Chronic Kidney Disease and Acute Kidney Injury
Chronic Kidney Disease (CKD)
CKD is a progressive, irreversible loss of kidney function with kidney damage or GFR < 60 mL/min/1.73 m² for >3 months.
There are 5 stages of CKD.
Prevalence: >26 million adults affected; about 1 out of 9 people. CKD is more common than AKI.
Leading causes: Diabetes (≈50%) and Hypertension (≈25%).
Other contributing factors: aging population, rising obesity, CVD risk factors, minority ethnicity (Native Americans and African Americans at highest risk), nephrotoxic drug exposure.
Often asymptomatic and underdiagnosed/untreated; prognosis highly variable.
Diabetes and hypertension are major drivers; management focuses on slowing progression and treating complications.
CKD: Definitions and Stages (GFR-based)
Stage 1: Kidney damage with normal or ↑ GFR ≥ 90; Diagnosis and treatment focus on CVD risk reduction and slowing progression.
Stage 2: Kidney damage with mild ↓ GFR 60–89; Estimation of progression.
Stage 3a: Moderate ↓ GFR 45–59; Evaluation and treatment of complications.
Stage 3b: Moderate ↓ GFR 30–44; More aggressive treatment of complications.
Stage 4: Severe ↓ GFR 15–29; Preparation for RRT (dialysis, kidney transplant).
Stage 5: Kidney failure < 15 (or dialysis); RRT if uremia present and patient desires treatment.
Equations/values summarized:
\text{Stage 1: GFR} \ge 90\,\text{mL/min/1.73 m}^2;
\text{Stage 2: }60 \le \text{GFR} \le 89;
\text{Stage 3a: }45 \le \text{GFR} \le 59;
\text{Stage 3b: }30 \le \text{GFR} \le 44;
\text{Stage 4: }15 \le \text{GFR} \le 29;
\text{Stage 5: }\text{GFR} < 15;Clinical trajectory varies; can progress to ESRD requiring dialysis or transplant.
CKD: Risk Factors
Age > 60 years
Cardiovascular disease (CVD)
Diabetes mellitus
Minority ethnicity
Exposure to nephrotoxic drugs
Family history of CKD
Hypertension (HTN)
CKD: Clinical Manifestations **KNOW IMAGE FROM SLIDE**
Affects all body systems; urinary and non-urinary signs
Urinary system: Early—no change in urine output (UO); Later—oliguria, fluid retention; diuretic therapy; dialysis may cause anuria.
Psychological: Depression, emotional lability, fatigue, lethargy; coping difficulties.
Reference: Fig 51.2 (12th edition).
CKD: Diagnostics
Matrix of staging and progression:
Stage 1: Kidney damage with normal or ↑ GFR ≥ 90
Stage 2: GFR 60–89
Stage 3a: GFR 45–59
Stage 3b: GFR 30–44
Stage 4: GFR 15–29
Stage 5: GFR < 15
Diagnostic components include:
Assessment of kidney damage and GFR trend
Estimation of progression risk and complication profiles
CKD: Interprofessional Care
Drug therapy targets several complications:
Hyperkalemia *
Hypertension *
CKD-MBD (mineral and bone disorder) → cannot convert D2 to D3 → calcium not absorbed.
Anemia
Dyslipidemia (often correlates with HTN)
STOP SMOKING
Nutrition Therapy: DASH DIET
Protein restriction (no keto diets)
Fluid restriction
600 ml (baseline) + whatever is lost in fluid over last 24 hours including blood, wound drainage, chest tube output, etc = fluid restriction next 24 hours.
Na (sodium) and K (potassium) restriction
Phosphate restriction
CKD: Nursing Management
Nursing process phases: Assessment → Clinical Problems → Planning/Goals → Implementation → Evaluation.
CKD: Nursing Assessment
Obtain a complete history (including OTC drugs, herbs, supplements).
Nephro-toxic drugs (ex. NSAIDS, vancomycin, etc)
Dietary assessment (quality of intake).
