What’s the prognosis of AkI?
uncomplicated AKI mortality is low, even when RRT is required. In AKI associated with sepsis and multiple organ failure, mortality is 50–70% and the outcome is usually determined by the severity of the underlying disorder and other complications, rather than by kidney injury itself
What’s the pathophysiology of AKI
PRE-RENAL
Impaired perfusion:
• Cardiac failure
• Sepsis
• Blood loss
• Dehydration
• Vascular occlusion
RENAL
Glomerulonephritis
Small-vessel vasculitis
Acute tubular necrosis
• Drugs
• Toxins
• Prolonged hypotension
Interstitial nephritis
• Drugs
• Toxins
• Inflammatory disease
• Infection
POST-RENAL
Urinary calculi (bilateral)
Retroperitoneal fibrosis
Benign prostatic
enlargement
Bladder cancer
Prostate cancer
Cervical cancer
Urethral stricture/valves
Meatal stenosis/phimosis
If the obstruction is not relieved,
the low GFR is maintained by a drop in renal blood flow rate
via
thromboxane A2 and angiotensin II.
What are the
KDIGO (Kidney Disease Improving Global Outcomes) criteria,
AKIN (Acute Kidney Injury Network) criteria,
RIFLE (Risk, Injury, Failure, Loss, End-stage) criteria.
Criteria of categorizing aki?
What are the clinical features of pre renal aki?
- Typical Clinical Presentation:
- Patients with pre-renal AKI often exhibit signs of hypotension (low blood pressure) and tachycardia (fast heart rate).
- There are also signs of poor peripheral perfusion, such as delayed capillary refill time, indicating that blood is not reaching the extremities efficiently.
- Tachycardia and postural hypotension (a drop in blood pressure of more than 20/10 mmHg when moving from lying to standing) are particularly important signs of early hypovolemia (low blood volume).
- Sepsis and Poor Perfusion:
- In cases of sepsis, patients may initially present with signs of poor peripheral perfusion, similar to hypovolemia.
- After resuscitation with intravenous fluids, these patients often develop peripheral vasodilation (widening of blood vessels), which can mask the true volume status.
- However, despite the vasodilation, the arterial system remains underfilled, and the kidneys respond by initiating renal vasoconstriction, behaving as if there were absolute hypovolemia.
Can Pre-renal AKI occur without Hypotension:
3.
- Interestingly, pre-renal AKI can occur without systemic hypotension, particularly in patients taking NSAIDs (non-steroidal anti-inflammatory drugs) or ACE inhibitors (angiotensin-converting enzyme inhibitors). These drugs interfere with the kidney’s ability to maintain adequate blood flow, even in the absence of obvious low blood pressure.
- Causes of Hypotension:
- The cause of hypotension is often easy to identify (e.g., dehydration, bleeding, sepsis), but sometimes, concealed blood loss may occur in less obvious places:
- Gastrointestinal tract (e.g., internal bleeding),
- Retroperitoneum (e.g., behind the abdominal cavity),
- Following trauma (e.g., fractures of the pelvis or femur),
- Pregnant uterus.
- Additionally, large volumes of fluid can be lost into tissues due to crush injuries, burns, severe inflammatory skin conditions, or sepsis.
- The cause of hypotension is often easy to identify (e.g., dehydration, bleeding, sepsis), but sometimes, concealed blood loss may occur in less obvious places:
- Progression to Acute Tubular Necrosis (ATN):
- If pre-renal AKI is not corrected (i.e., blood flow to the kidneys remains compromised), it can lead to acute tubular necrosis (ATN). ATN is a more severe form of kidney injury where the kidney’s tubular cells suffer damage due to prolonged hypoperfusion, potentially leading to longer-term renal failure.
Renal AKI:
- Glomerulonephritis:
Patients with glomerulonephritis typically present with hematuria (blood in the urine) and proteinuria (protein in the urine).
