Lecture 5 11.3 Renal Disorders Study Guide
Renal Disorders Overview
Introduction
Renal disorders discussed: Evaluation of kidney function, acute kidney injury (AKI), drug-induced kidney injury.
Emphasis on class participation through Turning Point questions (Session ID: AKI 2025).
Importance of Kidney Function
Essential for waste elimination from body to prevent toxicity.
Kidney function integral to medication adjustment.
Guidelines for class identification: 3 identifiers required for patient verification.
Key Laboratory Values
Memorization of lab values critical for NAPLEX and exams.
Variability in normal ranges across institutions acknowledged, e.g., Creatinine (0.6 to 1.2 mg/dL).
Evaluation of Kidney Function
Markers for Kidney Function
Blood urea nitrogen (BUN): Indicates waste filtration; varies with hydration status.
Elevated in dehydration due to increased urea reabsorption.
Creatinine: Muscle breakdown product; typically the best available kidney function marker.
Normal levels indicate kidney function but depend on muscle mass.
Higher muscle mass correlates with higher serum creatinine levels.
No reabsorption occurs in normal conditions; some 10% comes from tubular secretion.
Cystatin C: Newer renal marker not affected by muscle mass.
Ideal as a combination marker with creatinine for more accurate evaluation.
Estimating GFR (Glomerular Filtration Rate)
Normal GFR is ~120 mL/min; declines in renal insufficiency (
Correlation of GFR with blood markers: Increased BUN and serum creatinine with declining GFR.
Adjustments required in consideration of muscle mass, age, and nutritional status.
Introduction of newer equations like CKD-EPI without race as a factor.
Cockcroft-Gault equation still prevalent but requires serum creatinine at steady state.
Weight Considerations for Equations
Ideal body weight used generally; actual weight adjustments based on clinical scenarios for precision.
Adjusted body weight calculated when actual weight exceeds ideal by 30% or more.
Acute Kidney Injury (AKI)
Definition and Incidence
Sudden decrease in renal function leading to changes in creatinine, BUN, and urine output.
High incidence in hospitalized patients: 3-18.3% in non-critically ill; 30-60% in ICU settings.
Symptoms and Diagnosis
Often asymptomatic until significant Deterioration; leading indicators:
Drop in urine output precedes rise in serum creatinine.
Diagnostic criteria for AKI include:
Increase in serum creatinine by 0.3 mg/dL within 48 hours,
or a 1.5-fold increase within 7 days,
or urine output drop.
Phases of Renal Injury:
Pre-renal: Etiology before the kidneys resulting in decreased perfusion (dehydration, shock).
Common medications affecting blood flow: NSAIDs, ACE inhibitors, ARBs.
Intrinsic renal: Damage to renal tubules themselves; acute tubular necrosis common.
Post-renal: Obstruction of urinary flow from kidneys, e.g., stones.
Markers for AKI
BUN/creatinine ratios >20:1 indicative of pre-renal causes.
Fluid resuscitation and medication management are key supportive therapies.
Novel Biomarkers for Early Detection
Measurements such as Timp-2 and IGFBP7 can predict AKI risk, though not widely utilized in practice.
Management Strategies:
Fluids as first-line management; monitor intake/output.
Adjust medication dosing based on kidney function status.
Avoid nephrotoxic medications where possible.
Renal replacement therapy (dialysis) as a last resort for severe cases.
Pharmacologic Considerations
Drug Dosing Adjustments in AKI
Based on estimated GFR; medications given after dialysis may require readjustment.
Nephrotoxic Agents to Avoid
Common nephrotoxic drugs include NSAIDs, certain antibiotics (e.g., aminoglycosides), ACE inhibitors, ARBs under particular conditions.
Case Management in AKI
Insulin for glucose management in diabetic patients with AKI; targets for therapy established.
Pharmacological Correction Strategies
Use of loop diuretics for fluid overload without use to prevent AKI directly.
Patient Profiles in Management
Considerations differ significantly for populations including pediatrics and transplant patients.
Chronic Kidney Disease (CKD)
Definition and Stages
CKD defined by abnormal kidney function/structure persisting for 3+ months.
Classified by cause (most common: diabetes and hypertension) and stages based on GFR (1 through 5).
Importance of albuminuria in assessing kidney damage.
Clinical Presentation of CKD
Symptoms emerge in later stages; weight gain, edema, fatigue, anemia, itching, and alterations in urine output.
Laboratory Evaluations
Elevated levels of creatinine, BUN, potassium; low GFR indicative of renal impairment.
Management of CKD
Aims to slow progression of disease, typically through lifestyle modifications and pharmacologic interventions such as ACE inhibitors, ARBs, SGLT2 inhibitors, and tighter blood glucose control.
Preventative Strategies
Urged lifestyle changes (diet, exercise, smoking cessation) alongside pharmacotherapy.
Specific targets established for blood pressure (<120 systolic) and HbA1c levels (targeting 7% for diabetics).
Clinical Implications
Emphasis on prevention, recognition of renal decline early in course, and active monitoring of biomarkers.
Summary Considerations for CKD
The integral role of managing co-morbid chronic conditions to prevent deterioration of kidney function.
Coordination with care across specialties and attentive patient education.