Height/weight and recent weight changes.
Measure I/Os daily
Review support systems and psychosocial factors.
CKD: Clinical Problems
Fluid imbalance
I/Os
Weight
Electrolyte imbalance
Potassium levels rise (can’t excrete)
Impaired cardiac function
Coping difficulties
CKD: Planning/Goals Priorities
Adhere to current treatment plan
Develop effective coping strategies
Maintain ADLs within limitations
CKD: Implementation
Health Promotion:
Identify at-risk populations (Diabetics, HTN, family history, repeated UTIs).
Screen with UA and GFR, routine BUN/creatinine.
Need more than one GFR to diagnosis CKD
Acute Care:
CKD managed primarily in outpatient settings; exceptions for complications or kidney transplant management.
Ambulatory Care:
Patient education (diet, medications, follow-up, ER precautions).
Dietitian involvement
Kidney transplant evaluation (ideally before dialysis)
Palliative care consult if needed
Emotional support.
CKD: Evaluation
Fluid and electrolyte levels within normal range.
Acceptable weight with no more than 10% weight loss.
CKD: Objectives (Summary)
Classify AKI using RIFLE acronym (not detailed here).
Describe AKI clinical course.
Explain interprofessional and nursing management of AKI.
Define CKD and delineate its 5 stages by GFR.
Identify CKD risk factors.
Describe CKD care and nursing management.
Distinguish among renal replacement therapy (RRT) options for ESRD.
Compare nursing interventions for peritoneal dialysis (PD) vs. hemodialysis (HD).
Explain the role of nurses in kidney transplant care.
Acute Kidney Injury (AKI)
AKI is loss of kidney function with or without loss of urine output; leads to rises in BUN, creatinine, and potassium (potassium elevation occurs).
Azotemia (buildup of nitrogenous waste in blood) may develop; onset can be days or hours; AKI is potentially reversible.
Affects ~1/5 hospitalized patients; ICU AKI mortality can be ~80%.
Causes categorized into three classes: Prerenal, Intrarenal, Postrenal.
AKI: Etiology and Pathophysiology
AKI results in elevated blood waste products and electrolyte abnormalities.
Development varies; azotemia can be rapid or gradual; potentially reversible with timely treatment.
Key measures include monitoring BUN, creatinine, K⁺, and acid-base status.
AKI: Prerenal
Cause: Reduction in systemic circulation leads to decreased renal blood flow and GFR (decreased perfusion to kidneys).
Features: Pre-renal oliguria; no parenchymal damage yet.
Common etiologies: Hypovolemia, heart failure, decreased cardiac output.
Autoregulatory mechanisms attempt to preserve organ perfusion.
Pathophysiology: Pre-renal azotemia; decreased sodium excretion; increased sodium and water retention; decreased urine output.
Prognosis: Reversible with prompt treatment; if untreated, may progress to intrarenal AKI.
AKI: Intrarenal
Cause: Damage to the renal parenchyma (impaired nephron function).
Mechanisms: Nephrotoxins causing tubular epithelial cell damage; hemoglobin and myoglobin can obstruct tubules and cause vasoconstriction.
Common condition: Acute tubular necrosis (ATN) due to ischemia (kidneys can’t get better = critical), nephrotoxins, or sepsis.
Risk factors for ATN: Major surgery, shock, transfusion reactions, trauma, prolonged hypotension.
Potential for reversibility remains possible but less predictable.
Other intrarenal diseases: Acute glomerulonephritis, systemic lupus erythematosus.
Oliguria often persists.
AKI: Postrenal
Cause: Mechanical obstruction of urine outflow leading to backpressure and tubular damage.
Common etiologies: Benign prostatic hyperplasia (BPH), prostate cancer, stones, trauma, tumors; bilateral ureteral obstruction.
Bilateral Urethras Obstruction Consequences: Hydronephrosis, increased hydrostatic pressures, tubular blockages, declining kidney function.
