Alterations in Kidney Function and Elimination Flashcards

Key Functions of the Renal System

• Removal of Waste: Filters metabolic waste products, toxins, and excess substances from the bloodstream for excretion.

• Fluid and Electrolyte Balance: Regulates body fluid volumes and maintains precise concentrations of key electrolytes including sodium ($Na^+$), potassium ($K^+$), chloride ($Cl^-$), calcium ($Ca^{2+}$), and phosphate ($PO_4^{3-}$).

• Acid-Base Regulation: Maintains systemic blood pH within the narrow physiological range of $7.35\text{ to }7.45$ through the excretion of hydrogen ions ($H^+$) and the reabsorption/generation of bicarbonate ions ($HCO_3^-$).

• Regulation of Plasma/Serum Osmolarity: Controls water reabsorption and solute concentrations to stabilize extracellular fluid osmolarity.

• Erythropoietin Production: Synthesizes and secretes the hormone erythropoietin in response to renal hypoxia, stimulating red blood cell (RBC) production in the bone marrow.

• Renin Secretion: Releases the enzyme renin to initiate the renin-angiotensin-aldosterone system (RAAS), regulating systemic blood pressure and fluid balance.

• Vitamin D Conversion: Converts inactive Vitamin D into its active hormonal form, calcitriol ($1,25\text{-(OH)}_2\text{D}_3$), which is essential for intestinal calcium absorption and bone mineralization.

Gerontologic Considerations in Renal Function

• Structural and Vascular Changes:

  • Renal tissue mass and weight decrease by approximately $10\%$ per decade starting at age 30.

  • Renal blood flow decreases by approximately $10\%$ per decade starting at age 30.

  • Glomerular filtration capacity experiences a progressive decline starting around age 40.

  • Atherosclerosis accelerates the reduction of renal size and vascular perfusion with advancing age.

• Functional Aging Effects:

  • Decreased Glomerular Filtration Rate (GFR) and impaired urinary concentrating ability.

  • Under basal non-stress conditions, older adults continue to maintain fluid homeostasis despite anatomical and functional losses.

• Specific Organ Aging Changes:

  • Kidneys: Reduced renal blood flow leads to decreased GFR. Altered hormonal responsiveness results in impaired urine concentration and altered tubular excretion of water, sodium, potassium, and hydrogen ions (acid).

  • Urethra and Bladder (Female): Decreased tissue elasticity and loss of pelvic floor muscle support lead to an increased incidence of urinary tract infections (UTIs) and stress/urge urinary incontinence.

  • Urethra and Bladder (Male): Prostate gland enlargement (benign prostatic hyperplasia) compresses the urethra, altering voiding patterns and causing urinary hesitancy, frequency, and retention.

Diagnostic Studies for the Renal System

• Endoscopic and Radiologic Procedures:

  • Cystoscopy: Direct visual inspection of the bladder interior using a tubular lighted scope passed through the urethra. Enables direct biopsy, stone removal, and lesion identification.

  • Kidney, Ureters, Bladder (KUB) X-ray: Plain abdominal and pelvic radiograph that delineates the size, shape, and anatomical position of the kidneys, ureters, and bladder. Detects radiopaque urinary calculi (stones) and foreign bodies.

  • Magnetic Resonance Imaging (MRI) / Magnetic Resonance Angiography (MRA): Provides high-resolution visualization of renal parenchyma, soft tissues, and renal vasculature without ionizing radiation.

• Pre-Procedure Preparation and Nursing Considerations:

  • Bowel Preparation: Utilized prior to radiologic studies to evacuate bowel contents and enhance renal visualization.

  • Common bowel prep agents include magnesium citrate and Fleet enemas. These osmotic agents are strictly contraindicated in kidney failure due to the risk of severe hypermagnesemia or hyperphosphatemia.

  • Contrast-Induced Nephropathy (CIN): Administration of iodine-based intravenous contrast agents carries a risk of Contrast-Induced Kidney Injury (CIN) and severe allergic reactions. Prevention strategies include ensuring robust pre- and post-procedure intravenous hydration and administering N-acetylcysteine to reduce free radical renal damage.

  • NPO Protocols: Patients are placed NPO prior to procedures, requiring careful monitoring to prevent dehydration. Insulin dosages must be adjusted in diabetic patients during NPO periods.

Urinary Tract Infections (UTIs)

• Epidemiology and Etiology:

  • UTIs represent the most common outpatient bacterial infection and the most frequent Healthcare-Associated Infection (HAI).

