CLÍNICA 2 UNIDAD TRES 17MA CLASE INJURIA RENAL AGUDA JUEVES 22 MAYO
Understanding Acute Kidney Injury
Definition and Historical Context
The term "acute kidney injury" (AKI) has evolved since its introduction around 1820, initially referred to as acute renal failure, which focused on direct damage to the renal parenchyma.
In the early 2000s, the terminology shifted to "acute kidney injury," expanding the definition to include clinical characteristics and prior health status of patients, not just renal damage.
Recent Developments in Terminology
A 2024 editorial letter highlighted ongoing confusion regarding AKI definitions among authors, emphasizing that over 30 definitions have existed for this condition.
The distinction between "acute renal failure" and "acute kidney injury" is crucial; acute renal failure implies a progression from an initial injury to stage three AKI due to inadequate treatment.
Clarifying Terminology
The term "renal failure" is considered erroneous when used synonymously with acute kidney injury; it suggests a more severe progression of the condition.
Four key terms are identified: acute renal failure, acute kidney injury, and their synonymous term “renal lesion,” each with distinct implications for patient care.
Current Understanding of Acute Kidney Injury
A recent article from January 2025 defines AKI as a multifactorial condition leading to deteriorating renal function within hours or days, affecting 10%–15% of hospitalized patients and up to 50% in intensive care units (ICUs).
Risk Factors in Hospitalized Patients
Increased incidence of AKI in ICU patients is attributed to high medication demands due to intubation and multiple infusions, alongside potential nephrotoxic effects from sedatives and muscle relaxants.
Nutritional Support and Acute Kidney Injury
Nutritional Challenges in Patient Care
The speaker discusses the inadequacy of nutritional support provided to patients, emphasizing that simply giving a small amount of milk is insufficient for proper nourishment.
It is noted that irony exists in healthcare settings where monitoring should be higher, yet acute kidney injury (AKI) rates are significant, with complications leading to increased mortality.
Complications Associated with Acute Kidney Injury
Mortality related to AKI is primarily due to complications such as uremic encephalopathy and gastrointestinal hemorrhage rather than the injury itself.
Patients with pre-existing cardiovascular conditions like heart failure or myocardial infarction face even higher mortality risks when experiencing AKI.
Epidemiology of Acute Kidney Injury
Sources of Acute Kidney Injury
A graph presented shows that hospital-acquired AKI is prevalent, particularly in Latin America (45% hospital-acquired vs. 55% community-acquired).
In contrast, North America has a higher percentage of hospital-acquired cases (64%) compared to community cases (36%), while Africa shows a stark difference with only 15% being hospital-acquired.
Geographic Influence on Prevalence
The prevalence of AKI varies significantly based on geographic location and access to clean water, highlighting environmental factors' role in patient health outcomes.
Factors Contributing to Acute Kidney Injury
Identifying Key Risk Factors
Various factors contributing to AKI include cardiac surgery, shock, sepsis, and exposure to toxins or drugs; these are critical for understanding patient risk profiles.
Among these factors, drugs are identified as the most frequent cause of AKI due to their widespread impact on renal function.
Surgical Risks and Sepsis
Cardiac surgeries have a notable association with AKI (18.7%), while sepsis remains the leading factor at nearly 50%, underscoring its significance in clinical practice.
Pathophysiology of Acute Kidney Injury
Understanding Dysfunction vs. Damage
The speaker emphasizes two key terms: dysfunction and damage regarding kidney physiology; both play crucial roles in understanding AKI's pathophysiology.
Physiological and Pathological Influences
Factors affecting kidney function include age-related decline and physiological changes during pregnancy; pathological influences involve conditions like nephropathy and heart failure.
Structural Alterations Impacting Function
Understanding Renal Dysfunction and Structural Damage
Factors Affecting Renal Function
The discussion begins with the impact of physiological and pathological factors such as ischemia, hypoxia, toxins, and molecular modifiers on renal function.
It is noted that chronic kidney disease (CKD) results in smaller kidneys, while acute kidney injury (AKI) leads to hypertrophic kidneys that appear larger due to structural changes.