Prognosis: If obstruction treated within ~48 hours, recovery is probable; otherwise irreversible kidney fibrosis and tubular atrophy.
Contribution: Accounts for <10% of AKI cases.
AKI: Clinical Manifestations (3 Phases)
Oliguric Phase (Occurs within 1-7 days):
Urinary changes: Reduced urine output.
Fluid volume overload symptoms.
Metabolic acidosis develops; sodium balance disturbed; potassium excess.
Hematologic, neurologic problems; waste products accumulate.
Diuretic Phase (Being Treated → kidneys getting better):
Increased urine output (daily 1–3 L, up to 5 L/day) = high volume of UO.
Hyponatremia and hypokalemia risk; dehydration can occur.
ABGs and BUN/Cr stabilize.
Typically lasts 1–3 weeks.
Recovery Phase:
GFR begins to rise; BUN/Cr decrease.
Significant improvement may occur in first 1–2 weeks; complete stabilization can take up to 12 months.
Older adults have poorer recovery odds; some progress to ESRD; those who recover may still have early CKD.
AKI: Diagnostic Assessment
History and physical to identify cause.
Laboratory tests: Serum creatinine, BUN (first to change along with GFR); Serum electrolytes
Urinalysis: Sediment with cells, casts, or proteins suggests intrarenal disorders; urine osmolality, sodium content, and specific gravity help identify causes.
Imaging/biopsy: Renal ultrasound, renal biopsy, CT scan w/out contrast as indicated.
AKI: Interprofessional Care
Treat underlying cause; avoid nephrotoxins.
Fluid management: Fluid restriction (rough target ~600 mL plus prior 24-hour fluid losses). **
Nutrition: Oral, enteral, or parenteral nutrition with adequate protein (0.8–1.0 g/kg/day).
Diet restrictions: Potassium, phosphate (calcification), sodium (edema and HF risk); adjust based on levels.
Electrolyte management: Lower potassium with insulin IV, sodium bicarbonate, calcium gluconate as needed to lower potassium.
Dialysis options if indicated: Peritoneal dialysis (PD), Hemodialysis (HD), Continuous Renal Replacement Therapy (CRRT).
Dialysis indications and modality choice depend on hemodynamic status, uremia, electrolyte disturbances, and patient goals.
AKI: Clinical Problems
Electrolyte imbalances
Fluid imbalances
Risk for infection
Anxiety
AKI: Nursing Assessment
Daily weights and vital signs; strict intake/output monitoring.
Urine assessment: Color, specific gravity, glucose, protein, blood, sediment.
Assessment of overall appearance, edema, neck vein distention, bruising.
Monitoring dialysis access site (if applicable).
Mental status (fluctuates with sodium), oral mucosa hydration, lung and heart assessment (S3, murmurs, pericardial rub).
ECG review and labs/diagnostics review.
AKI: Goals/Planning
Achieve complete recovery of kidney function when possible.
Maintain normal fluid and electrolyte balance.
Reduce anxiety and ensure follow-up care.
AKI: Implementation
Health Promotion:
Identify high-risk populations; prevent nephrotoxic exposure; prevent prolonged hypotension/hypovolemia.
At-risk groups include older adults, major trauma/surgery, heart failure, sepsis, burns, CKD.
Monitor weight, I&O, fluid/electrolyte balance; replace significant losses.
Monitor kidney function; infection prevention = AKI may blunt febrile response.
Renal dosing adjustments if medications are renally cleared (no nephrotoxins); skin and oral care.
AKI: Evaluation
Regain and maintain normal fluid/electrolyte balance.
Adhere to treatment regimen.
Have no or minimal complications.
Achieve complete recovery when possible.
Dialysis
Dialysis is a technique where substances move from blood through a semipermeable membrane into a dialysis solution (dialysate).
Goals: Correct fluid/electrolyte imbalances; remove waste.
Two main types: Peritoneal dialysis (PD) and Hemodialysis (HD); Continuous Renal Replacement Therapy (CRRT) is also used in some settings.
