Acute kidney injury etc... Flashcards
(134 cards)
Renal Function
Normal Renal Function
THE KIDNEY IS NOT JUST A FILTER
REGULATION, REMOVAL, HORMONAL
Anatomy
Kidney
Nephrons
Renal vein & renal artery
Ureters
Bladder
Urethra
Renal Function
Think uric the c or k as in makla and acid as in lemons or oranges
- Fluid balance (absorbs/reabsorbs water)
- BP control (renin
- Acid/base (hydrogen (H+) and bicarbonate (HCO3)
- Electrolyte balance (sodium, potassium, calcium & phosphorus)
- Removal of wastes (urea which is a waste product of proteins, metabolites, toxins, uric acid which is a waste product of food)
- Erythropoietin (promotes the formation of RBCs in the bone marrow)
- Vitamin D (activation)
Nephron Anatomy
Functional Unit
1-2 million in each kidney
Glomerulus within Bowman’s capsule
**Afferent arteriole –caries blood to the glomerulus to get filtered.
**Efferent arteriole – carries blood from the glomerulus
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
Collecting duct
Renal Vasculature
The renal vasculature is responsible for supplying the kidneys with oxygen and nutrients to support their function. The kidneys receive a large percentage of cardiac output, about 20-25%, despite only comprising about 0.5% of the body’s total weight.
Renal blood flow (RBF) is about 1200 mL/min and is maintained by an intricate network of vessels that include the renal artery, interlobar arteries, arcuate arteries, and afferent and efferent arterioles that supply and drain the glomerulus, respectively. Capillaries surround all parts of the nephron, allowing for efficient exchange of solutes and fluids.
The afferent arteriole brings blood to the glomerulus, where it is filtered to form urine. The efferent arteriole then drains the glomerulus and supplies blood to the peritubular capillaries, which surround the renal tubules and allow for reabsorption and secretion of solutes.
Autoregulation of renal blood flow helps maintain a constant flow of blood to the kidneys despite changes in systemic blood pressure. The kidneys can increase or decrease resistance in the afferent and efferent arterioles to maintain perfusion pressure within a certain range. In particular, diastolic perfusion pressure (DPP), mean arterial pressure (MAP), and central venous pressure (CVP) are important parameters for maintaining renal perfusion and preventing acute kidney injury (AKI).
A decrease in DPP has been associated with an increased risk of AKI, while changes in MAP alone may not accurately reflect the risk of renal injury. Therefore, it is important to monitor and maintain adequate perfusion pressure to ensure proper kidney function.
Read slide 7 `
Monitoring Renal Function
Lab values:
Blood Urea Nitrogen (BUN) - BUN is a waste product generated from protein metabolism, which is filtered by the kidneys and excreted in urine. Elevated BUN levels can indicate hepatic or renal impairment, dehydration, high protein diet, infection, steroid use, GI bleed. Decreased BUN levels can indicate malnutrition, fluid volume excess, or severe hepatic damage.
Creatinine (Cr) - Creatinine is a waste product generated from muscle metabolism, which is also filtered by the kidneys and excreted in urine. Elevated creatinine levels can indicate chronic kidney disease (CKD), kidney obstruction, intense exercise, low muscle mass, pregnancy, or certain medications like cimetidine, trimethoprim-sulfamethoxasole (Bactrim), corticosteroids, vitamin D metabolites, salicylates, phenacemide, pyrimethamine. Creatinine levels are slightly higher in males than females due to their higher muscle mass.
BUN/Cr ratio - The BUN/Cr ratio is the ratio of BUN to creatinine levels in the blood. An increased ratio can indicate fluid deficit or hypoperfusion of the kidneys, while a decreased ratio can indicate fluid volume excess or malnutrition.
Glomerular Filtration Rate (GFR) - GFR is a measure of the amount of blood filtered by the kidneys per minute. It is considered the best indicator of renal function and is used to stage CKD. GFR can be estimated using equations based on serum creatinine, age, sex, and race.
Specific Gravity - Specific gravity is a measure of the concentration of solutes in urine, indicating the ability of the kidneys to concentrate urine. Low specific gravity can indicate diabetes insipidus or renal disease, while high specific gravity can indicate dehydration.