  • Primary Pathogen: Escherichia coli (E. coli) causes approximately $75\%$ of overall UTI cases and $65\%$ of complicated UTIs.

  • Fungal and Parasitic Pathogens: Less common causes, occurring primarily in patients who are immunosuppressed, diabetic, suffering from underlying kidney disease, receiving multiple courses of broad-spectrum antibiotics, or residing in/traveling to specific endemic developing regions.

• Anatomical and Clinical Classification:

  • By Anatomical Location:

  • Upper Tract Infection: Pyelonephritis—inflammatory infection involving the renal parenchyma, pelvis, and collecting system.

  • Lower Tract Infection: Cystitis (inflammation of the bladder) and Urethritis (inflammation of the urethra).

  • Systemic Spread: Urosepsis—a life-threatening systemic infection originating from a urinary tract source that requires immediate emergency intervention.

  • By Complexity:

  • Uncomplicated UTI: Infection occurring in a structurally and functionally normal urinary tract, typically in non-pregnant adult females.

  • Complicated UTI: Infection associated with coexisting factors such as structural or functional abnormalities (obstruction, neurogenic bladder), indwelling urinary catheters, renal calculi, diabetes, pregnancy, immunosuppression, or male gender.

• Risk Factors:

  • Female sex (shorter urethral length and proximity to the anus).

  • Indwelling urinary catheters (CAUTI).

  • Sexual intercourse.

  • Poor perineal hygiene practices.

  • Diabetes mellitus (DM) causing glucosuria and altered immune response.

  • Pregnancy causing urinary stasis due to mechanical pressure and hormonal changes.

• Clinical Manifestations:

  • Lower Urinary Tract Symptoms (LUTS):

  • Emptying Symptoms: Hesitancy, intermittency, post-void dribbling, urinary retention or incomplete bladder emptying, dysuria (painful urination).

  • Storage Symptoms: Urinary frequency, urgency, urge incontinence, nocturia (waking at night to void), nocturnal enuresis.

  • Urine Characteristics: Hematuria (gross or microscopic), cloudy appearance, foul odor.

  • Upper Urinary Tract Symptoms: Flank pain, costovertebral angle (CVA) tenderness, high fever, and rigors/chills.

  • Gerontologic Manifestations: Older adults frequently lack classic LUTS or systemic signs like fever. Instead, they present with non-localized abdominal discomfort, sudden onset cognitive impairment (confusion/delirium), fatigue, anorexia, or generalized functional deterioration.

  • Asymptomatic Bacteriuria: Bacterial colonization in the bladder without clinical symptoms. Treatment is not indicated for the general population but is mandatory in pregnant women to prevent preterm labor and pyelonephritis.

• Diagnostic Workup:

  • Initial Urine Dipstick Analysis: Tests for nitrites (indicating gram-negative bacterial conversion), white blood cells (WBCs), and leukocyte esterase.

  • Urine Culture and Sensitivity (C&S): Obtained via a clean-catch midstream urine technique. Indications for formal C&S include:

  • Recurrent UTIs (defined as more than 2 to 3 episodes per year).

  • Complicated UTIs.

  • Catheter-Associated UTIs (CAUTIs) or HAIs.

  • Infections unresponsive to empiric antibiotic therapy.

  • Imaging: Renal ultrasound or CT scans performed for suspected obstructions, structural anomalies, or recurrent pyelonephritis.

• Interprofessional Management:

  • Uncomplicated UTI Management: Patient education, aggressive fluid intake, short-course empiric antibiotic therapy (typically $\sim 3$ days), and urinary analgesics such as phenazopyridine for symptom relief.

  • Recurrent UTI Management: Urine culture and susceptibility testing, extended antibiotic courses ($7\text{ to }14$ days or longer), and continuous suppressive or post-coital prophylactic antibiotics.

• Nursing Process for UTI:

  • Assessment (Recognize Cues): Perform a complete history and physical exam, noting prior UTIs, surgical history, current medications, presence of fever/chills, dysuria, hematuria, and atypical cognitive changes in older adults.

  • Diagnosis (Analyze/Prioritize Cues): Impaired urinary elimination, Infection (risk of pyelonephritis or urosepsis), Acute pain (suprapubic or flank), Deficient knowledge regarding prevention.

  • Planning (Generate Solutions): Focus on resolving infection without renal damage, monitoring for pyelonephritis, strict intake and output (I&O) recording, and education regarding perineal hygiene and antibiotic compliance.

