renal Flashcards
What are prerenal causes of acute kidney injury (AKI)?
Prerenal causes reduce systemic circulation, decreasing renal blood flow and glomerular perfusion. Common causes include decreased cardiac output (e.g., cardiogenic shock, heart failure, MI), decreased peripheral vascular resistance (e.g., septic shock), decreased renovascular blood flow (e.g., embolism), and hypovolemia (e.g., dehydration).
What are intrarenal causes of AKI?
Intrarenal causes involve direct kidney tissue damage, impairing nephron function. Common causes include nephrotoxins (e.g., contrast media, aminoglycosides), prolonged ischemia, myoglobin from necrotic muscle cells, hemoglobin from hemolyzed RBCs, and interstitial nephritis (e.g., allergies to antibiotics and infections). Acute tubular necrosis (ATN) is the most common intrarenal cause, often due to sepsis, ischemia, or nephrotoxins.
What are postrenal causes of AKI?
Postrenal causes involve mechanical obstruction of urine outflow, leading to urine backup into the renal pelvis and impaired kidney function. Common causes include benign prostatic hyperplasia (BPH), prostate cancer, stones, extrarenal tumors, and trauma. Bilateral ureteral obstruction can cause hydronephrosis, tubular blockage, increased hydrostatic pressure, and progressive kidney decline.
What is the most common cause of intrarenal AKI in hospitalized patients?
Acute tubular necrosis (ATN) caused by ischemia, nephrotoxins, or sepsis accounts for 90% of intrarenal AKI cases in hospitals.
What are the three phases of AKI progression?
- Oliguric phase: Urine output <400 mL/day; fluid volume changes, metabolic acidosis, hyponatremia, hyperkalemia, leukocytosis, increased BUN/creatinine, neurologic problems (e.g., fatigue, seizures, stupor).
- Diuretic phase: Daily urine output 1-3 L (up to 5 L); fluid/electrolyte imbalance due to kidney’s inability to concentrate urine.
- Recovery phase: GFR improves, BUN/creatinine stabilize. Recovery can take up to 12 months, depending on overall health and injury severity.
What are the major electrolyte imbalances in AKI?
- Hyponatremia: Damaged tubules cannot conserve sodium, leading to excess urinary sodium excretion.
- Hyperkalemia: Impaired potassium excretion. Severe hyperkalemia may cause muscle weakness or ECG changes.
What happens in the oliguric phase of AKI?
- Urinary changes: Urine output <400 mL/day.
- Fluid volume changes: Hypovolemia may worsen; anuria or oliguria can lead to distended neck veins, edema, and hypertension.
- Metabolic acidosis: Impaired excretion of hydrogen ions.
- Electrolyte imbalance: Hyponatremia, hyperkalemia.
- Hematologic problems: Leukocytosis; infection is the most common cause of death.
- Waste accumulation: Increased BUN/creatinine.
- Neurologic issues: Fatigue, difficulty concentrating, stupor, coma, or seizures.
What occurs during the diuretic phase of AKI?
- Urine output increases to 1-3 L/day (may reach 5 L).
- Kidneys regain waste excretion ability but cannot concentrate urine.
- Hypotension and hypovolemia may result from excessive fluid loss.
- Phase lasts 1-3 weeks, with stabilization of acid-base, electrolyte, and BUN/creatinine levels by the end.
What marks the recovery phase of AKI?
The recovery phase begins when GFR increases, leading to decreased BUN and creatinine levels. Significant improvement occurs in the first 1-2 weeks, but it may take up to 12 months for full kidney function stabilization. Recovery depends on overall health and injury severity; some patients may progress to end-stage renal disease (ESRD).
What are diagnostic tests for AKI?
- History and physical exam.
- Identify the cause of AKI.
- Serum creatinine and BUN levels.
- Serum electrolytes.
- Urinalysis.
- Renal ultrasound.
- Renal scan.
- CT scan.
- RIFLE classification labs.
What medical treatments are used for AKI?
- Treat underlying cause.
- Dialysis if necessary.
- Continuous renal replacement therapy (CRRT) if necessary.
What are the interventions for managing AKI?
- Fluid restriction.
- Nutrition therapy: Adequate protein intake, enteral nutrition, parenteral nutrition, and dietary restrictions (e.g., potassium, phosphate, sodium).
- Measures to lower potassium (e.g., medications, dialysis).
- Calcium supplements or phosphate-binding agents.
What is chronic kidney disease (CKD)?
CKD involves the progressive, irreversible loss of kidney function over months to years. It is more common than acute kidney injury (AKI) due to aging populations and increasing rates of hypertension, diabetes, and obesity. CKD often goes unnoticed until significant nephron loss occurs, as the kidneys are highly adaptive.
What is CKD mineral and bone disorder pathophysiology?
- Decreased GFR and phosphate excretion lead to increased serum phosphate and vascular/soft tissue calcifications.
- Decreased activation of vitamin D impairs calcium absorption from the gut, leading to decreased serum calcium.
- Increased parathyroid hormone (PTH) causes osteitis fibrosa and bone demineralization, leading to osteomalacia.
- Bone demineralization increases serum calcium and phosphate, further contributing to vascular and soft tissue calcifications.
What are the risk factors for CKD?
- Age > 60 years
- Cardiovascular disease
- Diabetes
- Hypertension
- Ethnic minority
- Family history of CKD
- Exposure to nephrotoxic drugs
How does CKD affect the urinary system?
In the early stages, patients usually do not report changes in urine output. As CKD progresses, fluid retention becomes increasingly difficult to manage.
How does CKD affect the cardiovascular system?
CKD can cause hypertension (HTN), heart failure (HF), coronary artery disease (CAD), pericarditis, and peripheral artery disease (PAD).
What neurologic effects are seen in CKD?
Neurologic effects include fatigue, headache, sleep disturbances, and encephalopathy.
What musculoskeletal effects occur in CKD?
CKD causes vascular and soft tissue calcifications, osteomalacia, and osteitis fibrosa.
How does CKD affect the integumentary system?
CKD can cause pruritus, ecchymosis, and dry, scaly skin.
What diagnostic tests are used for CKD?
- History and physical exam
- Identification of reversible kidney disease
- Imaging: Renal ultrasound, renal scan, CT scan, renal biopsy
- Lab tests: BUN, serum creatinine, creatinine clearance, serum electrolytes, lipid profile, urinalysis, protein-to-creatinine ratio (first-morning void), hematocrit, and hemoglobin levels
What are the stages of CKD based on GFR?
- Stage 1: Kidney damage with normal/elevated GFR ≥ 90
- Stage 2: Kidney damage with mild decreased GFR 60-89
- Stage 3a: Moderately decreased GFR 45-59
- Stage 3b: Moderately decreased GFR 30-44
- Stage 4: Severely low GFR 15-29
- Stage 5: Kidney failure, GFR < 15 (or dialysis).
What medical treatments are used for CKD?
- Treat underlying cause
- Peritoneal dialysis
- Renal replacement therapy (RRT) with dialysis or kidney transplant
What are common drugs used in CKD management?
- Calcium supplementation and phosphate binders
- Antihypertensive therapy (ACE inhibitors, ARBs)
- Erythropoietin therapy
- Lipid-lowering drugs
- Adjust drug dosages to degree of renal function
What are nursing interventions for CKD?
- Correct fluid overload or deficit
- Nutrition therapy
- Measures to lower potassium
4o