Urinalysis - Urinalysis involves a physical and chemical examination of urine, which can provide information about renal function and the presence of various conditions such as urinary tract infections, kidney stones, and proteinuria. The test may include evaluating the appearance, pH, glucose, protein, ketones, bilirubin, urobilinogen, leukocytes, nitrites, and microscopic examination of cells and casts in the urine.
Glomerular Filtration Rate (GFR)
-Normal GFR (glomerular filtration rate) is the amount of blood that is filtered by the glomeruli (tiny blood vessels in the kidneys) per minute. It is typically estimated based on the level of creatinine in the blood, and a GFR of 100-125 ml/min is considered within the normal range for healthy adults.
Creatinine clearance (CrCl) is a measure of how efficiently the kidneys are able to remove creatinine from the blood. It is often used as an estimate of GFR.
As people age, their GFR gradually decreases, typically by around 1 cc/min/year after the age of 40. This can be due to various factors, including changes in blood flow to the kidneys and a reduction in the number of functioning nephrons (the basic filtering units in the kidneys).
If there is an abrupt decrease in GFR, there may be a corresponding increase in creatinine levels in the blood, since the kidneys are less able to clear it from the body. Creatinine is a waste product produced by the muscles that is filtered out of the blood by the kidneys.
In contrast, if the decrease in GFR is gradual, there may be little change in creatinine levels, since the kidneys are able to compensate and maintain relatively stable levels of creatinine clearance.
It is true that around 40% of people with decreased GFR may have a serum creatinine within the normal range, since the kidneys are able to maintain relatively stable creatinine levels even as GFR declines. However, other markers of kidney function may be abnormal in these cases, such as albuminuria (an excess of protein in the urine).
Urinalysis
Color: This refers to the color of the urine, which can vary from pale yellow to dark amber. Urine color can be affected by a variety of factors, including hydration status, diet, medications, and medical conditions.
Clarity: This refers to the transparency of the urine, which can range from clear to cloudy. Cloudy urine may be a sign of infection or the presence of crystals or other particles in the urine.
Sediment: This refers to the solid particles or material that may be present in the urine, such as cells, bacteria, crystals, or mucus. The presence of sediment may indicate an underlying medical condition.
Specific gravity: This measures the concentration of particles in the urine and reflects the kidney’s ability to regulate the water balance in the body. A low specific gravity may indicate kidney dysfunction or overhydration, while a high specific gravity may indicate dehydration or a problem with the kidney’s ability to concentrate urine.
pH: This measures the acidity or alkalinity of the urine. Normal urine pH ranges from 4.5 to 8.0. Abnormal pH levels may be an indicator of certain medical conditions or dietary habits.
Bacteria and leukocytes: These are markers of a possible urinary tract infection or inflammation.
Protein: This measures the amount of protein present in the urine. The presence of protein in the urine may be a sign of kidney damage or other medical conditions.
Ketones: This measures the presence of ketones in the urine, which may be an indicator of diabetes or other metabolic disorders.
Glucose: This measures the amount of glucose present in the urine, which may be an indicator of diabetes or other metabolic disorders.
Nitrites: This measures the presence of nitrites in the urine, which may be a sign of a urinary tract infection.
Bilirubin/urobilinogen: These are markers of liver function and may be elevated in the presence of liver disease or other medical conditions.
Toxins: A urinalysis does not usually include a direct measurement of toxins in the urine. However, some drugs or other substances may be detected in the urine as part of a drug screening or toxicology analysis.
Affects of Aging on the Renal system
Loss of skeletal muscle mass: The loss of muscle mass that occurs with aging is in proportion to the loss of glomerular filtration rate (GFR), so serum creatinine levels don’t change much. This can make it difficult to detect early kidney disease in older adults.
Loss of renal mass: As a person ages, there is a gradual loss of renal mass, which can affect the kidney’s ability to filter and excrete waste products. The reduction in renal mass is most profound in the renal cortex.
Changes in nephrons: The number of nephrons in the kidney decreases with age, which can lead to a decrease in renal function. Additionally, the remaining nephrons may undergo hypertrophy and hyperfiltration, which can lead to glomerular sclerosis.
Changes in hormonal regulation: The renin-angiotensin-aldosterone system (RAAS) becomes less efficient with age, leading to a decrease in renin and aldosterone production. This can affect blood pressure regulation and electrolyte balance.