  • Implementation (Take Actions):

  • Encourage maintenance of a 24-hour bladder diary.

  • Analyze urine labs (WBC count, nitrites, bacteria).

  • Educate female clients on wiping front-to-back to prevent urethral contamination.

  • Administer prescribed antibiotics and enforce complete compliance.

  • Encourage high fluid intake to flush the urinary tract.

  • Apply heating pads to the suprapubic area or lower back, or offer warm showers/baths to relieve dysuria and spasm.

  • Evaluation (Evaluate Outcomes): Relief of voiding manifestations (absence of burning, urgency, frequency, or suprapubic pain), urine return to a clear yellow color, negative repeat urine culture, and symptom resolution within $2\text{ to }4$ days of antibiotic initiation.

• Patient Education Checklist:

  • Complete the entire course of antibiotics even if symptoms resolve after $1\text{ to }2$ days.

  • Maintain adequate fluid intake throughout the day.

  • Void regularly, approximately every $3\text{ to }4$ hours.

  • Empty the bladder completely before and immediately after sexual intercourse.

  • Avoid vaginal douches, bubble baths, harsh soaps, powders, and perineal hygiene sprays.

  • Report signs of recurrent infection (fever, cloudy urine, dysuria) to the healthcare provider.

• Prevention of Catheter-Associated Urinary Tract Infections (CAUTI):

  • Avoid unnecessary urinary catheter placement.

  • Reassess catheter necessity daily and prompt early removal.

  • Maintain strict aseptic technique during insertion and use sterile gloves and proper hand hygiene.

  • Maintain a closed drainage system with unobstructed urine flow.

Acute Kidney Injury (AKI)

• Definition and Core Features:

  • AKI (formerly termed acute renal failure [ARF]) is characterized by a sudden decrease in kidney function occurring over hours to days.

  • Potentially reversible condition marked by a rise in serum creatinine, a reduction in urine output, and elevated Blood Urea Nitrogen (BUN) and serum potassium ($K^+$).

  • Leads to azotemia (accumulation of nitrogenous waste products like urea, ammonia, and uric acid) and dysregulation of extracellular fluid volume and electrolytes.

• Etiology and Classification:

  • Prerenal AKI: Caused by factors external to the kidneys that reduce systemic blood circulation, leading to decreased renal blood flow and renal hypoperfusion.

  • Causes: Hypovolemia (dehydration, severe hemorrhage), systemic vasodilation, acute heart failure, sepsis, vascular occlusion, or medication-induced impairment of renal autoregulation.

  • Intrinsic / Intrarenal AKI: Direct structural damage to kidney tissue (glomeruli, tubules, or interstitium).

  • Causes: Acute Tubular Necrosis (ATN) triggered by nephrotoxic medications (aminoglycosides, NSAIDs), contrast media, endogenous toxins (myoglobin from rhabdomyolysis), prolonged hypotension/ischemia, acute glomerulonephritis, autoimmune diseases, or severe infection.

  • Postrenal AKI: Mechanical obstruction of urine outflow distal to the kidneys, creating hydrostatic pressure buildup back into the renal pelvis and impairing filtration.

  • Causes: Benign prostatic hyperplasia (BPH), prostate or cervical cancer, nephrolithiasis (urinary calculi), meatal stenosis/phimosis, retroperitoneal fibrosis, or bladder outlet obstruction.

• Clinical Manifestations and Phases of AKI:

  • 1. Onset / Initiation Phase: The period between the initial renal insult (e.g., severe hypotension, toxin exposure) and the onset of cellular damage. Lasts hours to days.

  • Nursing Focus: Identify high-risk patients and treat the underlying insult immediately.

  • 2. Oliguric Phase:

  • Manifests within $1\text{ to }7$ days of the insult.

  • Characterized by a significant decrease in urine output to $< 400\,\text{mL/day}$.

  • Key Clinical Features: Fluid volume overload (peripheral edema, hypertension, pulmonary crackles, jugular vein distention, S3 gallop), severe electrolyte imbalances (hyperkalemia), metabolic acidosis, and progressive azotemia.

  • 3. Diuretic Phase:

  • Lasts $1\text{ to }3$ weeks as nephrons regain partial function.

  • Characterized by a marked increase in daily urine output, reaching up to $5\,\text{L/day}$ due to osmotic diuresis from high urea concentrations and unresponsiveness to ADH.

  • Key Clinical Features: Severe dehydration, hypovolemia, hypotension, and rapid loss of electrolytes (hyponatremia, hypokalemia).