They may also show clinical signs of an underlying systemic disease, such as Systemic Lupus Erythematosus (SLE) or systemic vasculitis.
Diagnosis of glomerulonephritis requires blood tests (e.g., immunological screening), but a renal biopsy is often necessary to confirm the diagnosis and understand the extent of the kidney damage.
Drug-Induced Acute Interstitial Nephritis:
This is more difficult to diagnose because the signs may not be immediately obvious.
Acute interstitial nephritis (AIN) should be suspected in a patient who was previously healthy but experiences an acute deterioration in renal function shortly after starting a new drug.
Common culprits include:
Proton Pump Inhibitors (PPIs),
NSAIDs (Non-Steroida Anti-Inflammatory Drugs),
Antibiotics.**
Post-Renal AKI:
Post-renal AKI is caused by obstruction to the flow of urine, which can occur at any point from the renal pelvis to the urethra.
Examination for Obstruction:
A clinical examination should be performed to assess for signs such as a distended bladder, which could indicate obstruction.
Imaging, particularly ultrasound, is critical for detecting obstructions above the level of the bladder. Ultrasound can reveal hydronephrosis (swelling of the kidney due to urine build-up), which is a hallmark of urinary obstruction.
How do you Manage AKI
The management of AKI (Acute Kidney Injury) involves addressing multiple critical aspects to prevent further complications. Here’s a breakdown of the key management steps:
- Correction of Hypovolemia:
- If the patient has hypovolemia (low blood volume), intravenous fluids or blood transfusions should be used to restore the volume.
- Avoid over-administration of fluids, as this can lead to pulmonary edema, worsening the patient’s condition.
- Monitoring central venous pressure (CVP) can help determine how fast and how much fluid should be given.
- Use balanced crystalloid solutions like Plasma-Lyte, Hartmann’s, or Ringer’s lactate when large amounts of fluids are needed to prevent hyperchloremic acidosis (an increase in chloride levels that may lead to acidosis).
- Avoid hydroxyethyl starch solutions, as they are linked to higher rates of established AKI.
- Critically ill patients may need inotropic drugs to maintain effective blood pressure, but there is no specific benefit of using low-dose dopamine for AKI.
- Hyperkalemia (high potassium levels) is common, particularly in conditions like rhabdomyolysis, burns, hemolysis, or metabolic acidosis.
- If potassium levels exceed 6.5 mmol/L, immediate treatment is essential to prevent cardiac arrhythmias, which could be life-threatening (as outlined in Box 14.17).
- Metabolic Acidosis:
- Acidosis may occur when the kidneys cannot remove acid or if the patient has lost hydrogen ions through vomiting.
- Severe acidosis can be managed with sodium bicarbonate, but only if the patient’s blood volume is stable.
- Correcting the blood volume will often reverse acidosis by restoring kidney function.
- If acidosis is severe, isotonic sodium bicarbonate infusions can also help treat hyperkalemia and prevent dangerous potassium levels from rising further.
- Pulmonary Edema:
- This can result from giving too much fluid relative to the patient’s urine output or due to increased pulmonary capillary permeability.
- If pulmonary edema is present and urine output cannot be increased, dialysis may be needed to remove the excess fluid.
- In some cases, temporary respiratory support using non-invasive ventilation may be necessary.
- After the initial resuscitation, the patient’s fluid intake should be adjusted to match their urine output plus 500 mL/day to account for insensible fluid loss (from breathing, sweating, etc.).
- If the patient has diarrhea, more fluid may need to be added to compensate for the extra loss.
These management strategies focus on stabilizing the patient’s overall status, correcting electrolyte imbalances, and preventing further complications like pulmonary edema or life-threatening arrhythmias.
The management of electrolyte disturbances and other complications in AKI (Acute Kidney Injury) is critical for patient recovery. Here’s a detailed explanation of each component:
- Dilutional Hyponatremia: This condition can occur when patients continue to drink fluids despite having reduced urine output (oliguria) or if they receive excessive amounts of intravenous fluids like dextrose. This can dilute the sodium levels in the blood.