Changes in bladder function: Aging can also affect bladder function, leading to urinary incontinence, retention, or frequency. In women, cystoceles (prolapse of the bladder into the vagina) may occur due to weakened pelvic muscles. In men, benign prostatic hyperplasia (BPH) can cause urinary retention, but androgen deprivation therapy can slow the progression of chronic kidney disease (CKD) associated with BPH.
Other factors: Other factors that can affect the renal system with aging include decreased cardiac output, hypertension, decreased thirst sensation, and changes in medication metabolism.
Overall, these changes can lead to a decreased ability to regulate fluid and electrolyte balance, excrete waste products, and maintain acid-base balance, which can increase the risk of kidney disease and other health problems in older adults.
Declining Renal Function
Renal function decline is a continuum that can progress from renal insufficiency to acute kidney injury, chronic renal failure, and end-stage renal disease. In renal insufficiency, the kidneys can still function to some degree, but nephrons compensate, and toxins may accumulate, leading to symptoms such as nocturia, polyuria, anorexia, nausea/vomiting, weakness, fatigue, and mild anemia. The BUN rises, and creatinine (Cr) is less than 2, and the glomerular filtration rate (GFR) decreases. Without intervention, renal insufficiency may progress to renal failure.
Acute kidney injury (AKI) is a sudden decline in renal function, often due to a decrease in blood flow to the kidneys or damage to the kidneys themselves. AKI can lead to a sudden rise in BUN and Cr, and a decrease in GFR. It can also cause oliguria (low urine output), volume retention, and hypertension. Treatment for AKI often involves addressing the underlying cause, such as fluid and electrolyte imbalances, and sometimes requires renal replacement therapy.
Chronic renal failure (CRF) occurs when the kidneys can no longer meet the body’s demands for waste removal and fluid and electrolyte balance. In the early stages of CRF, there may be an increase in urine output (polyuria), but the quality of the urine may be poor. As CRF progresses, the BUN increases with Cr greater than 5, and GFR continues to decrease. This can lead to oliguria (low urine output) or anuria (no urine output), volume retention, and hypertension. Other symptoms of CRF can include azotemia (an excess of nitrogenous waste products in the blood), acidosis (a buildup of acid in the body), anemia (a deficiency of red blood cells), and imbalances in electrolytes such as potassium, sodium, and calcium.
End-stage renal disease (ESRD) is the final stage of renal failure, where the kidneys have permanently failed, and dialysis or kidney transplant is necessary to sustain life. In ESRD, there is a severe elevation in BUN and Cr, with a GFR less than 15. There may also be imbalances in electrolytes such as high potassium, sodium, and phosphate levels, and low calcium levels, as well as acidosis. In addition to the renal symptoms, ESRD can cause systemic impairments, such as uremic syndrome, which can affect multiple organ systems in the body.
Kidney Disease Stages
Kidney disease is divided into 5 stages, based on filtration
Manifestations of impaired kidney function are not often seen until GFR is < 50%
Acute Kidney Injury (AKI)
AKI (Acute Kidney Injury) is a sudden and rapid decrease in kidney function, characterized by an abrupt decline in glomerular filtration rate (GFR). The etiology of AKI can be prerenal, intrarenal or postrenal. Prerenal causes include systemic hypoperfusion resulting from conditions such as hypovolemia, hypotension or sepsis. In response to systemic hypoperfusion, the renin-angiotensin-aldosterone system (RAAS), antidiuretic hormone (ADH) and sympathetic nervous system (SNS) are activated to increase vascular tone and reabsorption of sodium and water. However, this time-limited response can result in ischemia and infarction of nephrons if systemic pressures continue to fall. If the decrease in GFR persists, acute tubular necrosis (ATN) may develop.
The most common cause of AKI is prerenal volume depletion from loss of body fluids. Other causes of AKI include acute glomerulonephritis, acute interstitial nephritis, acute tubular necrosis, post-renal obstruction, and drug-induced nephrotoxicity. AKI can progress to chronic kidney disease (CKD) if not managed properly. The mortality rate for AKI with RRT (renal replacement therapy) can be as high as 50%.
AKI
Usually starts by oliguria but now always and marked increase in BUN & Cr and/or azotemia
The term “azotemia” refers to an accumulation of nitrogen-containing waste products in the blood that are normally excreted by the kidneys. In the context of AKI, azotemia is often used as a synonym for an increase in blood urea nitrogen (BUN) levels.