Understanding Renal Dysfunction
A graphical representation illustrates healthy nephrons versus those affected by dysfunction. Healthy nephrons are clean and undamaged.
An anecdote describes a student experiencing severe gastrointestinal symptoms after eating out, leading to concerns about renal health despite normal urination.
Functional Reserve of the Kidney
Despite ongoing issues like diarrhea and vomiting for several days, the student's creatinine levels remain normal due to renal functional reserve (RFR), which allows compensation for nephron damage.
The speaker emphasizes that while RFR can maintain stable renal function temporarily, it has limits beyond which kidney function will decline.
Critical Threshold of Nephron Loss
The relationship between glomerular filtration rate (GFR), creatinine levels, and nephron loss is discussed. GFR remains above 60 until more than 50% of nephrons are affected.
Once over 50% of nephrons are compromised, both GFR drops sharply and creatinine levels rise significantly.
Mechanisms of Structural Damage
Transitioning from dysfunction to structural damage involves stressors affecting the renal glomerulus.
The glomerulus employs compensatory mechanisms in response to damage but may lead to hyperfiltration as a maladaptive response.
Hyperfiltration Explained
Hyperfiltration occurs when the glomerulus attempts to compensate for damage by constricting afferent arterioles to filter more effectively.
Understanding Renal Injury and Disease
Mechanisms of Renal Injury
The discussion begins with the concept of hyperfiltration in renal function, indicating that a kidney functioning well (with a filtration rate over 60) may still be compensating for underlying issues.
Diabetic kidney disease is highlighted as a condition where microalbuminuria serves as an early marker of hyperfiltration, suggesting impending renal damage.
As injury progresses, podocytes are affected leading to endothelial compromise and decreased glomerular filtration rate (GFR), indicating worsening renal function.
Tubular cells also begin to suffer damage, particularly in the proximal tubule where significant electrolyte reabsorption occurs; this can lead to imbalances such as hypokalemia and hyponatremia.
Persistent damage results in maladaptive repair mechanisms, leading to sclerosis and fibrosis—irreversible changes that progress towards chronic kidney disease.
Criteria for Acute Kidney Injury
The NKDI criteria define stages of acute kidney injury: stable creatinine levels indicate no renal disease; however, exposure to nephrotoxins can lead to acute injury within days.
Acute kidney injury is classified based on duration: less than 7 days indicates acute injury; more than 7 days but less than 3 months suggests acute renal disease; beyond 3 months indicates chronic kidney disease.
Stage one involves a creatinine increase of 1.5–1.9 times baseline or urine output below 0.3 ml/kg over 48 hours; stage two shows higher increases with lower urine output over longer periods.
Stage three signifies severe impairment with creatinine rising above three times baseline or significant reductions in urine output, potentially requiring renal replacement therapy.
Evolution of Renal Conditions
A graphical representation illustrates how normal kidneys can transition into acute injuries or diseases while chronic conditions may also experience acute episodes—clarifying terminology around "chronic kidney disease exacerbation."
It emphasizes that terms like "chronic kidney disease reactivated" are incorrect; the proper term is "chronic kidney disease plus acute injury," highlighting the complexity of these conditions.
Recovery from Acute Kidney Injury
The trajectory of recovery from acute injuries is discussed through various scenarios: rapid recovery after an insult indicates transient injury versus prolonged dysfunction leading to permanent damage.
Understanding Acute Kidney Injury Through Graphical Representation
Analysis of Different Lines Representing Kidney Function
The line B shows a gradual decline in kidney function, indicating a transient acute kidney injury with slow recovery that approaches baseline levels.
Line C depicts a sharp drop in function, representing severe but transient acute kidney injury; it recovers partially but does not return to baseline.
Line D indicates persistent acute kidney injury, characterized by a failure to recover below baseline levels for over 48 hours.
Line E also represents persistent injury without recovery, while line F signifies patients requiring renal replacement therapy due to drastic declines in function.
The key takeaway is that all forms of acute kidney injury are potentially recoverable, although some may lead to chronic conditions or require dialysis.