- Prevention: It is essential to monitor the patient’s fluid balance carefully and administer intravenous fluids at a slow rate to avoid fluid overload.
- Hypocalcemia: Mild hypocalcemia (low calcium levels) is common in AKI, but it usually does not require treatment unless it becomes severe.
- Hyperphosphatemia: Elevated serum phosphate levels are typical in AKI but may drop during renal replacement therapy (RRT), such as continuous renal replacement therapy (CRRT). In such cases, phosphate replacement may be necessary to maintain balance.
- Nutritional support is crucial, especially in patients with conditions like sepsis or burns, where the body breaks down more proteins and energy (hypercatabolic state).
- A proper balance of calories and moderate protein intake should be ensured.
- Enteral or parenteral nutrition (feeding via the gastrointestinal tract or intravenously) may be required if oral intake is insufficient.
- AKI patients are prone to infections because their humoral and cellular immune responses are weakened. Regular clinical examinations and, when necessary, microbiological investigations are important to detect infections early.
- If infection is detected, it should be treated promptly according to the standard principles of infection management.
- Drug-induced AKI: If a drug is suspected to be causing AKI, it should be discontinued immediately.
- Vasoactive medications, such as NSAIDs and ACE inhibitors, should also be stopped as they may prolong the duration of AKI.
- H2-receptor antagonists or proton pump inhibitors (PPIs) are often prescribed to prevent gastrointestinal bleeding.
- All medications should be reviewed and adjusted based on the patient’s kidney function, with unnecessary drugs discontinued to avoid further kidney strain.
- In post-renal AKI, prompt relief of the obstruction is crucial. This may involve:
- Urinary catheterization to relieve bladder outflow obstruction.
- Ureteric stent or percutaneous nephrostomy to relieve ureteric obstructions.
- Conservative management involving careful attention to fluid balance, electrolyte levels, and nutrition can often manage AKI successfully. However, some patients may require RRT if their condition doesn’t improve.
- No specific cut-off for serum urea or creatinine levels necessitates the start of RRT. The decision is based on the patient’s overall condition, including the risk of uremic complications (such as pericarditis or encephalopathy), and the patient’s response to treatment.
- Two main options for RRT are:
- Intermittent hemodialysis: Conducted in intervals, where blood is filtered through a machine.
- Continuous renal replacement therapy (CRRT): A continuous form of dialysis, often used in critically ill patients.
- Peritoneal dialysis: This may be an alternative if hemodialysis is unavailable.
- Recovery from AKI typically occurs once the underlying cause is resolved, although it may be slower in patients with pre-existing Chronic Kidney Disease (CKD) or after severe or prolonged insults.
- Signs of Recovery:
- A gradual increase in urine output.
- Improvement in plasma biochemical markers (like creatinine and urea).
- Often, there is a diuretic phase, where urine output becomes excessive for a few days before normalizing. This occurs due to:
- Damage to the kidney tubules.
- Loss of the kidney’s ability to concentrate urine temporarily.
- As the kidneys recover, urine output gradually decreases back to normal levels, and the tubular function is restored.
- During recovery, temporary supplementation of electrolytes like bicarbonate, potassium, calcium, phosphate, and magnesium may be necessary to maintain balance.
By managing these different aspects—electrolyte disturbances, nutritional needs, infections, medication adjustments, and, if necessary, initiating renal replacement therapy—AKI can often be controlled effectively. However, the recovery process may vary depending on the severity and duration of the underlying causes.
Acute kidney injury (AKI) in the elderly presents unique challenges due to age-related physiological changes and the higher likelihood of comorbid conditions. Here’s a breakdown of both the impact of aging on AKI and the general management strategies:
- Physiological Changes:
- Nephron Decline & Reduced GFR: As people age, the number of functional nephrons (the kidney’s filtering units) decreases, leading to a gradual decline in glomerular filtration rate (GFR). Elderly patients often have established Chronic Kidney Disease (CKD), meaning that even small changes in renal function can have a significant impact.
