AKI

Definition: A term encompassing both slight deterioration and severe impairment of kidney function, characterized by rapid loss of kidney function.
Causes: Frequently due to hypertension, hypovolemia, or nephrotoxic agents. Common causes in the hospital include acute tubular necrosis (ATN) and prerenal causes.

Prerenal: External factors that reduce renal blood flow and decrease glomerular perfusion.
- Factors include reduced circulation leading to decreased blood flow.
- Body compensates by increasing blood volume through hormones (angiotensin II, aldosterone, norepinephrine, ADH).
- May progress to intrarenal if not addressed.
Intrarenal (Intravenous): Direct damage to kidney tissue leading to impaired nephron function. Common causes include:
- Prolonged ischemia
- Nephrotoxins
- Hemoglobin or myoglobin release from damaged cells (e.g., from trauma or necrosis).
- Acute tubular necrosis is a common cause.
Postrenal: Obstruction of renal flow below the kidneys (accounting for ~10% of cases).
- Common causes: Benign Prostatic Hyperplasia (BPH), prostate cancer, calculi, trauma, or tumors.
- Bilateral ureter obstruction can lead to kidney necrosis.
- Early intervention (e.g., removing the blockage within 48 hours) can lead to complete recovery.

Diagnosis: Defined by an increase in serum creatinine and/or a reduction in urine output.
Oliguria: Reduction of urine output to less than 400 mL/day, can occur within 1-7 days after injury, especially in ischemia cases where it may happen within 24 hours.
Anuria: Urine output less than 50 mL/day, typically seen in complete bilateral obstructions.
Non-oliguric AKI: Common with ATN or intrarenal causes.

Oliguric Phase: Decrease in urine output.
- Many people (50%) do not experience this phase, but it is critical for prognosis.
- Not solely indicative of AKI; further diagnostics needed.
Diuretic Phase: Kidneys start to excrete waste, resulting in hypovolemia and electrolyte loss; urine cannot be concentrated.
Recovery Phase: The timeline and quality depend on overall health, severity of AKI, and any complications.

Fluid Volume: Retention leading to distension and potential pulmonary edema or heart failure.
Metabolic Acidosis: Inability to excrete hydrogen ions results in acid build-up and decreased bicarbonate.
Sodium and Potassium Imbalance: Damaged tubules cannot conserve sodium, leading to high levels in urine and potential hyperkalemia, a serious complication.
Waste Product Accumulation: Increased levels of urea, impacting metabolic functions.
Neurological Disorders: Fatigue, cognitive disturbances due to uremia.

Urinalysis: May show casts, RBCs, WBCs, proteinuria, or abnormal electrolytes.
Imaging/Renal Biopsy: To identify underlying causes of AKI.

Introduction to Dialysis: Used to remove waste products and excess fluid due to kidney failure.
Types of Dialysis:
- Peritoneal Dialysis (PD): Involves infusing a dialysate solution into the peritoneum using a catheter.
  - Dwell Time: The period the solution remains in the abdomen to facilitate osmosis and diffusion.
  - Types of PD: Continuous ambulatory peritoneal dialysis (CAPD) and automated PD (APD).
  - Risks: Infection (peritonitis) and complications due to catheter placement.
- Hemodialysis (HD): Blood is filtered externally using a dialyzer.
  - Requires vascular access (fistula or graft).
  - Typically performed three times a week for several hours.
  - Complications may include hypotension, muscle cramps, thrombosis, and infections.
- Continuous Renal Replacement Therapy (CRRT): A slower method used for unstable patients, requiring special equipment.
  - Provides a more physiologic approach to filtering blood.
  - Nursing considerations include frequent hemofilter changes and careful monitoring.

Managing AKI and deciding on dialysis types involve assessing patient needs, symptoms, and underlying causes.
Education on treatment options and timely initiation of appropriate therapy is critical for patient outcomes.