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UTI in Children and Acute Kidney Injury
Urinary tract infection, abbreviated as UTI is common among children. It affects the urine and girls are more vulnerable to the condition since their urethra is closer to their anus. This makes it easier for E. coli to enter and cause the infection. As for acute kidney injury (AKI), it is a condition that lacks a standard definition but often characterized by diminished kidney functionality (Stein, et al. 2015). This paper is a comprehensive description of UTI in children and AKI.
UTI in infants and children
A bacterium known as E. coli which commonly causes UTI enters gets into a child’s urethra opening located at the bottom of the penis for boys and in the front part of the vagina and near the anus in girls. In most cases, the bacteria comes from the skin that surrounds the vagina or the anus. Normally, upon entering the urethra, the process of urination is supposed to flush them out. Nevertheless, the bacteria penetrates and invades the urinary tract if they are not expelled, causing UTI. The urinary tract consists of two kidneys and the ureters attached to each, the urinary bladder, and the urethra. The kidneys generate urine through the removal of waste and excess water from the blood (Schlager, 2016). The urine then moves from the kidneys through the ureters to the bladder where it is stored and emptied via the urethra during urination. When E. coli attacks the bladder, it causes a UTI known as cystitis while pyelonephritis is the UTI that results when the bacteria further invades the kidneys.
It is difficult to determine whether infants and very young babies have UTI as symptoms may not show.  However, younger children may experience varying symptoms of UTI depending on the part of the urinary tract that has been affected. Some of the most common indicators the condition on kids include fever, lack of appetite, irritability, vomiting, and diarrhea, as well as general body weakness. When the UTI has affected the bladder, children might present with bloody, smelly, and cloudy urine, pain during peeing, increased urgency to urinate, and bedwetting (Leung, et al. 2018). On the other hand, pyelonephritis is more serious and kids may exhibit symptoms such as high irritability and fever, excess abdominal aching, and fatigue as well as chills.
The diagnosis of UTI a child involves taking their urine sample and subjecting it to various tests. Urinalysis is one of the most common assessments for UTI. It involves using a special strip to check for indicators of the condition such as white blood cells and blood present in the urine. The presence of bacteria or pus in the urine may also be tested using a microscope during a urinalysis. Urine culture is also another way that a UTI infection could be detected. The method takes place in the laboratory and normally takes one or two days (Leung, et al. 2018). It includes analyzing a urine sample to determine the causative bacteria and what amount of it is present. Additional tests such as VCUG and kidney ultrasound might be recommended by a physician in situations where the kidney may have been infected or when an abnormality in the urinary tract has been suspected.
Antibiotic treatment is largely used to manage UTI in children. Drugs such as amoxicillin, cephalosporin, and nitrofurantoin, just to mention a few, inhibits kidney invasion. Factors such as the type of bacteria involved and the severity of the illness are used to make a decision of the type of antibiotic to be used and the treatment duration. Oral antibiotics to be consumed at home might be recommended for children who have bladder infection while hospitalization and IV fluids are likely to be suggested for severe UTI (Leung, et al. 2018). For instance, kids below 6 months, those who have a high and persistent fever, and those with kidney infections might undergo hospitalization when diagnosed with UTI.
Acute Kidney Injury (AKI)
Types of AKI
Pre-renal failure
Pre-renal AKI initially referred to as acute renal failure is the most predominant form of AKI. It takes place when the body experiences a reduction of blood flow in all the organs including the kidney. The term “renal hypoperfusion” is used to describe the unexpected drop of blood in the kidney. This, in turn, interferes with the kidneys’ functionality but they are totally okay. The interference of blood flow in the body which leads to pre-renal AKI may be due to existing illnesses or current medications (Kellum & Lameire, 2013). For instance, excess blood loss following major surgery, injury or sepsis can cause the condition. As for drugs, a variety of NSAIDs and ACE inhibitors have been associated with pre-renal AKI among individuals who are already vulnerable to renal problems.
Intrinsic renal failure
Also known as intrarenal acute renal failure (ARF), it happens when the kidneys are directly damaged, causing their functionality to diminish suddenly. One of the main causes of intrinsic AKI is acute tubular necrosis (ATN). It occurs when the kidneys’ tubular is damaged. Reduced kidney blood supply, severe burns, and muscle injury are some of the causes of ATN. Intrarenal AKI may also occur as a result of acute glomerulonephritis (AGN) ((Kellum & Lameire, 2013). This is a condition that results from damage in the glomeruli, making it not to filter the blood as required. The other main cause of intrinsic AKI is interstitial nephritis (AIN) which is an inflammation of the renal system.
Obstruction is also referred to as post-renal AKI and it is characterized by an abnormal flow of urine. This causes accumulation of pressure in the nephron (Kellum & Lameire, 2013). As a result, the nephrons stop working. The level of kidney failure reflects the amount of obstruction.
The pressure gradient emanating from the glomerulus directly impacts the glomerular filtration. On the other hand, the glomerular force depends principally on renal blood flow, abbreviated as RBF and constrained the renal afferent’ and efferent arterioles’ resistances. Despite the origin of AKI, a decline in RBF indicates a typical pathologic path for weakening glomerular filtration rate (GFR). AKI’s etiology is characteristic of 3 principle systems: prerenal, intrinsic, and obstructive.
As for prerenal failure, the GFR is negatively affected by low renal perfusion even though the functionality of the tubular and glomerular remains unaffected. Intrinsic renal failure is due to damage on the kidney itself, which further alters the glomerular or tubule, which are related to the dissemination of renal afferent vasoconstrictors. Ischemic renal damage is the most widely recognized condition that causes intrinsic renal distress (Chawla, et al. 2014). Obstruction of the urinary tract is responsible for the elevation pressure in the tubular, which lessens the filtration driving force. This force later balances, and the renal efferent vasoconstriction determines whether a low GFR remains intact.
The causes of AKI are grouped into pre-renal, intrinsic, and post-renal. Each category exhibit a wide range of factor that interferes with renal functionality. For instance, interference of blood pressure due to reduced supply of blood due to underlying medical conditions, bleeding, and medications trigger pre-renal AKI. Intrinsic causes are those that directly harm the kidney such as glomerulonephritis (Chawla, et al. 2014). On the other hand, post-renal causes are attributed to the urinary system blockage.
Diagnostic findings
Patients with AKI present with elevated serum creatinine levels within 48 hours. Determining the level of FENa is important as it helps in the distinction of pre-renal and intrinsic causes of AKI among patients who have oliguria. If the value is less than 1 percent, a pre-renal cause is assumed while more than 2 infers the presence of an intrinsic cause (Chawla, et al. 2014).
Chawla, L. S., Eggers, P. W., Star, R. A., & Kimmel, P. L. (2014). Acute kidney injury and chronic kidney disease as interconnected syndromes. New England Journal of Medicine371(1), 58-66.
Kellum, J. A., & Lameire, N. (2013). Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Critical care17(1), 204.
Leung, A. K. C., Wong, A. H. C., Leung, A. A. M., & Hon, K. L. (2018). Urinary tract infection in children. Recent patents on inflammation & allergy drug discovery.
Schlager, T. A. (2016). Urinary tract infections in infants and children. Microbiology spectrum4(5).
Stein, R., Dogan, H. S., Hoebeke, P., Kočvara, R., Nijman, R. J., Radmayr, C., & Tekgül, S. (2015). Urinary tract infections in children: EAU/ESPU guidelines. European urology67(3), 546-558.