- Clinical Implication: Older adults have less functional reserve, so mild AKI may manifest more severely than in younger patients.
- Nephron Decline & Reduced GFR: As people age, the number of functional nephrons (the kidney’s filtering units) decreases, leading to a gradual decline in glomerular filtration rate (GFR). Elderly patients often have established Chronic Kidney Disease (CKD), meaning that even small changes in renal function can have a significant impact.
- Serum Creatinine:
- With aging, muscle mass decreases, leading to reduced creatinine production. Since serum creatinine depends on muscle mass, lower levels may give a false impression of normal kidney function.
- Clinical Implication: Serum creatinine can be misleading in the elderly, and alternative assessments (like GFR estimations) should be considered for better evaluation of kidney function.
- With aging, muscle mass decreases, leading to reduced creatinine production. Since serum creatinine depends on muscle mass, lower levels may give a false impression of normal kidney function.
- Renal Tubular Function:
- Aging also affects the renal tubules, reducing the kidneys’ ability to concentrate urine.
- Clinical Implication: Elderly patients may struggle with maintaining fluid and electrolyte balance, increasing the risk of dehydration or overhydration.
- Aging also affects the renal tubules, reducing the kidneys’ ability to concentrate urine.
- Drug-Related Risks:
- Older adults often have higher rates of drug prescriptions, including diuretics, ACE inhibitors, and NSAIDs, which can increase the risk of AKI by impacting renal perfusion or causing direct nephrotoxicity.
- Clinical Implication: Careful monitoring of drug use and doses is essential to avoid exacerbating renal injury.
- Older adults often have higher rates of drug prescriptions, including diuretics, ACE inhibitors, and NSAIDs, which can increase the risk of AKI by impacting renal perfusion or causing direct nephrotoxicity.
- Common Causes of AKI in the Elderly:
- Factors like infection, renal vascular disease, prostatic obstruction, hypovolemia, and severe cardiac dysfunction are frequent contributors to AKI in this age group.
- Mortality:
- Mortality rates rise with age, mainly because elderly patients often have multiple comorbid conditions (e.g., heart disease, diabetes), making recovery from AKI more difficult.
The management of AKI involves assessing and addressing fluid balance, electrolyte disturbances, medication review, and managing complications. Here are key management steps:
- Fluid Status Assessment:
- Hypovolemic patients: If the patient is dehydrated or hypovolemic, focus on restoring fluid balance by administering intravenous fluids or using inotropic drugs if needed. This helps optimize blood flow to the kidneys.
- Euvolemic patients: Once the patient achieves normal fluid balance (euvolemia), fluid intake should be matched to urine output plus an additional 500 mL/day to account for insensible fluid losses (e.g., sweating, breathing).
- Fluid-overloaded patients: If there is excess fluid, high doses of loop diuretics (e.g., furosemide) may be required. If diuretics are ineffective, dialysis may be necessary to remove excess fluid.
- Hyperkalaemia Management:
- Hyperkalaemia (elevated potassium levels) is a life-threatening complication of AKI. When serum potassium exceeds 6.5 mmol/L, treatment should be initiated immediately.
- Calcium Resonium: Given to stabilize the myocardium.
- Glucose and Insulin: Administered to shift potassium into cells temporarily, buying time until the underlying cause is corrected (either through dialysis or recovery of renal function).
- Hyperkalaemia (elevated potassium levels) is a life-threatening complication of AKI. When serum potassium exceeds 6.5 mmol/L, treatment should be initiated immediately.
- Acidosis Management:
- If the patient has severe metabolic acidosis (H+ concentration > 100 nmol/L or pH < 7.0), sodium bicarbonate (100 mmol) may be administered to correct the acidosis.
