The effects of prolonged CO2 insufflation on kidney function in a rat pneumoperitoneum model

Abstract

Introduction: Pneumoperitoneum (PP) is known to cause ischemia in kidneys and other intra-abdominal organs because of decreased splanchnic blood flow.

Aim: We aimed to determine the degree of renal injury that occurs due to a PP and prolonged PP. We measured renal injury biomarkers and made a histopathological evaluation to estimate the degree of injury and assessed the correlation of biomarkers with histopathological findings.

Material and methods: Twenty-one female Sprague Dawley rats were separated randomly into three groups. Group 1 was the control group and was given anesthesia for 3 h. In group 2, a PP was administered under anesthesia for 1 h. A pneumoperitoneum was administered under anesthesia to animals in group 3 for 3 h.

Results: Pathological analysis showed a significant statistical difference between the 3 groups. In particular, neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C (Cys C) levels at the 24^th h and preoperative mean urea levels showed a significant difference between the groups. The 24^th-hour NGAL level in group 3 was significantly higher than that of group 1. The preoperative Cys C level was higher in group 1 than in either group 2 or 3. Cys C was decreased significantly in group 1 and increased significantly in both groups 2 and 3.

Conclusions: The increase in NGAL and Cys C levels directly correlated with the duration of PP and intra-abdominal pressure, and they are therefore good biomarkers in diagnosing acute renal injury in the early phase. Serum creatinine level is not a good biomarker in the early phase of renal injury.

Keywords: acute kidney injury; cystatin C; neutrophil gelatinase-associated lipocalin; pneumoperitoneum; rats.

Figure 1

The relationship between NGAL level and PP duration

Figure 2

Early events in ischemic acute renal failure. The initial ischemic insult results in morphological and functional alterations in the renal tubules and the renal vasculature. Following the initial ischemic insult, further alterations in the renal vascular endothelium of the cortico-medullary junction contribute to inflammation and vascular congestion. These processes are proposed to extend the initial injury to the renal tubules [52]

Figure 3

Graph of total scores of histopathological analysis of the kidneys by groups

Photo 1

Histopathological features (light microscopy). A – control group: tubulointertitial features in normal limits (1 × 200), B – 1 h pnp.: mild edema, mild congestion and glomerular lobutation (1 × 200), C – 3 h pnp.: congestion of glomeruli, edema of tubular epithelium, swelling of endothelial cells and vascular congestion (1 × 200), D – 3 h pnp.: congestion of glomeruli, edema of tubular epithelium, swelling of endothelial cells and vascular congestion (1 × 400)