Renal

Renal Anatomy Review

• Kidneys located in the retroperitoneal space.
• Fibrous capsule covers each kidney (connective tissue, lymphatics, blood vessels).
• Hilum: Area where blood vessels, lymphatics, nerves, and ureter enter the kidney.
• 20% of cardiac output delivered to the kidneys; compromised cardiac output affects kidneys early.

Nephron

The functional unit of the kidneys.

• Composed of capillaries (glomerulus).
• Filtration occurs in the glomerulus and depends on intracapillary blood pressure.
• Afferent arteriole: Supplies blood to the glomerulus.
• Efferent arteriole: Carries blood away from the glomerulus.
• Renal tubule: Proximal convoluted tubule, loop of Henle, distal convoluted tubule, collecting duct.
• Fluid filtered through glomerulus passes through the renal tubule to the collecting duct.

Normal Urine Output

• Infants: $1-2$ milliliters per kilo per hour.
• Child: $1$ milliliter per kilo per hour.
• Adolescent: $0.5$ milliliters per kilo per hour (well-hydrated).
• Individual baseline normal is most important.
• Consider changes and responses to interventions.

Renal System Functions

• Urine formation.

• Waste excretion.

• Erythropoietin secretion (erythrocyte production).

• Water and sodium balance.

• Blood pressure maintenance.

• Electrolyte and acid-base balance.

• Kidney development continues until around age two.

  Functional limitations in young patients:

  • Inability to excrete excess sodium.
  • Decreased serum bicarbonate concentrations.
  • Limited reabsorption of bicarbonate and secretion of hydrogen ions (affects acid-base balance).
  • Inability to concentrate urine.
  • Decreased glomerular filtration rate.
  • Decreased renal blood flow (especially with low cardiac output).
  • Immature kidneys are less able to adjust to stress from acute illness.

Acute Kidney Injury (AKI) Categorization

• Categorized by the location of the abnormality

  • Prerenal.
  • Renal (intrarenal, intrinsic, acute tubular necrosis).
  • Postrenal.

Prerenal Failure

• Most common cause of AKI.

• Usually caused by decreased perfusion, but not structural renal defect.

• Decreased perfusion related to diminished preload or cardiac failure.

• Decreased renal blood flow leads to decreased glomerular perfusion and glomerular filtration rate.

• Decreased urine output results from increased intravascular volume via sodium and water conservation (compensatory mechanism).

• Increased venous return to heart improves perfusion.

• Potential causes of decreased renal perfusion:

  • Altered cardiac function (cardiogenic shock, congenital heart defects, cardiomyopathy).
  • Positive pressure ventilation (impacts thoracic pressure and venous return).
  • Peripheral vasodilation (septic shock, anaphylaxis, liver failure).
  • Intravascular volume depletion (hemorrhage, third spacing from sepsis, GI losses).
  • Altered renal blood supply (renal artery thrombosis, renal vascular obstruction).

• Early recognition and restoration of blood flow lead to a good prognosis.

Physiologic Responses

• Autoregulation: Intrarenal mechanism to maintain constant renal blood flow despite altered blood or renal perfusion pressure.

  • Kidneys readjust vascular resistance to regulate blood flow (up to a point).
  • Vital organs (heart, lungs, brain) prioritize blood flow over non-vital organs (kidneys).

• Extrarenal mechanisms to maintain constant renal blood flow:

  • Increased cardiac output.
  • Changes in systemic vascular tone (vasodilation or vasoconstriction).
  • Antidiuretic hormone (ADH) role in water balance.
  • Extrarenal changes to systemic blood flow and blood pressure.

• These responses are time-limited; untreated prerenal AKI can lead to permanent damage.

Prerenal Failure Presentation

• Oliguria (decreased urine output) as compensation.
• Non-oliguric responses with normal or high urine output are possible.
• Assess urine output in relation to total fluid balance.
• Acid-base disturbances (unexplained metabolic acidosis) may be an early indicator.
• Azotemia (high urea and creatinine, and nitrogen-rich waste products in the blood).
• Diagnosis is based on the presence of azotemia or uremia.
• Decreased glomerular filtration rate increases BUN and creatinine.
• BUN to creatinine ratio is a more sensitive indicator of renal function.
• Urine specific gravity may be elevated if the body is reabsorbing water and concentrating urine.