- Clinical Caution: Sodium bicarbonate should only be used if acidosis is severe and may not be appropriate in all patients, as overcorrection can lead to complications.
- If the patient has severe metabolic acidosis (H+ concentration > 100 nmol/L or pH < 7.0), sodium bicarbonate (100 mmol) may be administered to correct the acidosis.
- Medications:
- Discontinue nephrotoxic drugs: Any medications that could worsen kidney function, such as NSAIDs or certain antibiotics, should be stopped.
- Dose adjustments: For necessary medications, their dosages should be adjusted based on the patient’s current level of kidney function.
- Nutritional Support:
- Ensure the patient receives adequate nutrition, balancing energy needs while avoiding excessive protein intake, which could further stress the kidneys.
- Preventing Gastrointestinal Complications:
- Consider prescribing proton pump inhibitors (PPIs) to reduce the risk of upper gastrointestinal bleeding, which can occur in critically ill patients, especially those with kidney injury.
- Infection Screening:
- Regularly screen for and treat infections, as AKI patients are at increased risk of infections due to weakened immune function. Quick identification and treatment of infections are critical to prevent worsening kidney function.
- Urinary Tract Obstruction:
- If the AKI is caused by a urinary tract obstruction, such as an enlarged prostate or blockage of the ureters, the obstruction should be relieved promptly.
- Management Options: This may involve urinary catheterization for bladder outlet obstruction or insertion of a ureteric stent or percutaneous nephrostomy to relieve ureteric obstructions.
- If the AKI is caused by a urinary tract obstruction, such as an enlarged prostate or blockage of the ureters, the obstruction should be relieved promptly.
In conclusion, managing AKI, particularly in older patients, requires careful attention to fluid balance, medication management, and preventing complications like hyperkalaemia and acidosis. Each patient’s treatment should be individualized based on their clinical status and the underlying cause of AKI.
Describe the pathophysiology of pre-renal, renal, and post-renal causes of acute kidney injury (AKI).
Pre-renal AKI is caused by reduced renal perfusion without direct damage to the kidneys. The kidneys receive inadequate blood flow, leading to a decreased glomerular filtration rate (GFR). Common causes include hypovolaemia (e.g., from dehydration or blood loss), decreased cardiac output (e.g., in heart failure), and systemic vasodilation (e.g., in sepsis). The kidneys respond by reabsorbing sodium and water to preserve volume, leading to concentrated urine with low sodium. If untreated, prolonged pre-renal AKI can lead to ischemic injury and progress to intrinsic AKI.
Renal (intrinsic) AKI involves direct damage to the kidney tissue itself, most commonly due to acute tubular necrosis (ATN). This can be caused by ischemia (prolonged pre-renal state), toxins (e.g., nephrotoxic drugs, contrast agents), or inflammatory processes (e.g., glomerulonephritis or interstitial nephritis). Tubular cells die, slough off, and obstruct the renal tubules, reducing GFR. Renal causes also include glomerular diseases (e.g., lupus nephritis) and vascular disorders (e.g., thrombotic microangiopathy). The urine in renal AKI often has cellular debris and a high sodium concentration.
Post-renal AKI occurs due to obstruction of urine flow at any level from the renal pelvis to the urethra. Causes include ureteric stones, benign prostatic hyperplasia, or tumours compressing the urinary tract. The obstruction increases hydrostatic pressure in the urinary system, impairing glomerular filtration. If left untreated, backpressure can lead to hydronephrosis and permanent kidney damage. Relief of the obstruction can quickly restore renal function if addressed early.
A 68-year-old man presents with hypotension, tachycardia, and signs of hypovolaemia after a traumatic injury. He subsequently develops oliguria. Discuss the clinical assessment and management of pre-renal AKI in this patient.
