Acute kidney injury (AKI) is one of the silent killers of the world. Studies in developed and developing countries have documented the high incidence of acute kidney injury. Luyckx, V. A., Tonelli, M., and Stanifer have quantified the global burden of acute kidney injury. Acute kidney injury is a major contributor to the burden of chronic kidney disease.
Nephrotoxic drugs
Patients admitted to the intensive care unit (ICU) may be exposed to a variety of nephrotoxic drugs, which can affect kidney function. These drugs include some pain relievers, antibiotics, and NSAIDs. Some of these drugs can lead to severe acute kidney injury. In order to reduce the risk of renal toxicity, patients should minimize exposure to multiple nephrotoxic drugs.
Nephrotoxic drugs can also cause multiple types of kidney damage, which is a risk for people who are taking more than one type of medication. It is important to discuss the potential for nephrotoxicity with your healthcare provider before starting a new medication. You should also ask about the combinations of medications that you are currently taking. Also, be sure to make regular visits to your physician to have your kidneys checked.
Radiocontrast agents
The association between radiocontrast agents and acute kidney injury is well known. All formulations of contrast media are cytotoxic, and in vitro studies have revealed significant effects on endothelial cells. This cytotoxicity leads to cell damage and apoptosis, thereby affecting the nephron’s tubules. The cellular damage is also associated with oxidative stress and a rise in free radical levels.
In early publications, CI-AKI was defined as an increase in creatinine of 0.5 mg/dL or more from baseline within two to five days. However, the Kidney Disease Improving Global Outcomes Working Group proposed a new definition for CI-AKI: a rise in creatinine of more than 50% within 7 days or 0.3 mg/dL within 48 hours of exposure. These definitions have become accepted terminology for acute kidney injury caused by iodinated contrast media.
Acute tubular necrosis
Treatment for acute tubular necrosis depends on the underlying disorder. If the cause of necrosis was poisoning, the first goal is to remove the poison from the body. Treatment will also focus on keeping the kidneys from overproducing waste products and fluids. While the majority of people recover fully after treatment, some may need dialysis to maintain normal kidney function.
If left untreated, acute tubular necrosis may develop and result in acid-base and electrolyte disturbances. Renal function may decline over time, and blood flow and electrolyte levels may be impaired. If the kidneys are not able to repair themselves, the condition may progress to chronic tubular necrosis.
NAG
Acute kidney injury (AKI) is a serious medical condition that occurs when the kidney fails to function properly. AKI is classified into three phases: onset, diuretic, and recovery. During the onset phase, the kidney produces more urine than normal, increasing tubular edema. Once this is over, the kidney recovers and returns to normal renal function. The blood urea nitrogen (BUN) level is a key marker of renal failure, but this test is not always a good indicator of actual renal function.
Besides NAG, other important markers for kidney injury include HIV infection and Interleukin-8 (IL21). Interleukin-2 (IL2) is a protein produced by cells in the body that fights infection. This protein is also a marker of a variety of other diseases, including Tuberculosis and HIV infection.
L-FAB
The urinary concentration of L-FABP has been used to predict acute kidney injury. It is a highly sensitive biomarker, more sensitive than uKIM-1 and uL-FABP. However, in some cases, a person may develop hepatocellular carcinoma, which may lose staining for L-FABP. The protein is regulated by HBx, the hepatitis B virus X protein. In addition, an allele called rs2919872A reduces transcriptional activity of the FABP1 promoter.
In a study published in the Journal of Clinical Chemistry, a group of researchers showed that a small increase in L-FAB in patients with acute kidney injury was associated with better clinical outcomes. These results supported the clinical benefits of implementing the biomarker in the first few hours after the surgery. The findings also showed that L-FAB may increase the rate of kidney recovery in children with acute kidney injury.