Prerenal AKI Treatment

• Early recognition and intervention are essential.
• Maintain intravascular volume.
• Assess for signs and symptoms of fluid volume deficit or dehydration, and respond with a fluid bolus.
• Remove potassium from IV fluids.
• Diuretics may help distinguish between prerenal and renal failure (kidneys may respond well to diuretics in early renal failure).
• Avoid agents that harm the kidneys (certain antibiotics).

Intrinsic Acute Kidney Injury

Occurs due to an acute insult to the kidneys.

• Immune-related (glomerulonephritis, lupus).
• Vascular causes (hemolytic uremic syndrome, disseminated intravascular coagulation, thrombotic thrombocytopenia purpura).
• Infectious or drug-related interstitial nephritis.
• Renal trauma.
• Nephrotoxins (antibiotics, radiographic contrast agents).
• Over 50% of pediatric cases are related to acute glomerulonephritis, hemolytic uremic syndrome, or drug-induced nephritis.

Phases of Intrinsic Kidney Injury

• Oliguric or anuric phase (abrupt onset).
• Diuretic phase (exponential increase in urine output; monitor fluid volume status).
• Recovery phase (lasts longer in children and can take years).
• Supportive care is the primary focus (no known therapy to change the course).
• Improve renal perfusion and remove any identifiable cause (discontinue nephrotoxic medications).

Postrenal Acute Kidney Injury

• Obstruction of urine flow (ureters, bladder, urethral meatus).
• Uncommon in children; may be congenital.
• Obstruction leads to increased intratubular pressure, decreased renal blood flow, and decreased glomerular filtration rate.
• Presents as decreased urine output.
• Abdominal or flank pain; palpable mass.
• Risk of failure to thrive.
• Management: Decompression of the urinary collecting system by removing the obstruction, or diverting urine around the obstruction.

General Management of Acute Kidney Injury

• Affects all body systems.
• Electrolyte balance.
• Acid-base balance.
• Intravascular volume management.
• Respiratory status (fluid overload can lead to respiratory distress and failure).
• Neurologic status.
• Hematologic function.
• Adequate nutrition (may need more calories with limited fluid intake).
• Infection prevention.

Intravascular Volume Management

• Maintain normal intravascular fluid volume.
• Strict intake and output monitoring.
• Watch for signs and symptoms of dehydration or fluid overload.
• Administer fluids for hypovolemia.
• Fluid restriction and diuretics for hypervolemia.
• Hypertension can be related to hypervolemia and the renin-angiotensin system.

Common Electrolyte Imbalances During AKI

• Related to changing volume status and kidney's inability to regulate electrolyte excretion.
• Hyperkalemia.
• Hyponatremia.
• Hypocalcemia.

Hyperkalemia

• Most dangerous electrolyte imbalance.

• Kidneys clear over 90% of potassium normally; compromised kidney function affects clearance.

• Clinical manifestations:

  • Muscle weakness.
  • Confusion
  • Ascending paralysis.
  • Nausea and diarrhea.
  • Cardiac manifestations are most dangerous.
    • Tall, peaked T waves, widened QRS, prolonged PR interval.
    • Ventricular arrhythmias.
    • Cardiac arrest.

• Managing hyperkalemia:

  • Watch for ECG changes or altered cardiac function.
  • Stabilize myocardium (calcium gluconate or calcium chloride to reduce cardiac toxicity).
  • Decrease serum potassium level.
    • Shift potassium back into cells.
      • Insulin-glucose combination (promotes cellular uptake of potassium).
      • Sodium bicarbonate (facilitates movement of potassium into the cell).
      • Albuterol (shifts serum potassium into the cellular space).
    • Remove potassium from the body.
      • Lasix (excretion of potassium).
      • K oxalate (exchanges sodium for potassium in the gastrointestinal tract).
      • Dialysis (most effective method).

Hyponatremia

• Sometimes occurs due to overestimation of the patient's free water needs, leading to too much fluid replacement.

• Body can't diurese excess water; dysfunctional kidneys may not excrete sodium well.

• Patients undergoing the diuretic phase of intrinsic failure have an increased risk of developing hyponatremia.

• Neurologic symptoms (lethargy, disorientation, seizures, coma) are most dangerous.

