Acute Kidney Injury - Lecture Notes PDF

Acute kidney injury Lecture Number 9.1 Status Done Type Lecture 9.1 Acute Kidney Injury (AKI) Overview Acute Kidney Injury (AKI) is a sudden decline in renal excretory function occurring over hours to days. This results in an inability to maintain fluid, ele...

Acute kidney injury Lecture Number 9.1 Status Done Type Lecture 9.1 Acute Kidney Injury (AKI) Overview Acute Kidney Injury (AKI) is a sudden decline in renal excretory function occurring over hours to days. This results in an inability to maintain fluid, electrolyte, and acid-base balance. It is part of a continuum of acute kidney diseases that can progress to chronic kidney disease (CKD) if unresolved within three months. AKI is diagnosed using two primary criteria: an acute rise in serum creatinine and a reduction in urine output (oliguria). This condition is potentially treatable, and early detection significantly improves patient outcomes. Learning Objectives Objective 1: Define acute kidney injury (AKI) and its diagnostic criteria. Objective 2: Differentiate between pre-renal, renal, and post-renal causes of AKI. Objective 3: Describe the pathophysiological mechanisms involved in the development of AKI. Objective 4: Identify risk factors for AKI and strategies for primary prevention. Objective 5: Evaluate clinical assessment and management principles for AKI. Key Concepts and Definitions Acute Kidney Injury (AKI): A sudden decrease in kidney function causing disruption in fluid, electrolyte, and acid-base balance. Oliguria: Reduced urine output, often a key diagnostic feature of AKI. Prerenal AKI: Caused by reduced renal perfusion without structural damage; reversible if perfusion is restored promptly. Renal AKI: Results from structural damage to the kidney, affecting tubules, glomeruli, interstitium, or vasculature. Postrenal AKI: Results from obstruction to urine outflow, causing increased intratubular pressure and reduced glomerular filtration rate (GFR). Clinical Applications Case Study: A 70-year-old patient with a history of heart failure presents with oliguria and elevated serum creatinine after starting NSAIDs. Diagnostic Approach: History: Assess for volume depletion, nephrotoxic drug use, and obstruction symptoms. Examination : Fluid status, signs of heart failure, and symptoms of obstruction (e.g., flank pain). Tests: Urine output monitoring, serum creatinine, urea, electrolytes, and renal ultrasound. Treatment Options: Fluid resuscitation for prerenal causes. Withdrawal of nephrotoxic agents for renal causes. Relief of obstruction for postrenal causes. Complications/Management: Monitor for hyperkalemia, metabolic acidosis, and need for renal replacement therapy if medical management fails. Pathophysiology Prerenal AKI: Caused by hypovolemia, reduced cardiac output, or systemic vasodilation. Reduced renal perfusion triggers  autoregulation to maintain GFR. If mean arterial pressure drops below 75-80 mmHg, autoregulation fails, causing ischemia and potential acute tubular necrosis (ATN). Renal AKI: Involves direct damage to the kidney structure, often through ischemic or nephrotoxic injury. The S3 segment of the proximal tubule and thick ascending limb of the loop of Henle are most vulnerable due to high energy demands and low oxygen supply. Postrenal AKI: Obstruction of urinary outflow increases tubular pressure, reducing GFR. If untreated, this can cause irreversible kidney damage. Pharmacology Nephrotoxic Drugs: NSAIDs: Cause afferent arteriole constriction, reducing renal perfusion. ACE Inhibitors/ARBs: Dilate efferent arterioles, reducing glomerular pressure. Aminoglycosides: Cause direct tubular toxicity. Radiocontrast Agents: Cause nephrotoxicity via renal vasoconstriction and direct cellular toxicity. Differential Diagnosis Prerenal AKI: History of dehydration, hypovolemia, heart failure. Renal AKI: History of drug exposure, systemic illness, or nephrotoxic exposure. Postrenal AKI: Symptoms of urinary obstruction, e.g., flank pain or anuria. Investigations Serum Creatinine: Key diagnostic marker for AKI. Urine Output: Monitored for oliguria (6 hours). Urinalysis: Prerenal: Normal sediment or hyaline casts. Renal: Muddy brown casts or tubular epithelial cells. Postrenal: Red/white blood cells or crystals in the urine. Imaging: Renal ultrasound to identify postrenal obstruction. Key Diagrams and Visuals Summary and Key Takeaways Takeaway 1: AKI is a potentially reversible condition that requires early diagnosis and intervention. Takeaway 2: Key diagnostic criteria are increased serum creatinine and reduced urine output. Takeaway 3: Causes of AKI are categorized as prerenal, renal, and postrenal, each with distinct pathophysiology and treatment approaches. Takeaway 4: Early intervention can prevent progression to chronic kidney disease. Further Reading/References  KDIGO Clinical Practice Guideline for AKI (Kidney Int Suppl. 2012;2(1):1-138). Comprehensive Clinical Nephrology: Relevant chapters on AKI. Questions/Clarifications Question 1: What are the best clinical strategies to distinguish between prerenal and renal AKI? Question 2: How can the use of ACE inhibitors in patients with heart failure lead to AKI? Question 3: Why are the S3 segment of the proximal tubule and the thick ascending limb particularly susceptible to ischemic injury? Question 4: How can early identification of nephrotoxic drugs prevent AKI progression?