Understanding Renal Health and Damage Progression
Four types of kidneys are discussed: healthy (filtration >90), susceptible (reduced functional reserve), structurally damaged (good filtration but structural issues), and chronic (severe damage).
All four types can experience an acute kidney injury; the extent of recovery varies based on initial health status and functional reserve.
Complete recovery is possible for those with normal or slightly reduced functional reserves; partial recovery occurs more frequently in those with significant pre-existing damage.
Patients with structural damage are at higher risk for progressing to chronic kidney disease after an acute event compared to healthier individuals.
Key Components of Acute Kidney Injury Diagnosis
Acute kidney injury assessment relies on two main factors: creatinine levels and urine output; elevated creatinine alone does not confirm the diagnosis.
Creatinine production originates from liver metabolism involving arginine and glycine; understanding its production helps clarify diagnostic challenges.
Factors Influencing Creatinine Levels
Various factors can alter creatinine production or excretion rates, complicating diagnoses.
Medications like trimethoprim can interfere with tubular secretion, leading to misleadingly high creatinine readings without actual renal damage.
Conditions such as chronic liver disease reduce creatinine production, which may mask underlying renal issues during evaluation.
Understanding Renal Injury and Its Causes
Importance of Diuresis in Assessing Renal Function
In chronic liver disease patients, creatinine levels are less reliable; diuresis is a more critical measure for renal function.
Various conditions like obesity and pregnancy can affect fluid retention and overload, impacting both creatinine and diuresis.
Types of Renal Injury
There are three main types of renal injury: prerenal, intrinsic, and postrenal.
Prerenal injuries occur at the level of the afferent arteriole.
Intrinsic injuries affect the glomerulus.
Postrenal injuries arise from retrograde effects starting from the arterioles.
Intrinsic Renal Injuries
Intrinsic injuries can be categorized into glomerular, tubular, interstitial, and vascular types. Tubular injuries are most common (90%).
Ischemic causes are frequently responsible for tubular injuries.
Common Causes of Prerenal Injury
Sepsis is a leading cause of prerenal injury; other factors include hypovolemia due to hemorrhage, burns, vomiting, diarrhea, or poor oral intake.
Certain medications (e.g., NSAIDs, ACE inhibitors) can also contribute to prerenal injury.
Contrast-Induced Nephropathy
Contrast agents used in imaging studies have been shown not to significantly increase the risk of acute kidney injury in healthy individuals.
However, patients with comorbidities such as hypertension or diabetes may be at higher risk for contrast-induced nephropathy.
Prevention Strategies
For patients with susceptible kidneys undergoing procedures involving contrast agents:
Hydration with sodium chloride (1 to 1.5 ml/kg/hour for 6 to 12 hours before and after).
Discontinuation of certain medications prior to the procedure is advised.
Intrinsic Causes of Renal Injury
Various intrinsic causes include thrombotic microangiopathy and renal artery stenosis; however, nephrotoxic drugs like antibiotics pose significant risks.
Antibiotic-Induced Kidney Damage
The discussion emphasizes monitoring antibiotic use that could lead to acute kidney injury.
Factors influencing susceptibility include both modifiable (e.g., hydration status) and non-modifiable factors (e.g., age).
Specific Antibiotics Linked to Kidney Damage
Different antibiotics have varying impacts on renal health:
Vancomycin: Associated with tubular necrosis.
Aminoglycosides: Known for causing interstitial nephritis.
Other Notable Antibiotics
Beta-lactams (e.g., cephalosporins).
Fluoroquinolones (e.g., ciprofloxacin).
Macrolides (e.g., azithromycin).
Postrenal Causes of Renal Injury
Conditions like benign prostatic hyperplasia or tumors can lead to obstructive uropathy by compressing ureters.
Clinical Manifestations
Patients may experience symptoms such as uremic encephalopathy or strokes due to fluid overload affecting cardiac function.
Diagnostic Tools Beyond Creatinine Levels
Etiology and Differentiation of Acute Kidney Injury
Understanding Types of Acute Kidney Injury
The etiology of acute kidney injury (AKI) can be classified as prerenal if the urine is hyaline. If granular casts are present, it indicates intrinsic renal injury, specifically acute tubular necrosis (ATN).