AKI: S & Sx
Increased BUN and Cr: As the kidney function decreases, the BUN and Cr levels in the blood will increase.
Decreased GFR: GFR is a measure of the rate at which blood is filtered by the kidneys. In AKI, the GFR will decrease.
Increased specific gravity or fixed: In AKI, the urine specific gravity may be increased or fixed at 1.010 despite fluid intake. The specific gravity of normal urine ranges from 1.002 to 1.035, with higher values indicating more concentrated urine. A fixed specific gravity of 1.010 despite fluid intake may indicate a problem with the kidneys’ ability to concentrate urine, which can be seen in conditions such as AKI or chronic kidney disease.
Anemia: AKI can cause a decrease in the production of erythropoietin, which can lead to anemia.
HTN and CHF: AKI can lead to the retention of fluid and electrolytes, which can cause hypertension and congestive heart failure.
A,N,V: AKI can cause symptoms of nausea, vomiting, and abdominal pain.
Puritis: AKI can cause itching due to the buildup of uremic toxins in the bloodstream.
AKI Acid-base, fluid & electrolytes, toxins
pH depends on number of functioning nephrons
Metabolic acidosis. it’s called metabolic because the problem is in the kidneys and their lack of production of bicarbonate. It’s not a lungs problem..
pH of the blood becomes more acidic than normal (less than 7.35). The severity of metabolic acidosis depends on the number of functioning nephrons, as the kidneys are responsible for regulating acid-base balance in the body.
Categories of Renal Injury
Prerenal injury:
Prerenal injury is caused by decreased blood flow to the kidneys, which leads to reduced renal perfusion and ischemia. This can happen due to various conditions such as hypovolemia, sepsis, hypotension, heart failure, liver failure, and renal artery stenosis. The decreased blood flow causes a reduction in filtration pressure, because less fluid means less pressure in the hose and eventually, glomerular filtration pressure falls. However, no structural damage to the kidney has yet occurred, and the condition is reversible. If not addressed, prerenal injury can progress to acute kidney injury (AKI). (One of the primary mechanisms is the reduction in effective circulating volume. People with advanced liver disease often have a reduced effective circulating volume due to increased vasodilation, increased capillary permeability, and decreased plasma oncotic pressure. This can lead to a reduction in renal perfusion pressure, which can cause renal vasoconstriction, reduced glomerular filtration rate (GFR), and eventually AKI.)
Intrinsic renal injury:
Intrinsic renal injury, also called intrarenal injury, is caused by problems within the renal tissue itself. This can result from a wide range of conditions such as ischemia, toxins, infections, autoimmune disorders, and genetic disorders. Intrinsic renal injury is categorized based on the primary site of injury, which includes acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vascular damage. ATN, one of the most common causes of intrinsic renal injury, is characterized by the death of renal tubular epithelial cells due to ischemia, toxins, or sepsis. Nephrotoxicity, another cause of intrinsic renal injury, can be caused by medications like aminoglycosides, contrast media, and non-steroidal anti-inflammatory drugs (NSAIDs). Rhabdomyolysis, a condition that occurs when muscle tissue breaks down and releases toxic substances, can also cause intrinsic renal injury. Hepatorenal syndrome, a complication of liver cirrhosis, is another cause of intrinsic renal injury.
Postrenal injury:
Postrenal injury occurs when there is obstruction in the urinary outflow tract, which prevents the urine from leaving the kidneys. This can be caused by mechanical or functional issues, such as tumors, kidney stones, benign prostatic hyperplasia (BPH), and urethral strictures. The obstruction can lead to an increase in pressure within the renal system, causing damage to the kidney’s tissues and impairing renal function. The severity of the injury depends on the duration and degree of obstruction.
It is essential to identify the type of renal injury accurately to initiate appropriate treatment and prevent further damage. Diagnostic tests like urine tests, blood tests, and imaging studies can help identify the underlying cause of renal injury. Treatment may include addressing the underlying cause, providing supportive care, and in severe cases, renal replacement therapy may be needed.
Causes of AKI slide 19
The list you provided outlines various causes and types of acute kidney injury (AKI). Here is a brief explanation of each:
Intrinsic AKI: This refers to damage to the kidney tissue itself, such as the glomeruli, tubules, or interstitium. Causes include ischemia, nephrotoxins (both exogenous and endogenous), infections, and systemic conditions like vasculitis and malignant hypertension.