  • Nursing Focus: Monitor blood pressure, electrolyte levels, and strict intake/output.

  • 4. Recovery Phase:

  • Can require several months up to $1\text{ year}$.

  • GFR increases, allowing BUN and serum creatinine levels to plateau and return to normal range. Normalization of fluid balance and electrolyte regulation occurs.

• Interprofessional Care and Management:

  • Intravascular Volume and Cardiac Output Optimization: Fluid boluses for prerenal hypovolemia. Diuretic administration (loop diuretics such as furosemide [Lasix] or osmotic diuretics such as mannitol) if fluid overload is present without acute tubular necrosis.

  • Fluid Restriction in Oliguric Phase: Calculated formula: Total Fluid Restriction = All measured fluid losses over the previous 24 hours + $600\,\text{mL}$ (for insensible loss).

  • Hyperkalemia Emergency Therapies:

  • Temporary Shifting into Cells: Intravenous regular insulin (given with IV dextrose) and intravenous sodium bicarbonate.

  • Myocardial Membrane Stabilization: Intravenous calcium gluconate to prevent life-threatening cardiac dysrhythmias.

  • Potassium Removal from Body: Sodium polystyrene sulfonate (Kayexalate) or Patiromer (Veltassa) via GI tract, or emergency hemodialysis.

  • Nutritional Therapy: Provide adequate protein calories to prevent catabolism ($0.8\text{ to }1.0\,\text{g/kg/day}$ if not on dialysis), utilize enteral or parenteral nutrition if oral intake is insufficient, administer calcium supplements or phosphate-binding agents, and restrict sodium, potassium, and phosphate intake.

  • Treat Underlying Cause: Discontinue nephrotoxic agents, correct perfusion deficits, and treat underlying systemic sepsis or obstruction.

  • Renal Replacement Therapy (RRT): Hemodialysis or Continuous Renal Replacement Therapy (CRRT) indicated for acute severe hyperkalemia, metabolic acidosis, fluid volume overload compromising respiratory function, uremic encephalopathy, or pericarditis.

• Nursing Process for AKI:

  • Assessment (Recognize Cues): Take detailed past and current medical history; measure vital signs, daily weights, and strict I&O; inspect urine characteristics; evaluate general appearance, mental status/LOC, oral mucosa, lung sounds (crackles), heart rhythm (dysrhythmias, S3), and observe hemodialysis access sites.

  • Diagnosis (Analyze Cues): Electrolyte imbalance (hyperkalemia, rash), Fluid imbalance (edema, hypertension, crackles, JVD), Risk for infection, Anxiety.

  • Planning (Generate Solutions): Complete recovery of renal function, restoration of fluid/electrolyte balance, management of oliguria and acidosis, education on disease management and dietary restrictions.

  • Implementation (Take Actions): Identify nephrotoxic meds and notify providers; maintain precise I&O and daily weight logs; administer diuretics as ordered; continuously monitor mental status, blood pressure, and serum potassium levels.

  • Evaluation (Evaluate Outcomes): Restoration of kidney function, achievement of adequate hydration, alert mental status, absence of peripheral/pulmonary edema, and return of BUN and creatinine to normal limits.

Chronic Kidney Disease (CKD)

• Definition and Criteria:

  • Progressive, irreversible loss of kidney function over time.

  • Complete functional recovery is impossible due to permanent nephron destruction and fibrosis.

  • Diagnostic criteria: Demonstrated kidney damage OR an Estimated Glomerular Filtration Rate (eGFR) $< 60\,\text{mL/min/1.73\,m}^2$ for longer than 3 months.

• eGFR Staging of Chronic Kidney Disease:

  • Stage 1: eGFR $\ge 90\,\text{mL/min/1.73\,m}^2$ with kidney damage (e.g., microalbuminuria).

  • Stage 2: eGFR $60\text{ to }89\,\text{mL/min/1.73\,m}^2$ (mildly reduced kidney function).

  • Stage 3: eGFR $30\text{ to }59\,\text{mL/min/1.73\,m}^2$ (moderately reduced kidney function).

  • Stage 4: eGFR $15\text{ to }29\,\text{mL/min/1.73\,m}^2$ (severely reduced kidney function; prepare for RRT).

  • Stage 5: eGFR $< 15\,\text{mL/min/1.73\,m}^2$ (End-Stage Renal Disease [ESRD]; requires dialysis or transplantation for survival).

• Etiology:

  • Leading Cause: Diabetes Mellitus—accounts for $50\%$ of all CKD cases (Type 2 DM: $30\text{--}50\%$, Type 1 DM: $3.9\%$).