Two key differentiators for identifying whether AKI is prerenal or intrinsic include urinary sediment analysis and fractional excretion of sodium (FENa). A FENa less than 1% suggests prerenal causes, while greater than 2% indicates ATN.
Additional Diagnostic Tools
Fractional excretion of urea (FEU) is another metric used when FENa results are altered due to conditions like nephrotoxicity or glomerulopathy. An FEU less than 35% suggests a prerenal cause, while more than 35% points to intrinsic renal issues.
Renal ultrasound can help diagnose potential obstructions or hydronephrosis by assessing kidney dilation due to obstruction at various levels such as the renal pelvis or ureters.
Imaging Techniques in Diagnosis
Urography without contrast aids in evaluating urinary lithiasis across the ureter, bladder, or kidneys. Contrast-enhanced urography is reserved for suspected obstructive masses like tumors compressing the ureter.
Doppler ultrasound assesses renal congestion and monitors fluid therapy and diuretics in patients with AKI. Advanced multiparametric MRI evaluates specific aspects like morphology and tissue microstructure.
Stress Testing with Furosemide
The furosemide stress test has gained traction since its introduction around 2016 for predicting outcomes in established AKI cases rather than diagnosing them directly.
In this test, a dose of furosemide (1 mg/kg for naive patients; 1.5 mg/kg for those previously on diuretics) is administered, followed by monitoring urine output over two hours to assess kidney function response.
Interpreting Test Results
If a patient produces more than 200 ml of urine within two hours post-furosemide administration, there’s a low probability they will progress to stage three AKI or require renal replacement therapy (RRT).
Conversely, if urine output is less than 200 ml, there’s a high likelihood that the patient may progress to stage three AKI or need RRT. This test shows an 87% sensitivity and an 84% specificity in predicting outcomes.
Biomarkers in Acute Kidney Injury
What Are the Current Insights on Biomarkers in Acute Kidney Injury?
Understanding Biomarkers
Current discussions highlight that biomarkers can be utilized not only for diagnosing acute kidney injury (AKI) but also for monitoring progression and prognosis.
Two significant biomarkers, tissue inhibitor of metalloproteinase A2 and insulin-like growth factor binding protein 7, have been identified as predictors for whether a patient will require renal replacement therapy (RRT).
These biomarkers are particularly notable because they can be detected early, with peak levels occurring between 6 to 24 hours after injury.
Fluid Therapy in Acute Kidney Injury Management
Fluid therapy is emphasized as a foundational treatment approach in managing AKI. Three phenotypes of patients are discussed:
Phenotype A: Hypovolemic (dehydrated or hypotensive)
Phenotype B: Euvolemic (normal hydration status)
Phenotype C: Hypervolemic (congested or edematous)
Managing Different Patient Types
The management strategies differ based on the patient's phenotype:
For hypovolemic patients, hydration should involve stable solutions that maintain electrolyte balance.
Optimal Solutions for Hydration
In cases of hypovolemia due to conditions like diarrhea or vomiting, balanced crystalloids such as lactated Ringer's solution are recommended as the best option.
Isotonic saline (0.9% sodium chloride) is considered a secondary option if lactated Ringer's is unavailable but is not ideal.
Use of Albumin in Specific Cases
Albumin has shown benefits primarily in specific scenarios involving chronic liver disease or significant fluid removal needs (>5L), spontaneous bacterial peritonitis, and certain renal syndromes treated with terlipressin.
It’s crucial to assess the patient's condition before administering albumin; it should not be used indiscriminately.
Considerations for Hypervolemic Patients
Diuretic Resistance and Management Strategies
Understanding Diuretic Response
The discussion begins with the concept of diuretics, specifically focusing on their role in managing congestion. The speaker mentions furosemide as a commonly used diuretic.
When faced with diuretic resistance, the first recommended action is to increase either the dosage or frequency of administration. For example, if a patient is receiving 20 mg every 12 hours, it may be beneficial to adjust this to every 6 or 8 hours.