Prerenal AKI: This is caused by a decrease in blood flow to the kidneys, which can be due to hypovolemia (low blood volume), decreased cardiac output, congestive heart failure, liver failure, or impaired renal autoregulation.
Postrenal AKI: This occurs when there is an obstruction of urine flow out of the kidneys or bladder. Causes include bladder outlet obstruction, bilateral pelvoureteral obstruction, or unilateral obstruction of a solitary functioning kidney.
Some specific examples of AKI causes listed in your statement are:
NSAIDs (nonsteroidal anti-inflammatory drugs) and ACE-I/ARB (angiotensin converting enzyme inhibitors/angiotensin receptor blockers) can cause prerenal AKI by affecting renal blood flow and vasoconstriction.
Cyclosporine, a medication used to prevent transplant rejection, can cause intrinsic AKI by damaging the renal tubules.
Hemolysis (the breakdown of red blood cells), rhabdomyolysis (the breakdown of muscle tissue), and intratubular crystals can all cause intrinsic AKI by obstructing or damaging the renal tubules.
Prerenal Causes of AKI
Prerenal causes of acute kidney injury (AKI) refer to conditions that lead to a decrease in renal blood flow, which subsequently results in a reduction in glomerular filtration rate (GFR) and impaired kidney function. These causes are typically reversible if promptly identified and managed. Common prerenal causes of AKI include:
Reduced effective circulating volume (ECV): This can result from volume depletion due to factors such as dehydration, diuretic use, third-spacing (i.e. fluid accumulation in body cavities or interstitial spaces), blood loss or gastrointestinal losses such as vomiting or diarrhea.
Cardiovascular causes: Conditions that affect cardiac output or blood pressure can lead to prerenal AKI. These may include myocardial infarction (MI), heart failure (HF), cardiac tamponade, tension pneumothorax, cardiac dysrhythmia, valve dysfunction or abdominal aortic aneurysm (AAA).
Shock states and sepsis: In conditions such as sepsis, the body’s inflammatory response can lead to decreased blood flow to the kidneys, resulting in prerenal AKI.
Obstructed renal blood flow: Any condition that obstructs blood flow to the kidneys, such as renal artery stenosis or thrombosis or obstruction of the inferior vena cava, can result in prerenal AKI.
Medications: Certain medications can cause prerenal AKI by affecting blood flow to the kidneys. These may include drugs that lower blood pressure, such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and nonsteroidal anti-inflammatory drugs (NSAIDs).
Causes of Renal Hypoperfusion
When PVR is increased, the resistance to blood flow in the peripheral blood vessels is higher. This means that the heart has to work harder to pump blood through the vessels, and there is a decrease in blood flow to the organs and tissues of the body. This can lead to a decrease in perfusion, which can cause ischemia (a lack of oxygen) in the affected organs and tissues.
In the kidneys, decreased perfusion due to increased PVR can lead to renal hypoperfusion, which can cause kidney damage or failure over time. Conditions that increase PVR, such as sepsis, hepatorenal syndrome, drug overdose, and the use of vasodilators, can all lead to renal hypoperfusion.
Therefore, it is important to identify and treat the underlying cause of increased PVR to prevent damage to the organs and tissues of the body due to decreased perfusion. Treatment may involve medications to reduce PVR (such as vasodilators), or addressing the underlying condition that is causing the increased PVR.
Intrarenal Causes of AKI
Interstitial nephritis: Inflammation of the kidney’s interstitial tissue can cause AKI. Causes of interstitial nephritis include drug reactions (e.g., antibiotics, NSAIDs), infections (e.g., pyelonephritis), and autoimmune diseases (e.g., lupus).
Glomerulonephritis: Inflammation of the glomeruli (the kidney’s filtering units) can cause AKI. Causes of glomerulonephritis include infections (e.g., streptococcal), autoimmune diseases (e.g., lupus), and certain medications.
Vasculitis: Inflammation of the blood vessels in the kidney can cause AKI. Causes of vasculitis include autoimmune diseases (e.g., lupus), infections (e.g., hepatitis B and C), and certain medications.
Nephrotoxins: Certain substances can be toxic to the kidneys and cause AKI. Examples of nephrotoxins include contrast media, heavy metals (e.g., lead), and certain medications (e.g., aminoglycoside antibiotics, nonsteroidal anti-inflammatory drugs, and cimetidine/ranitidine).
