NR 325 Week 3 Acute Kidney Injury CAE PNCI Medical Surgical
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Chamberlain University
NR-325 Adult Health II
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Acute Kidney Injury (AKI): Pathophysiological Changes, Diagnostic Differentiation, and Management
Pathophysiology of Acute Kidney Injury
Acute kidney injury (AKI) refers to an abrupt decline in renal function that results in the accumulation of metabolic wastes, fluid imbalance, and disturbances in electrolyte regulation. One of the key mechanisms contributing to AKI is obstruction of urinary outflow, which impairs normal urine passage and leads to retrograde pressure in the renal pelvis. This process, known as hydronephrosis, causes dilation of the renal structures, an increase in hydrostatic pressure, and eventual tubular compression.
If obstruction is relieved within 48 hours, renal function is often restored, but prolonged blockage can cause permanent damage. Tubular epithelial cell death, disruption of the basement membrane, and ischemia-related injury result in tubular atrophy and fibrosis, both of which compromise long-term kidney function. Severe ischemic injury may cause loss of large portions of the tubular epithelium, worsening renal dysfunction.
Classification of AKI: Prerenal, Intrarenal, and Postrenal
AKI can be divided into three main categories depending on the underlying cause:
Prerenal AKI occurs when renal perfusion decreases, most commonly due to dehydration, hemorrhage, heart failure, or myocardial infarction. Shock states and neurologic injuries may also contribute.
Intrarenal AKI develops from direct damage to the renal parenchyma. Causes include nephrotoxic drugs (e.g., aminoglycosides, contrast agents), infections such as acute pyelonephritis, and autoimmune conditions like lupus nephritis.
Postrenal AKI results from urinary tract obstruction, frequently caused by benign prostatic hyperplasia (BPH), renal calculi, or neuromuscular disorders that impair bladder emptying.
What are the common signs and symptoms of AKI?
Patients with AKI often present with oliguria (decreased urine output), shortness of breath due to fluid overload, peripheral edema, chest discomfort, and fatigue. In advanced cases, neurological complications such as seizures or coma may occur due to severe electrolyte disturbances and uremia.
Electrolyte and Fluid Imbalances in AKI
Electrolyte abnormalities are hallmark features of AKI and may pose life-threatening risks:
Hyperkalemia results from impaired potassium excretion and metabolic acidosis. Patients may experience muscle weakness, bradycardia, and cardiac dysrhythmias.
Hyponatremia can arise from either excessive fluid retention or dehydration. Symptoms include confusion, irritability, dry mucous membranes, headache, and in severe cases, seizures.
Hypocalcemia is frequently associated with hyperphosphatemia due to reduced glomerular filtration. It manifests as tetany, muscle cramps, tingling sensations in the extremities or perioral region, and bronchospasms.
NR 325 Week 3 Acute Kidney Injury CAE PNCI Medical Surgical
Table 1: Overview of AKI Characteristics, Causes, Symptoms, and Imbalances
| Category | Description | Signs/Symptoms |
|---|---|---|
| Pathophysiology | Urinary obstruction leads to hydronephrosis, increased pressure, and impaired kidney function. | Tubular atrophy, kidney fibrosis, irreversible damage if prolonged. |
| Causes of AKI | – Prerenal: hypovolemia, heart failure, shock – Intrarenal: nephrotoxicity, infections, lupus – Postrenal: BPH, calculi, neuromuscular disorders | Oliguria, shortness of breath, edema, fatigue, seizures or coma in severe cases. |
| Electrolyte Imbalances | – Hyperkalemia: renal insufficiency, metabolic acidosis – Hyponatremia: dehydration, fluid overload – Hypocalcemia: increased phosphorus levels | Dysrhythmias, cramps, confusion, dry mucous membranes, tetany, bronchospasm. |
Management and Treatment of AKI
The cornerstone of AKI management is identifying and treating the underlying cause while supporting renal recovery. Care involves strict monitoring of fluid balance, serum electrolytes, and renal function markers.
Fluid Therapy: Restoring renal perfusion through IV fluids or diuretics (if fluid overload is present) helps optimize kidney function.
Electrolyte Management: Hyperkalemia may require IV insulin with glucose, sodium bicarbonate, or calcium gluconate to stabilize cardiac membranes. Sodium polystyrene sulfonate enemas or hemodialysis may be necessary for persistent cases.
Dialysis: Indicated when conservative measures fail or when life-threatening complications (e.g., severe hyperkalemia, uremia, or acidosis) occur. Dialysis provides rapid clearance of toxins and maintains fluid-electrolyte balance.
What nursing interventions are important in patients undergoing dialysis?
Nursing actions include maintaining aseptic technique during access site care, preventing compression or trauma to the vascular access, and monitoring for complications such as hypotension, disequilibrium syndrome, or infection. Nurses also play a key role in patient education, emphasizing proper hand hygiene, infection prevention, and adherence to prescribed medications.
How should infection risks, such as MRSA, be managed in AKI patients?
In patients with multidrug-resistant infections like MRSA, strict isolation precautions are essential. Nurses must provide meticulous wound care, educate patients about hygiene, and monitor for systemic infection signs. Preventing the spread of infection within healthcare facilities is a critical part of AKI management.
References
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. (2012). KDIGO clinical practice guideline for acute kidney injury. Kidney International Supplements, 2(1), 1–138.
National Institute for Health and Care Excellence. (2019). Acute kidney injury: Prevention, detection and management. NICE Guideline.
NR 325 Week 3 Acute Kidney Injury CAE PNCI Medical Surgical
Thomas, R., & Balogun, R. A. (2018). Dialysis modalities: An evidence-based review. Clinics in Chest Medicine, 39(3), 557–566. https://doi.org/10.1016/j.ccm.2018.04.009
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