It’s emphasized that increasing the dose or frequency should be the initial approach before considering switching to another diuretic.
Additional Diuretic Options
If resistance persists after adjusting dosages, additional diuretics can be introduced such as hydrochlorothiazide and spironolactone. Other options include SGLT2 inhibitors and metolazone.
In cases where these measures fail, particularly in patients who remain congested despite treatment, therapy with vasopressors may become necessary.
Fluid Management in Euvolemic Patients
Hydration Strategies
For euvolemic patients, continuous hydration is crucial. However, caution is advised for patients with sepsis-induced renal injury; management should focus on treating the underlying infection rather than aggressive fluid replacement.
Regular monitoring for signs of hypoperfusion (e.g., cyanosis, pallor, capillary refill time over two seconds) is essential to assess patient status effectively.
Fluid Therapy Adjustments
If signs of hypoperfusion are observed, fluid therapy should be initiated. A positive response would lead to administering crystalloid fluids in fractional doses rather than large boluses.
If clinical improvement does not occur despite adequate fluid therapy, discontinuation may be warranted and consideration for vasoactive agents like norepinephrine should be made.
Goals and Considerations in Renal Injury Management
Targeting Hemodynamic Goals
The target mean arterial pressure (MAP) for patients experiencing acute kidney injury (AKI) should ideally reach at least 65 mmHg. This metric takes precedence over systolic or diastolic pressures.
Nutritional Support
Nutritional strategies must prioritize caloric intake while avoiding excessive protein consumption and high levels of potassium and sodium.
Antibiotic-Induced Acute Kidney Injury
Managing Antibiotic Dosing
Attention is drawn to antibiotics that can cause AKI; adjustments based on renal function are critical but differ from chronic kidney disease protocols.
Misconceptions about CADEPI Usage
There’s a common misconception among interns regarding using CADEPI for AKI management; it’s clarified that creatinine levels and urine output are more relevant indicators for AKI than filtration rates used in chronic conditions.
Renal Replacement Therapy in Acute Kidney Injury
Overview of Antibiotic Dosing in AKI
In acute kidney injury (AKI) patients, it is not necessary to apply the CDPI (Creatinine-Dose Pharmacokinetic Index) for antibiotic dosing adjustments. Other measures can be utilized for appropriate antibiotic therapy.
Indications for Initiating Renal Replacement Therapy (RRT)
RRT should be initiated in cases of refractory hyperkalemia, particularly when potassium levels exceed 5.5 or 6.5 mEq/L and are associated with cardiovascular complications like arrhythmias.
Severe metabolic acidosis is defined as a pH below 7.1; this condition warrants RRT initiation.
Fluid overload leading to pulmonary edema that does not improve with diuretics also indicates the need for RRT.
Uremic complications such as uremic encephalopathy, pericarditis, and bleeding may necessitate starting RRT.
Modalities of Renal Replacement Therapy
Various modalities exist for RRT: continuous, intermittent, non-conventional, prolonged intermittent, and peritoneal dialysis. Clinical trials have shown no significant survival difference among these modalities.
Continuous and intermittent therapies show superiority over peritoneal dialysis specifically in patients with traumatic brain injury or acute cerebral lesions.
Transitioning Between Dialysis Modalities
Patients typically start on continuous dialysis three times a week; if stabilized after three days, they may transition to an intermittent schedule.
The progression from continuous to intermittent therapy is common once patient stability is achieved.
Anticoagulation Strategies in Dialysis
Intermittent renal replacement therapy often uses low molecular weight heparins like enoxaparin or unfractionated heparin as anticoagulants.
Continuous renal replacement therapy employs regional anticoagulation using citrate to prevent clotting by chelating calcium.
Discontinuation Criteria for Dialysis
Dialysis can be suspended when urine output exceeds 500 mL/day or 2.4 L/day while on diuretics; however, diuretic use does not necessarily expedite discontinuation of RRT.
Markers Indicating Successful Transition from Dialysis
Urinary markers such as NGAL (Neutrophil Gelatinase Associated Lipocalin) and cystatin C can indicate favorable outcomes during renal replacement therapy.