• Management:

  • Identify and treat the underlying cause.
  • Treat serum sodium levels with hypertonic saline (if levels are less than 120 or the patient is symptomatic).
  • Frequent neurologic assessments.
  • Monitor serum sodium levels frequently.

Hypocalcemia

• Occurs due to increased phosphate, decreased vitamin D production, or hypoalbuminemia.

• Hyperphosphatemia occurs due to the inability of the kidneys to excrete phosphate and hypercatabolic state.

• Clinical manifestations:

  • Kavacic's sign (twitching with tapping on the facial nerve).
  • Trousseau's sign (hand and finger spasms with blood pressure cuff inflation).
  • Lethargy; seizures.
  • Hypotension; prolonged QT interval.

• Management:

  • Treat the underlying condition.
  • Treat hyperphosphatemia.
  • Administer IV calcium replacements.
  • Check for hypomagnesemia.

Medication Clearance

• Altered kidney function affects medication clearance.
• Partner with a clinical pharmacist.
• Monitor medication levels and adjust doses.

Renal Replacement Therapy

Used to remove excess intravascular volume and correct electrolyte or acid-base imbalances.

• Peritoneal dialysis: Removes fluid slowly (over a few days); used in newborns, infants, and young pediatric patients; can be used for chronic management.
• CVVH (continuous venovenous hemofiltration): Slow, continuous removal of fluid via ultrafiltration and convection; maintained at the bedside by a trained critical care nurse.
• Hemodialysis: Rapidly restores fluid, electrolyte, and acid-base balances; can cause significant fluid shifts; patient must tolerate rapid correction.

Chronic Kidney Disease/Failure

Acute kidney injury can progress to chronic kidney disease and chronic kidney failure.

• Medications for growth, bone density, and anemia.
• Diuretic medications can increase urine output and maintain fluid balance.
• Diet restrictions.
• Dialysis (chronic peritoneal dialysis or chronic hemodialysis) may be needed for months or years.
• Kidney transplant may ultimately be needed.

Kidney Transplantation

• Candidates have end-stage renal disease from congenital renal disorder, glomerulonephritis, or secondary to another disease/treatment.

• Postoperative management:

  • Monitor urinary output.
  • Urine replacement may be needed.
  • Monitor labs (BUN and electrolytes).
  • Appropriate pain management.
  • Lifelong immunosuppressive therapy to prevent kidney graft rejection.

• Outcomes are better with living donor kidneys; transplants have a 90-95% success rate at five years.

Hemolytic Uremic Syndrome (HUS)

• Triad:

  • Hemolytic anemia (lysis of red blood cells).
  • Thrombocytopenia (low platelet count).
  • Acute kidney injury.

• One of the most common causes of acquired renal failure in pediatric patients.

• Primary effects are hematologic and renal, but multisystem involvement (GI, neurological) is possible.

Etiology

• Typical HUS is often associated with E. coli strains (80-90% of cases), shigella, salmonella, campylobacter, strep pneumoniae, and coxsackievirus;.
• Atypical HUS is a hereditary form related to a genetic deficiency of a prostacyclin stimulating hormone.

Pathophysiology

• Microangiopathy with platelet aggregation and fibrin deposition in small vessels of the kidney, gut, and central nervous system.
• Hemolytic anemia (lysis) occurs due to shearing of red cells as they pass through narrow vessels.
• Gastrointestinal symptoms (bloody diarrhea) may occur early.
• Thrombocytopenia and hemolytic anemia develop acutely.
• Acute kidney injury and renal failure.
• Symptoms may also include hemorrhagic, thrombotic, and necrotic lesions that can occur in the central nervous system, the lungs, adrenal glands, and the heart.

Assessment of HUS

• Anemia (pale, lethargic, irritable).
• Abdominal pain with gastrointestinal involvement.
• Bruising, petechiae, purpura (hemorrhagic perspective).
• Seizures (neurologic perspective).
• Oliguria or anuria (renal perspective).

Labs

Signs and symptoms of acute kidney injury (elevated BUN/creatinine).

• Management of HUS:

  • Rapid recognition.
  • Restore fluid and electrolyte balance.
  • Support renal function (peritoneal dialysis is usually best tolerated).
  • Treat anemia (if symptomatic) and bleeding (platelet transfusion).
  • Manage CNS complications symptomatically.
  • Restrict oral intake (affect GI function);
  • Provide more calories from glucose versus protein to minimize azotemia.