Trauma: Physical injury to the kidney can cause AKI. Examples of trauma that can cause AKI include blunt trauma (e.g., from a car accident) and penetrating trauma (e.g., from a gunshot wound).
Acute tubular injury: Injury to the renal tubules can cause AKI. Causes of acute tubular injury include ischemia, nephrotoxins, and infections.
Contrast-Induced Acute Kidney Injury (CI-AKI)Contrast Inducted Nephropathy (CIN)
Contrast-induced acute kidney injury (CI-AKI) and contrast-induced nephropathy (CIN) are both conditions that can occur as a result of exposure to contrast agents used in medical imaging procedures such as CT scans and angiography.
CI-AKI typically occurs 24-48 hours after contrast administration, while CIN has a slower onset, typically taking 3-5 days to develop. CI-AKI is associated with a peak in creatinine levels in 3-4 days and has a mortality rate of around 34%.
There are several strategies that can be used to minimize the risk of CI-AKI/CIN, including pre-contrast prophylaxis, hydration with normal saline, hemofiltration, bicarbonate, and the use of non-ionic, low molecular weight contrast agents. However, patient factors such as hydration and hemodynamic status, underlying kidney disease or compromise, volume of contrast administered, and repeated doses within 48 hours, as well as the use of vasopressors, can also impact the risk of developing CI-AKI/CIN.
N-acetyl cysteine has been studied as a potential prophylactic agent for CI-AKI/CIN, but a 2016 meta-analysis found that oral administration did not offer much benefit. Overall, the prevention of CI-AKI/CIN requires a multifactorial approach that takes into account both patient and procedural factors.
Postrenal Causes of AKI
Stones, clots, hypertrophy (BPH), tumors leading to obstruction and backup or stasis
Bilateral ureteric obstruction (Bilateral ureteric obstruction refers to the blockage or obstruction of both ureters)
Bladder outlet obstruction
Urethral obstruction
Obstruction of a single functioning kidney
When postrenal AKI occurs, urine flow is blocked from both kidneys or from a single functioning kidney, causing urine to back up into the kidneys and damaging them. It’s important to identify and treat the underlying cause of postrenal AKI as soon as possible to prevent permanent damage to the kidneys.
Common Causes of Renal Injury
Prerenal: Excessive fluid loss, Decreased renal perfusion, Increased vascular capacity, Vascular obstruction, Drugs that alter renal hemodynamics
Intrarenal: Ischemia, Nephrotoxicity, Rhabdomylosis, Intratubular obstruction
Postrenal: Mechanical: blood clots calculi, tumors, prostatic hypertrophy, prostate CA, urethral strictures. Functional: Diabetic neuropathy, neurogenic bladder, drugs
Factors Affecting Renal Excretion
Blood flow to the kidneys: The kidneys receive about 20% of the cardiac output, which allows for proper filtration and waste removal. Any conditions that affect blood flow to the kidneys, such as arterial blockages or constriction, can cause renal injury.
Urine flow rate: The rate of urine flow is determined by several factors, including blood pressure, volume status, and hormone levels. A low urine flow rate can be a sign of kidney disease, obstruction, or dehydration.
Urine pH and pKa: Urine pH is a measure of the acidity or alkalinity of urine. The lower the pH, the more acidic the urine. pKa is a measure of the strength of an acid. In the kidneys, urine pH and pKa can affect renal fluid secretion and the formation of kidney stones.((protein kinase-attaches phosphates to proteins))
Physicochemical properties: The physicochemical properties of drugs can impact their absorption, distribution, metabolism, and excretion. These properties can also affect their interactions with the kidneys and their ability to be eliminated from the body.
Distribution and binding: The distribution and binding of drugs within the body can affect their concentration in the kidneys and their ability to interact with renal transporters and enzymes.
Drug interactions: Many drugs can interact with each other and affect their pharmacokinetics and pharmacodynamics. These interactions can also impact renal function and lead to adverse effects.
Biological factors: Biological factors such as age, gender, genetics, and body weight can affect drug metabolism, renal function, and drug interactions.
Disease states: Various disease states such as hypertension, diabetes, and kidney disease can affect renal function and drug metabolism, leading to altered drug effects and interactions.