  • Second Leading Cause: Hypertension—accounts for $27.2\%$ of cases.

  • Other Causes: Glomerulonephritis (primary/secondary), chronic tubulointerstitial nephritis, cystic/hereditary diseases (e.g., polycystic kidney disease), renal neoplasms, or sickle cell nephropathy.

  • Approximately $70\%$ of affected individuals are unaware of their disease; CKD remains heavily underdiagnosed and untreated in early stages.

• Systemic Clinical Manifestations (Uremia):

  • Psychologic: Anxiety, depression.

  • Neurologic: Fatigue, severe headache, sleep disturbances, uremic encephalopathy, peripheral neuropathy (paresthesias, restless legs syndrome), lethargy, and altered consciousness.

  • Ocular: Hypertensive retinopathy.

  • Cardiovascular: Refractory hypertension, accelerated coronary artery disease, heart failure, uremic pericarditis, peripheral artery disease.

  • Pulmonary: Pulmonary edema, uremic pleuritis, kussmaul respirations (compensatory for metabolic acidosis), pneumonia.

  • Gastrointestinal: Anorexia, nausea, vomiting, uremic fetor (urinous odor of breath), GI mucosal bleeding, gastritis.

  • Integumentary: Severe pruritus, ecchymosis, dry scaly skin, uremic frost (rare end-stage presentation).

  • Musculoskeletal (CKD-MBD): Vascular and soft tissue calcifications, osteomalacia, osteitis fibrosa (due to secondary hyperparathyroidism, low active calcium, high phosphate).

  • Endocrine/Reproductive: Hyperparathyroidism, thyroid dysfunctions, amenorrhea, infertility, erectile dysfunction.

  • Metabolic: Carbohydrate intolerance (insulin resistance caused by uremia), hyperlipidemia.

  • Hematologic: Normocytic anemia (due to deficient erythropoietin production), bleeding tendencies (uremia-induced platelet dysfunction), increased infection susceptibility.

• Interprofessional and Drug Therapy:

  • Hyperkalemia: Potassium-binding medications (e.g., Patiromer, Sodium polystyrene sulfonate).

  • Hypertension: Lifestyle modification (TLC), DASH diet, ACE inhibitors or ARBs (early stage; used with caution in advanced stages).

  • CKD-Mineral and Bone Disorder (CKD-MBD): Phosphate binders (taken directly with meals; e.g., calcium acetate, sevelamer), calcium supplements, active Vitamin D (calcitriol).

  • Anemia: Erythropoietin-stimulating agents (ESAs such as epoetin alfa), oral/IV iron supplementation, folic acid.

  • Dyslipidemia: Statin drug therapy to reduce cardiovascular risks.

  • Nephrotoxic Drug Management: Dose reduction or complete discontinuation of nephrotoxic medications.

• Nutritional Management:

  • Protein Intake:

  • Pre-Dialysis: Normal protein intake; high-protein diets and supplements must be strictly avoided to prevent early uremia.

  • On Dialysis: No protein restriction; patients require increased protein intake to replace amino acids lost during dialysis procedures.

  • Fluid Restriction: Pre-dialysis patients utilize diuretics to minimize fluid retention. Dialysis patients require strict fluid restriction based on 24-hour urine output plus $600\,\text{mL}$.

  • Electrolyte Restriction:

  • Sodium: Restrict to less than $2,300\,\text{mg/day}$.

  • Potassium: Restrict in advanced stages based on serum levels.

  • Phosphate: Restrict high-phosphate foods (dairy, dark sodas, nuts). Because high-protein foods are often high in phosphate, phosphate binders are administered alongside meals.

• Nursing Process for CKD:

  • Assessment (Recognize Cues): Perform a comprehensive physical assessment, gather detailed family history, evaluate baseline disease understanding, and review diagnostic tests (urinalysis, eGFR, BUN/creatinine, renal ultrasound, KUB).

  • Diagnosis (Analyze Cues): Excess fluid volume (bilateral lower extremity edema, shortness of breath, lung crackles, JVD, S3 sound, ascites), Electrolyte imbalance (potassium elevation), Impaired cardiac function, Ineffective coping.

  • Planning (Generate Solutions): Preserve remaining nephron function, promote physical/psychological well-being, monitor disease progression, and manage metabolic complications.

  • Implementation (Take Actions): Enforce strict fluid restrictions and order diuretics; log precise I&O and daily weights; provide extensive patient education regarding blood pressure control, glycemic control, diet compliance, avoidance of nephrotoxins, daily weight tracking, and routine follow-up care.

