The observed bulging in cilia undergoing shortening may indicate potential mechanisms underlying ciliary fragmentation.