Urinary Tract Obstructions - Renal Notes

**Urinary Tract Obstructions** **Urinary tract obstructions** occur when the flow of urine is impeded at any point in the urinary tract. Obstructions can be caused by anatomical or functional abnormalities. **The severity of the obstruction is determined by its location, the degree of blockage, the...

**Urinary Tract Obstructions** **Urinary tract obstructions** occur when the flow of urine is impeded at any point in the urinary tract. Obstructions can be caused by anatomical or functional abnormalities. **The severity of the obstruction is determined by its location, the degree of blockage, the duration of the blockage, and the underlying cause**. - **Upper urinary tract obstructions** involve blockages in the kidneys or ureters. Common causes include: - Kidney stones - Ureteral strictures - Tumors - Blood clots - Congenital anomalies in children - **Lower urinary tract obstructions** occur in the bladder or urethra. Common causes include: - Urethral strictures - Prostate enlargement in men - Pelvic organ prolapse in women - Tumors - Neurogenic bladder **Pathophysiological Mechanisms of Urinary Tract Obstructions:** When an obstruction occurs, urine backs up behind the blockage, increasing hydrostatic pressure and dilating the urinary structures upstream. This dilation can lead to: - Hydroureter: Dilation of the ureter - Hydronephrosis: Dilation of the renal pelvis and calyces - Increased pressure in the Bowman\'s capsule, reducing glomerular filtration rate - Urinary stasis, increasing the risk of infection - Tubulointerstitial fibrosis, damaging renal nephrons and potentially leading to chronic kidney disease **Clinical Manifestations of Urinary Tract Obstructions:** The clinical presentation of urinary tract obstructions depends on the location and severity of the blockage. **Upper Urinary Tract Obstructions:** - Renal colic: Moderate to severe pain, often originating in the flank and radiating to the groin. Pain radiating to the lateral flank or lower abdomen indicates midureter obstruction. - Nausea and vomiting - Hematuria - Urgency and frequent voiding, especially with lower ureter or ureterovesical junction obstruction. **Lower Urinary Tract Obstructions:** - Frequent daytime voiding - Nocturia - Weak or intermittent urinary stream - Urinary urgency and hesitancy - Feelings of incomplete bladder emptying **Types of Urinary Incontinence** **Urinary incontinence** is the involuntary leakage of urine. The different types of incontinence include: - **Stress incontinence:** Urine leakage with sudden increases in intra-abdominal pressure, such as during coughing, sneezing, laughing, or exercise. This type is most common in women younger than 60 and men who have had prostate surgery. - **Urge incontinence:** Urine loss accompanied by a strong, sudden urge to urinate. This type is most common in older adults and may be associated with neurologic disorders or decreased bladder wall compliance. - **Overflow incontinence:** Involuntary urine loss due to bladder overdistention. This may be caused by neurologic lesions, polyneuropathies, urethral obstruction (such as an enlarged prostate), or detrusor underactivity. - **Functional incontinence:** Urine leakage resulting from cognitive impairment (such as dementia) or physical limitations that prevent timely toileting. **Cystitis and Pyelonephritis** **Urinary tract infections (UTIs)** occur when pathogens infect any part of the urinary tract, from the urethra to the kidneys. UTIs are typically caused by the retrograde movement of bacteria from the gut into the urethra and bladder. - **Cystitis** is an infection of the bladder, while **pyelonephritis** is an infection of one or both upper urinary tracts (kidneys). **Causative Microorganisms:** - The most common cause of UTIs is *Escherichia coli* ( *E. coli*). - Other causative organisms include *Klebsiella, Proteus, Pseudomonas, Staphylococcus saprophyticus*, fungi, viruses, and parasites. **Pathophysiology of Cystitis:** - Bacteria, typically *E. coli*, enter the urethra and ascend to the bladder. - Uropathic *E. coli* have fimbriae that allow them to adhere to the uroepithelium, resisting the flushing action of urine. - Infection triggers an inflammatory response in the bladder wall, leading to redness, pus formation, and potentially ulceration or necrosis. **Pathophysiology of Pyelonephritis:** - Infection usually ascends from the bladder up the ureters to the kidneys - Alternatively, bacteria can spread to the kidneys through the bloodstream - Inflammation primarily affects the renal pelvis, calyces, and medulla - In severe cases, abscesses can form in the medulla and extend to the cortex **Clinical Manifestations:** **Cystitis:** - Frequency, dysuria, urgency - Lower abdominal and/or suprapubic pain - Hematuria and cloudy urine may also occur **Pyelonephritis:** - Symptoms of cystitis may precede systemic signs - Fever, chills, nausea, vomiting - Flank or groin pain - Costovertebral tenderness **Glomerulonephritis** **Glomerulonephritis** is an inflammation of the glomeruli, the filtering units of the kidneys. It can be acute or chronic and is categorized as primary or secondary. - **Primary glomerulonephritis** originates in the glomeruli themselves, often triggered by infections or immune responses. - **Secondary glomerulonephritis** develops as a consequence of systemic diseases like diabetes mellitus, hypertension, or lupus. **Risk Factors for Glomerulonephritis:** **Acute Glomerulonephritis:** - Infections, particularly those caused by group A beta-hemolytic streptococci - Immune disorders, such as IgA nephropathy - Exposure to certain toxins or drugs **Chronic Glomerulonephritis:** - Systemic diseases like diabetes mellitus, hypertension, and systemic lupus erythematosus - Prolonged or recurrent episodes of acute glomerulonephritis - Family history of kidney disease **Pathophysiology of Glomerulonephritis:** Glomerulonephritis is often caused by immune responses that damage the glomerular filtration membrane. - Immune