In pre-renal AKI, the first step is to assess the patient’s fluid status. Clinical signs of hypovolaemia include dry mucous membranes, decreased skin turgor, hypotension, tachycardia, and reduced urine output (oliguria). Blood urea nitrogen (BUN) and serum creatinine are elevated, and the BUN/creatinine ratio may be high (>20:1), which is typical of pre-renal causes. Urinalysis shows concentrated urine with a low sodium concentration (<20 mEq/L).
Management involves rapid restoration of intravascular volume. Isotonic crystalloids like normal saline or balanced solutions like Hartmann’s solution are used. Blood products may be required if there’s significant haemorrhage. Central venous pressure (CVP) monitoring may guide fluid resuscitation in critically ill patients to prevent fluid overload. It is important to correct hypovolaemia promptly to prevent progression to ischemic injury and ATN.
Monitoring urine output is crucial, and if oliguria persists despite adequate fluid resuscitation, other causes of AKI, such as intrinsic or post-renal, should be considered. Care should be taken to avoid fluid overload, as it can lead to pulmonary oedema, especially in elderly or heart failure patients.
Discuss the role of electrolyte disturbances, particularly hyperkalaemia and acidosis, in the management of acute kidney injury.
In AKI, impaired kidney function leads to the accumulation of waste products and electrolytes, causing serious disturbances. Hyperkalaemia is one of the most life-threatening electrolyte imbalances. It occurs because the kidneys fail to excrete potassium. When serum potassium exceeds 6.5 mmol/L, it can result in life-threatening cardiac arrhythmias, such as ventricular fibrillation. Hyperkalaemia is managed emergently by administering calcium gluconate to stabilize the myocardium, insulin and glucose to shift potassium into cells, and other medications like sodium bicarbonate if acidosis is present.
Metabolic acidosis develops because the kidneys cannot excrete hydrogen ions or produce bicarbonate, especially in conditions like rhabdomyolysis or severe sepsis. Severe acidosis (pH < 7.0) can cause arrhythmias, hypotension, and impaired oxygen delivery. Sodium bicarbonate can be given in severe acidosis to buffer the excess hydrogen ions, but this is typically a temporary measure until kidney function recovers or dialysis is initiated.
Early recognition and management of these electrolyte disturbances are essential in preventing fatal complications, especially while awaiting definitive treatment like renal replacement therapy (RRT).
Critically evaluate the use of renal replacement therapy (RRT) in the management of AKI.
Renal replacement therapy (RRT) is indicated in AKI when conservative management (fluid balance, electrolyte correction) fails or if the patient has life-threatening complications. Indications for RRT include severe hyperkalaemia, metabolic acidosis, fluid overload unresponsive to diuretics, and uremic complications like pericarditis or encephalopathy.
There are several modalities of RRT:
- Intermittent haemodialysis (IHD): performed 3–4 times weekly, it allows rapid removal of waste products and excess fluid but can cause haemodynamic instability.
- Continuous renal replacement therapy (CRRT): typically used in critically ill, haemodynamically unstable patients, CRRT allows for slower, continuous removal of fluids and solutes, reducing the risk of hypotension. However, it requires prolonged vascular access, which can increase the risk of infection.
- Peritoneal dialysis (PD): an option when haemodialysis is unavailable. PD is less commonly used in AKI due to its slower solute clearance.
RRT is not without risks. Placement of central venous catheters for dialysis access increases the risk of infection, and aggressive ultrafiltration may cause hypotension in unstable patients. Therefore, the decision to start RRT should be individualized, weighing the potential risks and benefits, especially in patients with multiple comorbidities.
Explain the management of AKI in elderly patients, with a focus on physiological changes that occur with aging and how these influence both the development of AKI and its treatment.
In elderly patients, the kidney’s structural and functional reserve diminishes with age. There is a natural decline in the number of functioning nephrons, resulting in a lower baseline glomerular filtration rate (GFR). As a result, even small reductions in renal perfusion can cause significant decreases in kidney function. Additionally, the elderly have reduced renal tubular function, limiting their ability to concentrate urine, which predisposes them to dehydration and electrolyte imbalances.
