The results of our study show that the use of the ratio is a reliable tool for predicting the development of contrast-induced nephropathy (CIN) in patients undergoing contrast-requiring procedures. We found that a ratio cutoff value of ≤ 7.91 had an excellent predictive value for forecasting CIN with a sensitivity of 98.9% and specificity of 83.3%. This finding is consistent with previous studies that have also reported the efficacy of the ratio in predicting CIN, as it is a simple, low-cost, and minimally invasive method that can easily be used in routine clinical practice. [1]
In this study, we considered patients undergoing the procedure with only one type of contrast agent as mentioned before, thus minimising the bias. However, to assess the usefulness of HCR for predicting CIN in a situation where the type of contrast agent is not known, larger studies need to be conducted with different types of contrast agents.
Direct toxic effects of contrast agents on renal tubular cells are thought to be a significant factor in the development of CIN. The contrast agents cause a direct injury to the renal tubular epithelial cells, which results in decreased renal function. This injury may be caused by the osmotic and ionic effects of the contrast agents, leading to cellular swelling, and the formation of intracellular vacuoles. [9]
Oxidative stress is another important mechanism in the pathophysiology of CIN. Contrast agents generate reactive oxygen species (ROS) which can cause oxidative damage to the renal tubular cells, leading to inflammation and cell death. The gap between generation of ROS and ability to neutralise it leads to production of oxidative stress. [10]
Finally, alterations in renal hemodynamics, including decreased renal blood flow and increased renal vascular resistance, are thought to contribute to the development of CIN. Contrast agents can cause vasoconstriction of the renal arterioles, leading to decreased renal blood flow, decreased oxygen delivery, and increased hypoxia in the renal tubular cells. This decreased renal perfusion and hypoxia can lead to renal injury and contribute to the development of CIN.
Our study found that a HB1 cutoff value of ≤ 8.8 g/dL had a high sensitivity of 100% but a lower specificity of 66.7% for predicting CIN. This result may indicate that the Hb1 level alone may not be a true predictor of CIN as the ratio, as it lacks the supplemental information provided by the creatinine level. The high sensitivity of the Hb1 cutoff value suggests that it may be a useful tool for identifying patients at risk for CIN. Also, the AUC for CR1 is 0.566 and p-value is 0.590 which indicates that CR1 alone is a terrible predictor for CIN whereas HCR has a better prognostic significance.
Low levels of haemoglobin may cause hypoxia owing to the decreased oxygen transport capacity [11] and their increased affinity for oxygen when exposed to contrast media [12], which aggravates hypoxic injury and further results in renal dysfunction. [13,14,]
Although ratio and Hb1 cutoff values observed in our study may be useful for predicting CIN, they should not be used as the only method for diagnosing or treating CIN. When assessing a patient's risk for CIN, several clinical factors should be taken into consideration in addition to the use of contrast agents. These include underlying medical conditions, such as chronic kidney disease, diabetes, and hypertension, which are known to increase the risk of CIN. Patients with a history of congestive heart failure, liver disease, or advanced age may also be at higher risk. [15]
Medication use is another important factor to consider when assessing the risk of CIN. Certain medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme (ACE) inhibitors, and diuretics, can interfere with renal blood flow and increase the risk of kidney damage following exposure to contrast agents.
Additionally, the dose and type of contrast agent used can also affect the risk of CIN. Higher doses of contrast agents are associated with a greater risk of kidney damage, as are certain types of agents, such as those containing high-osmolality or ionic compounds.
Overall, a comprehensive assessment of a patient's medical history, medications, and the type and dose of contrast agent to be used should be performed to determine their risk for CIN and to identify appropriate preventive measures. Nonetheless, it is important to note that the optimal cutoff value for the ratio may alter depending on the demographic being studied.
Biomarkers may offer a more sensitive and specific approach to diagnosing and predicting CIN. For example, neutrophil gelatinase-associated lipocalin (NGAL), which is a protein expressed by neutrophils and other cells in response to kidney injury can be measured in the urine. NGAL levels have been shown to correlate with the severity of CIN and the need for renal replacement therapy. Other markers such as KIM-1 have also been investigated; however, further research is needed to determine the optimal biomarker(s) to use in clinical practice and to establish standardised cutoff values for diagnosis and risk stratification. Therefore, future studies should explore the use of these biomarkers in conjunction with HCR and HB1 in predicting CIN.
LIMITATIONS:
One limitation of our study is the small sample size. Further research with larger sample sizes may be needed to confirm the utility of the ratio and HB1 cutoff values in predicting CIN.
Our study did not examine the potential impact of interventions such as hydration and medication adjustments on the development of CIN. Future research could investigate whether these interventions, in conjunction with the use of the ratio or HB1 cutoff values, may be effective in preventing or mitigating the development of CIN.
Despite these limitations, our study is a guide for future studies.