  • Evaluation (Evaluate Outcomes): Maintain serum potassium within normal limits, achieve stable BUN/creatinine levels, and maintain body weight with no more than a $10\%$ undesirable loss.

Renal Replacement Therapy (RRT) and Dialysis

• Indications and Principles:

  • RRT involves the movement of fluid and molecules across a semipermeable membrane from one compartment to another.

  • Indicated to correct fluid/electrolyte imbalances and remove waste products when uremia can no longer be managed conservatively, typically at eGFR $< 15\,\text{mL/min/1.73\,m}^2$.

• Peritoneal Dialysis (PD):

  • Mechanism: Infusion of sterile dialysate solution into the peritoneal cavity through an surgically implanted catheter (e.g., Tenckhoff catheter). The peritoneum acts as the semipermeable membrane.

  • The 3 Phases of a PD Exchange Cycle:

  • 1. Inflow (Fill): Approximately $2\,\text{L}$ of dialysate solution infused over $\sim 10\text{ minutes}$.

  • 2. Dwell: Solution remains in peritoneal cavity for $20\text{ to }30\text{ minutes}$ (or up to $8\text{ hours}$ depending on protocol) for diffusion and osmosis to occur.

  • 3. Drain: Effluent fluid drained by gravity over $15\text{ to }30\text{ minutes}$.

  • PD Modalities:

  • Continuous Ambulatory Peritoneal Dialysis (CAPD): Manual exchanges performed up to 4 times throughout the day.

  • Automated Peritoneal Dialysis (APD): Automated cycler machine performs 3 to 4 exchanges overnight while the patient sleeps.

• Complications of Peritoneal Dialysis:

  • Catheter exit-site infection.

  • Peritonitis: Primary major complication. Manifests as cloudy peritoneal effluent, severe abdominal pain, rebound tenderness, and fever.

  • Abdominal hernias (due to increased intra-abdominal pressure).

  • Protein loss in effluent fluid.

  • Lower back pain.

  • Intra-abdominal bleeding.

  • Pulmonary complications (atelectasis, pneumonia from diaphragmatic displacement).

  • Hemodialysis (HD):

• Schedule: Typically performed $3\text{ to }5\text{ hours}$ per session, $3\text{ times per week}$ (or overnight at home or dialysis centers).

• Vascular Access Types:

  • Arteriovenous Fistula (AVF): Surgical anastomosis of a native artery and vein (preferred access). Requires placement at least 3 months prior to initiation to allow maturation.

  • Arteriovenous Graft (AVG): Synthetic bridge tube connecting an artery and vein.

  • Temporary Access: Central venous catheter placed in the subclavian or internal jugular vein.

• Vascular Access Care and Protections:

  • Confirm patency by palpating a thrill (vibratory sensation) and auscultating a bruit (swishing sound).

  • Strictly prohibit blood pressure measurements, IV insertions, blood draws, or tight/restrictive clothing on the arm with an active AV fistula or graft.

• Nursing Considerations for HD Treatment:

  • Evaluate fluid status prior to treatment (determine ultrafiltration goal).

  • Review scheduled medications; hold antihypertensives and dialyzable medications until after the procedure to prevent severe hypotension.

• Complications of Hemodialysis:

  • Hypotension: Caused by rapid fluid removal, decreased systemic vascular resistance, or low-sodium dialysate. Symptoms include lightheadedness, nausea, vision changes, chest pain, and seizures. Treatment: Reduce ultrafiltration rate and infuse IV normal saline bolus ($0.9\%$ NaCl).

  • Muscle Cramps: Caused by rapid fluid/electrolyte shifts. Treatment: Reduce ultrafiltration rate and administer hypertonic saline or dextrose.

  • Blood Loss: Results from incomplete blood return from dialyzer, accidental tubing separation, membrane rupture, or bleeding at needle entry sites post-dialysis.

  • Hepatitis: Infection transmission risk (Hepatitis B incidence reduced via universal precautions and mandatory vaccination).

  • Advanced and Novel Renal Therapies:

• Wearable Artificial Kidney (WAK): Miniature, lightweight ($\sim 10\,\text{lbs}$) dialysis device worn on a tool-belt harness, connecting via catheter to run continuously on battery power for ESRD filtration.

• Kidney Transplantation: Definitive treatment choice for ESRD, offering excellent long-term outcomes and high 1-year graft survival rates.