Rat Study Finds Artery-Only and Artery-Vein Clamping Cause Similar Acute Kidney Injury

When surgeons remove a kidney tumor while sparing the rest of the organ, they must briefly cut off the blood supply to keep the field dry and visible. A long-running question in urological surgery is whether it is better to clamp only the renal artery or to clamp both the artery and the vein. A new experimental study in rats, published in the African Journal of Urology, reports that after eight minutes of warm ischemia in a solitary kidney model, the two clamping strategies produced no statistically significant differences in a panel of blood-based inflammatory, oxidative and antioxidant markers, and no significant differences in most measures of acute kidney tissue damage three days after surgery.

The research team, led by Tunahan Ates with colleagues from institutions in Turkey, set out to test the prevailing hypothesis that artery-only clamping is gentler on the kidney. The theoretical argument is well established in the literature: occluding both vessels traps blood inside the renal vasculature, producing venous stasis, raised intrarenal pressure and vascular congestion, whereas artery-only clamping leaves the venous system patent so residual blood can drain. Previous animal work has suggested that venous or combined clamping causes greater histological damage, more severe acute kidney injury and stronger inflammatory responses than arterial occlusion alone, and some clinical meta-analyses have reported slightly better long-term preservation of estimated glomerular filtration rate with artery-only clamping. Yet the clinical literature remains divided, with other studies and meta-analyses finding no significant difference between the techniques and attributing outcomes mainly to patient and tumor factors.

To isolate the biological effect of clamping from these confounders, the investigators designed a tightly controlled experiment. Twenty-four female albino rats, each weighing between 250 and 300 grams, were divided into three groups of eight: a control group, an artery-only group and an artery-vein group. Every rat first underwent removal of the right kidney, creating a left solitary kidney model. This design choice matters, because a functioning opposite kidney can compensate for injury and mask damage to the operated side. Based on earlier studies indicating that compensatory hypertrophy signs can appear as early as the second or third day after unilateral nephrectomy in rats, the procedures were spaced at three-day intervals.

Three days after the right nephrectomy, rats in the two ischemia groups underwent a left partial nephrectomy. Under the operating microscope, the left renal vessels were dissected, and in the artery-only group only the artery was clamped while in the artery-vein group both vessels were occluded, each for eight minutes. A 25 square millimeter wedge of tissue was resected from the anterior surface of the left kidney. The surgeons deliberately omitted deep parenchymal suturing to avoid suture-induced strangulation and secondary ischemia, achieving hemostasis instead with gentle compression using sterile cotton swabs. Bleeding was controlled in all animals without major hemorrhage, and no intraoperative or postoperative complications, including vascular thrombosis or perioperative mortality, occurred across the 24 animals. The control group underwent hilar dissection of the artery and vein without clamping, a sham step designed to ensure that later comparisons would reflect the specific effect of ischemia rather than dissection alone.

The ischemia duration was not chosen arbitrarily. In a pilot study before the main experiment, rats subjected to 20 or 15 minutes of ischemia lost viability at a rate of 50 percent by postoperative day two, and animals exposed to 12 minutes showed significant hypertrophy and discoloration of the left kidney at exploratory examination. Because the animals needed to survive at least three days after the procedure, the team reduced the ischemic time to eight minutes, which preserved macroscopic kidney integrity and was well tolerated. The authors note that this duration cannot be translated one-to-one to humans: rodents have a far higher mass-specific metabolic rate and oxygen consumption, so they experience accelerated energy depletion and cellular injury during vascular occlusion. While human kidneys typically tolerate warm ischemia times of 20 to 25 minutes, an eight-minute interval in a solitary rat kidney serves as a biologically potent surrogate for clinically significant acute warm ischemic injury rather than a direct temporal equivalent.

Three days after the partial nephrectomy, the researchers performed a left nephrectomy in both ischemia groups, aspirated blood from the heart under terminal anesthesia, and euthanized the animals. Blood samples were analyzed with enzyme-linked immunosorbent assays for creatinine, total antioxidant status, total oxidant status, oxidative stress index, malondialdehyde, superoxide dismutase, nitric oxide, tyrosine hydroxylase, 8-isoprostane and interleukin-6. The removed kidneys were fixed in formalin, sectioned at four microns, stained with hematoxylin and eosin, and examined by two blinded pathologists from Cukurova University. Six histopathological features were graded from zero to four: Bowman’s capsule enlargement, tubular necrosis, leukocyte infiltration of the vasa recta, tubular regeneration, interstitial inflammation and tubular dilation, while mitosis was recorded as present or absent.