Dialysis is started when uremia cannot be adequately managed with conservative therapy, typically when GFR < 15 mL/min/1.73 m².
Peritoneal Dialysis (PD)
Catheter placement through the anterior abdominal wall.
Dialysate infused into the peritoneal space.
Three phases per exchange:
Inflow (fill)
Dwell (equilibration)
Drain
One exchange takes about 30–50 minutes; several exchanges per day depending on system.
Systems include Automated PD (APD) and Continuous Ambulatory PD (CAPD).
Complications: Site infection, peritonitis, hernias, bleeding, back pain, protein loss, pulmonary issues.
Hemodialysis (HD)
Requires arteriovenous (AV) access: AV fistulas or AV grafts.
Assessment: Thrill (palpable) and bruit (audible). **
Healing time: 2–4 weeks for fistulas; grafts have higher infection and thrombosis risk and may need removal.
Procedure: One needle draws blood from circulation to HD machine; the other returns dialyzed blood to the patient.
Complications: Hypotension, muscle cramps, blood loss, hepatitis.
Continuous Renal Replacement Therapy (CRRT)
Used to treat AKI in hemodynamically unstable patients.
Uremia toxins and excess fluids are removed while acid-base/electrolytes are corrected slowly and continuously over ~24 hours.
Slower rate improves hemodynamic stability; can be used for 30–40 days if needed.
Contraindicated in life-threatening conditions requiring rapid correction.
May be used with HD; access typically via dual-lumen catheter in jugular or femoral vein.
Many types exist; choice depends on patient needs.
Kidney Transplant
Best option for ESRD when feasible.
Waitlist: >120,000 with donor shortage; average cadaver kidney wait 2–5 years; live donor wait is longer.
>90% success rate; most people die waiting for transplant if not transplanted.
Nursing Management:
Pre- and post-operative care.
Immunosuppressive therapy management for life.
Transplant-related complications: Rejection, infection, cardiovascular disease (CVD), cancer, CKD recurrence, steroid complications.
Test Your Knowledge (NCLEX-style Questions)
NCLEX Question #1: When a patient is in the diuretic phase of AKI, which serum electrolyte imbalances should the nurse monitor?
a. hyperkalemia and hyponatremia
b. hyperkalemia and hypernatremia
c. hypokalemia and hyponatremia
d. hypokalemia and hypernatremia
NCLEX Question #2: Nurses can screen patients at risk for developing CKD, recognizing CKD is characterized by:
a. progressive irreversible destruction of the kidneys.
b. a rapid decrease in urine output with an elevated BUN.
c. an increasing creatinine clearance with a decrease in urine output.
d. prostration, somnolence, and confusion with coma and imminent death.
NCLEX Question #3: At-risk groups for CKD include (SATA): Older Black patients; Patients >60 years old; History of pancreatitis; History of hypertension; History of type 2 diabetes (T2DM).
NCLEX Question #4: An ESRD patient considering kidney transplant: which statement is true?
a. Successful transplant usually provides better quality of life than dialysis.
b. If rejection occurs, no further treatment for renal failure is available.
c. HD replaces normal kidney functions, so there is no fear of rejection.
d. Immunosuppressive therapy after transplant makes the person ineligible for other treatments if the kidney fails.
NCLEX Question #5: A kidney transplant recipient has fever, chills, and dysuria for 2 days. What is the first action?
a. Assess temperature and start a workup to rule out infection.
b. Reassure the patient this is common after a transplant.
c. Provide warm covers and give acetaminophen.
d. Notify the nephrologist that there are manifestations of acute rejection.
Notes:
All numerical values, stages, and ranges are included as shown in the transcript. LaTeX formatting has been used for important numerical expressions and stage definitions (e.g., GFR thresholds and phase descriptions).
Figures and tables referenced in the transcript (e.g., Fig 51.2, Fig 51.4, Figures 51.5–51.7, 51.12–51.14) are acknowledged but not reproduced here; the notes summarize the concepts they represent.