complexes can deposit in the glomeruli, activating complement and triggering an inflammatory response that damages the filtration barrier. - This damage leads to: - Increased permeability, allowing proteins and red blood cells to leak into the urine - Reduced glomerular filtration rate - Fluid retention, leading to edema and hypertension - Potential progression to chronic kidney disease **Clinical Manifestations of Glomerulonephritis:** - Hematuria with red blood cell casts, resulting in brown-tinged urine - Proteinuria, often accompanied by hypoalbuminemia - Edema, particularly around the eyes (periorbital) and in the legs (pedal) - Hypertension - In severe cases, oliguria and renal failure **Nephrotic and Nephritic Syndromes** **Nephrotic and nephritic syndromes** are distinct clinical presentations that can result from glomerular injury. **Nephrotic Syndrome:** - Characterized by: - **Massive proteinuria** (more than 3.5 grams per day) - **Hypoalbuminemia** - **Edema** - **Hyperlipidemia** - The main pathophysiological mechanism is increased glomerular permeability, leading to the loss of large amounts of protein in the urine. - This protein loss reduces plasma oncotic pressure, causing fluid to shift into the interstitial spaces, resulting in edema. **Nephritic Syndrome:** - Key features include: - **Hematuria** with red blood cell casts - **Oliguria** - **Decreased glomerular filtration rate** - **Hypertension** - Often associated with immune-mediated glomerular injury, where inflammation and damage disrupt the filtration barrier, leading to the passage of red blood cells and protein into the urine. **Acute Kidney Injury, Chronic Kidney Disease, and End-Stage Renal Disease** **Acute Kidney Injury (AKI):** - **Definition:** Sudden decline in kidney function, characterized by a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood. - **Causes:** AKI is classified into three categories based on the cause: - **Prerenal AKI:** Most common type, resulting from reduced blood flow to the kidneys (renal hypoperfusion). Examples include: - Severe dehydration - Heart failure - Hemorrhage - **Intrarenal AKI:** Caused by direct damage to the kidney structures, particularly the nephrons. Causes include: - Acute tubular necrosis (ATN), often due to ischemia or nephrotoxic agents - Glomerulonephritis - Acute interstitial nephritis - **Postrenal AKI:** Relatively rare, caused by an obstruction in the urinary tract downstream from the kidneys. This leads to a buildup of pressure in the kidneys, impairing their function. Examples include: - Kidney stones - Prostate enlargement - Tumors - **Pathophysiology:** - **Reduced perfusion (prerenal):** Decreased blood flow triggers compensatory mechanisms to maintain filtration initially, but prolonged hypoperfusion leads to ischemia and cell damage, particularly in the tubules - **Direct damage (intrarenal):** Various insults can directly injure the nephrons, leading to inflammation, cell death, and impaired filtration - **Obstruction (postrenal):** Blockage increases pressure upstream, reducing glomerular filtration and potentially causing hydronephrosis - **Clinical Manifestations:** - **Decreased urine output (oliguria)**: One of the hallmarks of AKI - **Elevated serum creatinine and blood urea nitrogen (BUN)**: Indicate a buildup of waste products in the blood - **Electrolyte imbalances:** Hyperkalemia and other electrolyte disturbances can occur - **Fluid overload**: Edema and even heart failure can develop due to fluid retention **Chronic Kidney Disease (CKD):** - **Definition:** Progressive, irreversible loss of kidney function over a period of months or years - **Causes:** - **Diabetes mellitus:** Leading cause of CKD - **Hypertension:** Contributes significantly to CKD development - **Glomerulonephritis:** Can lead to chronic scarring and loss of kidney function - **Polycystic kidney disease:** Inherited disorder characterized by multiple cysts in the kidneys - **Obstructive uropathies:** Long-term obstruction can cause irreversible damage - **Pathophysiology:** - **Nephron loss and hypertrophy:** As nephrons are damaged, the remaining nephrons try to compensate by filtering more, leading to further stress and damage - **Glomerular hyperfiltration and proteinuria:** Increased pressure within the glomeruli damages the filtration barrier, leading to protein leakage into the urine - **Tubulointerstitial fibrosis:** Chronic inflammation and damage lead to scarring and loss of functional tissue in the kidneys - **Oxidative stress and inflammation:** Play a significant role in the progression of CKD - **Clinical Manifestations:** - Early stages may be asymptomatic. - As kidney function declines: - **Fluid and electrolyte imbalances:** Sodium and water retention, hyperkalemia, and metabolic acidosis \[ - **Anemia:** Due to reduced erythropoietin production - **Hyperphosphatemia and hypocalcemia:** Impaired phosphate excretion and reduced vitamin D activation - **Cardiovascular complications:** Hypertension, heart failure, and pericarditis - **Gastrointestinal disturbances:** Nausea, vomiting, and loss of appetite - **Neurologic complications:** Fatigue, confusion, and even seizures **End-Stage Renal Disease (ESRD):** - **Definition:** Final stage of CKD, where kidney function is less than 10% of normal - **Causes:** Same as CKD, as ESRD is the result of progressive kidney damage. - **Pathophysiology:** Extensive nephron loss and widespread scarring, leading to a profound inability to filter waste products and maintain homeostasis - **Clinical Manifestations:** - **Uremic syndrome:** A constellation of symptoms resulting from the buildup of toxins in the blood - **Severe fluid and electrolyte imbalances** - **Marked anemia** - **Significant cardiovascular, gastrointestinal, neurologic, and other systemic complications** **Treatment for ESRD:** - **Dialysis:** Artificial filtration of the blood to remove waste products and excess fluid - **Kidney transplantation:** Replacement of the damaged kidneys with a healthy kidney from a donor