The biochemical results were largely negative. Creatinine, total oxidant status, superoxide dismutase and tyrosine hydroxylase were elevated in the ischemia groups compared with controls, but none of these differences reached statistical significance, with p-values ranging from 0.178 to 0.893. Conversely, total antioxidant status, oxidative stress index, malondialdehyde and 8-isoprostane were unexpectedly higher in the control group, again without statistical significance. Total antioxidant status, total oxidant status, tyrosine hydroxylase and interleukin-6 were significantly higher in the artery-vein group than in the artery-only group, but taken together the authors concluded that no biochemical parameter demonstrated clear superiority of either technique. The absence of a creatinine difference may partly reflect the well-known time lag with which serum creatinine mirrors abrupt drops in filtration rate, a recognized blind spot in hyperacute post-ischemic assessment, and the study lacked baseline blood values because the required sampling volume could have destabilized the animals hemodynamically.

The histopathological picture told a more nuanced story. For every measured feature, the striking contrast was between the ischemia groups and the controls, not between the two clamping techniques. Bowman’s capsule enlargement, tubular necrosis, vasa recta leukocyte infiltration, mitosis and tubular dilation all differed significantly across the three groups, driven primarily by the control group, with p-values of 0.003, 0.016, 0.003, 0.014 and 0.0001 respectively. Tubular necrosis was absent in all controls but present in both ischemia groups, and tubular dilation appeared in every animal that underwent ischemia but in only one control animal, making it the most sensitive histological marker of acute warm ischemic injury in this model. Between the two ischemia groups, however, none of these features differed significantly. Interestingly, several findings, including Bowman’s capsule enlargement, tubular necrosis, vasa recta leukocyte infiltration and interstitial inflammation, showed non-significant numerical trends that actually favored the artery-vein group, the opposite of the expected direction, and the authors caution that this may reflect inter-individual variability rather than a true histological difference.

The authors are explicit about the limits of their findings. With eight animals per group, the study cannot establish true biological equivalence between the techniques, and the three-day observation window captures only acute injury, not long-term functional outcomes. The model also used healthy, non-tumor kidney, whereas clinical partial nephrectomy follows the plane around a tumor pseudocapsule through tissue that has been compressed and remodeled by the mass, so ischemic tolerance may differ. Blood loss was visually monitored but not quantitatively measured, although the authors report it was minimal and well controlled in every case. No baseline renal function was assessed, and none of the biochemical markers used is organ-specific.

Within those constraints, the conclusion is cautiously practical. In this experimental solitary kidney model, artery-only clamping showed no statistically significant acute structural or oxidative advantage over artery-vein clamping, and the authors suggest that when intraoperative conditions require clamping both vessels, the combined approach appears to be a safe alternative, yielding similar short-term histopathological changes at three days. They also note that artery-only clamping demands more extensive hilar dissection, which can prolong the operation and increase the risk of hilar injury, while combined clamping shortens warm ischemia time in some clinical series and provides a bloodless field for evaluating surgical margins. The team emphasizes that these results should not be read as definitive clinical equivalence, and that long-term follow-up studies in larger animal models and human cohorts are needed to determine whether the subtle micro-differences observed here matter for preserved renal function over years, particularly given that chronic kidney disease affects a substantial share of patients with renal cancer.

Subject of Research: Acute kidney injury from artery-only versus artery-vein clamping during partial nephrectomy in a rat solitary kidney model

Article Title: The clamping technique of renal circulation blockage during partial nephrectomy in rats

Article References: Ates, T., Deger, M., Akdogan, N., Yilmaz, I. O., Goruroglu Ozturk, O., Toyran, T., Erdogan, S., Izol, V., & Arıdogan, I. A. (2026). The clamping technique of renal circulation blockage during partial nephrectomy in rats. African Journal of Urology, 32(1), Article 71. https://doi.org/10.1186/s12301-026-00620-3

Image Credits: AI Generated

DOI: 10.1186/s12301-026-00620-3

Keywords: partial nephrectomy, renal ischemia, artery-only clamping, artery-vein clamping, warm ischemia, rat model, histopathology, oxidative stress, solitary kidney, nephron-sparing surgery, kidney injury, surgical technique