Elderly patients often have multiple comorbidities, such as diabetes, hypertension, and heart failure, which increase the risk of AKI. The use of medications like NSAIDs, ACE inhibitors, and diuretics also heightens this risk, as these drugs impair renal autoregulation or promote volume depletion.
Management involves careful attention to fluid balance. Volume status must be optimized, but fluid overload should be avoided, as elderly patients are more prone to develop pulmonary oedema. Drug dosing must be adjusted according to renal function, and nephrotoxic drugs should be avoided or discontinued. In elderly patients with severe or prolonged AKI, conservative management may be insufficient, and RRT may be required. However, frailty and comorbidities must be considered when deciding on the aggressiveness of treatment.
Describe the approach to managing a patient with AKI secondary to rhabdomyolysis.
Rhabdomyolysis results from the breakdown of muscle tissue, releasing myoglobin, potassium, and phosphate into the bloodstream, which can overwhelm the kidneys and cause AKI. The key factor is the accumulation of myoglobin in the renal tubules, leading to obstruction and direct toxicity to tubular cells.
Management begins with aggressive fluid resuscitation to maintain urine output and dilute myoglobin concentrations in the kidneys. Intravenous isotonic fluids (normal saline) are preferred. The goal is to achieve a urine output of at least 200-300 mL/hour. Sodium bicarbonate may be added to alkalinize the urine, preventing myoglobin precipitation in the tubules, though its benefit is debated.
Hyperkalaemia, common in rhabdomyolysis, must be monitored and treated, as it can lead to cardiac arrhythmias. Calcium gluconate, insulin with glucose, and potassium binders can be used to manage severe hyperkalaemia.
Dialysis may be required if there is severe hyperkalaemia or metabolic acidosis unresponsive to medical therapy, or if fluid overload occurs. Early recognition and prompt treatment are critical to preventing further renal damage in rhabdomyolysis-induced AKI.
List three common causes of post-renal acute kidney injury.
Answer:
1. Ureteric stones
2. Benign prostatic hyperplasia (BPH)
3. Tumours compressing the urinary tract (e.g., pelvic or abdominal malignancies causing obstruction).
What is the role of diuretics in managing fluid overload in AKI, and when might dialysis be required?
Answer:
Diuretics, particularly loop diuretics like furosemide, are used to manage fluid overload in AKI by promoting diuresis. However, if the response to diuretics is unsatisfactory or the fluid overload is severe, dialysis may be required to remove excess fluid and prevent complications like pulmonary oedema.
Why is serum creatinine an unreliable marker of renal function in elderly patients?
Answer:
In elderly patients, serum creatinine is unreliable because muscle mass decreases with age, resulting in lower creatinine production. This can lead to deceptively normal or low serum creatinine levels despite significant declines in kidney function, making creatinine a poor indicator of actual GFR.
What is the significance of hyperkalaemia in AKI, and how is it managed?
Answer:
Hyperkalaemia, often seen in AKI, is significant because it can lead to life-threatening cardiac arrhythmias, such as ventricular fibrillation. It is managed by administering calcium gluconate to stabilize the myocardium, insulin with glucose to shift potassium into cells, and sodium bicarbonate if metabolic acidosis is present. Definitive treatment may involve dialysis to remove excess potassium.
What is the most common cause of pre-renal acute kidney injury, and how does it lead to AKI?
Answer:
The most common cause of pre-renal AKI is hypovolaemia (e.g., from dehydration, blood loss, or excessive diuresis). Hypovolaemia leads to reduced renal perfusion, resulting in decreased glomerular filtration rate (GFR) and impaired kidney function. If not corrected, pre-renal AKI can progress to ischemic injury and intrinsic AKI (acute tubular necrosis).
