Urinary and Renal Disorders - Acute Kidney Injury Midterm Notes PDF

**URINARY AND RENAL DISORDERS -- *Acute Kidney Injury*** **Acute Kidney Injury (AKI)** Acute Kidney Injury (AKI) is defined as a **sudden decline in kidney function**, resulting in reduced glomerular filtration, fluid and electrolyte imbalances, and accumulation of **nitrogenous waste products** i...

**URINARY AND RENAL DISORDERS -- *Acute Kidney Injury*** **Acute Kidney Injury (AKI)** Acute Kidney Injury (AKI) is defined as a **sudden decline in kidney function**, resulting in reduced glomerular filtration, fluid and electrolyte imbalances, and accumulation of **nitrogenous waste products** in the blood. **1. Most Likely Cause** The causes of AKI are classified into three major categories: 1. **Prerenal Causes** (most common) - **Hypoperfusion** of the kidneys due to conditions such as: - **Low blood pressure (hypotension)** from hemorrhage, shock, or sepsis. - **Hypovolemia** (severe dehydration or blood loss). - **Heart failure** or reduced cardiac output, causing inadequate blood flow to the kidneys. 2. **Intrarenal Causes** (damage within the kidney itself) - **Direct damage to the kidney structures**, including: - **Acute tubular necrosis (ATN)** caused by **ischemia or nephrotoxins** (e.g., drugs, toxins). - **Glomerulonephritis** (immune-mediated injury to the glomeruli). - **Acute interstitial nephritis** (inflammation of the kidney\'s interstitial space, often caused by allergic reactions to drugs). 3. **Postrenal Causes** (blockage of urine flow) - **Obstruction of urinary outflow**, which increases pressure in the nephrons, causing injury. Examples include: - **Kidney stones** (nephrolithiasis). - **Prostate enlargement** (benign prostatic hyperplasia). - **Tumors** or **ureteral strictures**. **2. Pathophysiology** The pathophysiology of AKI differs based on the type (prerenal, intrarenal, or postrenal), but generally follows a sequence of events: 1. **Prerenal Pathophysiology** (renal hypoperfusion) - **Decreased renal blood flow** reduces **glomerular filtration rate (GFR)**, leading to insufficient blood flow to the nephrons. - **Hypoxia** in the renal tissue causes **cell injury** and **ischemia**, which may progress to **acute tubular necrosis (ATN)** if untreated. - GFR can recover quickly if blood flow is restored. 2. **Intrarenal Pathophysiology** (direct injury to the kidney) - Injury to **renal tubules** (as in ATN) results from: - **Ischemia**: Prolonged prerenal failure progresses to ischemic necrosis of the renal tubular cells. - **Nephrotoxins** (e.g., certain antibiotics, NSAIDs) cause damage to the **proximal tubular cells**, which are responsible for reabsorption. - Damaged tubular cells form **casts** that block urine flow, worsening the injury by increasing intratubular pressure. - In **glomerulonephritis**, **immune complexes** deposit in the glomerulus, triggering inflammation and injury, leading to proteinuria and hematuria. 3. **Postrenal Pathophysiology** (urinary tract obstruction) - **Urinary obstruction** (from kidney stones, tumors, or prostate enlargement) increases pressure in the nephrons, which opposes the normal pressure gradient required for filtration. - Prolonged obstruction leads to **hydronephrosis** (swelling of the kidney due to backed-up urine) and compression of the renal tissue, which damages nephron function. **3. Disease Transmission** - **Transmission:** - **Not transmissible**. AKI is a non-infectious disease. - However, certain **infections (e.g., sepsis)** may lead to prerenal AKI due to **shock and reduced perfusion**. **4. Risk Factors** The risk factors for AKI depend on the category (prerenal, intrarenal, or postrenal). **Risk Factors for Prerenal AKI** - **Age**: Older adults have reduced renal reserve. - **Dehydration**: Can result from excessive diarrhea, vomiting, or inadequate fluid intake. - **Shock**: Hypotension from trauma, hemorrhage, or septic shock can decrease renal perfusion. - **Heart Failure**: Reduced cardiac output decreases blood flow to the kidneys. - **Use of diuretics**: Excessive diuresis may result in dehydration and reduced blood volume. **Risk Factors for Intrarenal AKI** - **Medications**: Use of nephrotoxic drugs (e.g., **aminoglycosides**, **NSAIDs**, **contrast agents** for imaging) increases risk of ATN. - **Infections**: Infections like **glomerulonephritis** can cause immune-mediated injury to the kidneys. - **Autoimmune diseases**: Conditions like **lupus nephritis** may result in immune complexes that deposit in the kidneys. - **Sepsis**: Sepsis-induced ischemia and endotoxins can damage renal tubules. **Risk Factors for Postrenal AKI** - **Kidney Stones (Nephrolithiasis)**: Stones block the outflow of urine, leading to **hydronephrosis** and increased intratubular pressure. - **Prostatic Hypertrophy (BPH)**: Enlargement of the prostate can block urine flow in men, especially older men. - **Urethral Strictures**: May develop as a result of **trauma, infection, or surgery**, increasing the risk of postrenal AKI. - **Tumors**: Cancers that invade or compress the urinary tract can lead to postrenal AKI. **Summary Table** **Criteria** **Acute Kidney Injury (AKI)** ----------------------- ----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- **Most Likely Cause** Prerenal (hypoperfusion), intrarenal (tubular injury), postrenal (obstruction). **Pathophysiology** Prerenal: Reduced blood flow → reduced GFR. Intrarenal: Tubular injury (ischemia, nephrotoxins) → casts, obstruction, and backpressure. Postrenal: Obstruction increases nephron pressure, reducing filtration. **Transmission** **Not transmissible**. AKI is not an infectious disease. **Risk Factors** **Prerenal:** Dehydration, hemorrhage, shock, heart failure. **Intrarenal:** Nephrotoxins, glomerulonephritis, sepsis. **Postrenal:** Kidney stones, prostatic hypertrophy, tumors.