Acute Pyelonephritis

Acute Pyelonephritis 150 150 Tony Guo

Acute Pyelonephritis

  • Etiology and Pathophysiology
    • Inflammation of renal parenchyma and collecting system (including the renal pelvis)
    • Most common cause is bacterial infection
    • Fungi, protozoa, or viruses can also infect kidneys
    • Cortical surface shows grayish white areas of inflammation and abscess formation

 

  • Urosepsis

 

  • Systemic infection from urologic source
  • Prompt diagnosis/treatment critical 
    • Can lead to septic shock and death unless promptly treated
  • Usually begins with colonization and infection of lower tract via ascending urethral route
  • Frequent causes 
    • Escherichia coli
    • Proteus
    • Klebsiella
    • Enterobacter
  • Preexisting factor usually present
    • Vesicoureteral reflux
      • Retrograde (backward) movement of urine from lower to upper urinary tract
    • Dysfunction of lower urinary tract
      • Obstruction from BPH
      • Stricture
      • Urinary stone
    • CAUTI
  • Clinical manifestations
    • Mild fatigue
    • Chills
    • Fever
    • Vomiting
    • Malaise
    • Flank pain
    • LUTS characteristic of cystitis
      • Dysuria, urgency, frequency
    • Costovertebral tenderness to percussion typically present on affected side
    • Manifestations may subside in a few days, even without therapy
      • Bacteriuria and pyuria still persist
  • Diagnostic Studies
    • History and physical examination
      • Palpation for CVA pain
    • Laboratory tests
      • Urinalysis
      • Urine for culture and sensitivity
      • CBC with WBC differential
      • Blood culture (if bacteremia is suspected)
    • Ultrasound
    • CT Scan
  • Interprofessional Care
    • Hospitalization for patients with severe infections and complications 
      • Such as nausea and vomiting with dehydration
    • Signs/symptoms typically improve within 48 to 72 hours after therapy starts
    • Drug therapy
      • Antibiotics
        • Parenteral administration in hospital to rapidly establish high drug levels
      • NSAIDs or antipyretic drugs
        • Fever
        • Discomfort
      • Urinary analgesics
    • Relapses may be treated with 6-week course of antibiotics
      • Antibiotic prophylaxis may be used for recurrent infection
      • Follow-up urine culture and imaging studies
    • Urosepsis is characterized by bacteriuria and bacteremia
      • Close observation and vital sign monitoring are essential
      • Prompt recognition and treatment of septic shock may prevent irreversible damage or death

Nursing Management

  • Nursing Assessment
    • Mild Symptoms
      • Outpatient management or short hospitalization
        • Adequate fluid intake
        • Nonsteroidal anti-inflammatory drugs (NSAIDs) or antipyretic drugs
        • Follow-up urine culture and imaging studies
    • Severe Symptoms
      • Hospitalization
      • Adequate fluid intake (parenteral initially; switch to oral fluids as nausea, vomiting, and dehydration subside)
      • NSAIDs or antipyretic drugs to reverse fever and relieve discomfort
      • Follow-up urine culture and imaging studies
  • Nursing Planning
    • The overall goals are that the patient with pyelonephritis will have 
      • Normal renal function
      • Normal body temperature
      • No complications
      • Relief of pain
      • No recurrence of symptoms
  • Nursing Implementation
    • Nursing interventions vary depending on the severity of symptoms. 
    • These interventions include teaching the patient about the disease process with emphasis on
      • Continuing medications as prescribed
      • Having a follow-up urine culture
      • Recognizing manifestations of recurrence or relapse
      • In addition to antibiotic therapy, encourage the patient to drink at least eight glasses of fluid every day, even after the infection has been treated. 
      • Rest will increase patient comfort.

 

Acute Kidney Injury and Chronic Kidney Disease

 

Comparison of Acute Kidney Injury and Chronic Kidney Disease

Acute Kidney Injury Chronic Kidney Disease
Onset Sudden  Gradual, often over many years
Most common cause Acute tubular necrosis Diabetic nephropathy
Diagnostic criteria Acute reduction in urine output and/or Elevation in serum creatinine GFR <60 mL/min/1.73 m2 for >3 mo. and/or Kidney damage >3 mo.
Reversibility Potentially Progressive and irreversible
Primary cause of death Infection Cardiovascular disease

  • Acute Kidney Injury
    • Causes of Acute Kidney Disease
      • Prerenal
      • Intrarenal
      • Postrenal 
    • Etiology and Pathophysiology
      • Prerenal
        • Causes are factors that reduce systemic circulation, causing reduction in renal blood flow
          • Severe dehydration, heart failure, lowered CO
        • Decreases glomerular filtration rate
          • Causes oliguria
        • Autoregulatory mechanisms attempt to preserve blood flow
      • Intrarenal
        • Causes include conditions that cause direct damage to kidney tissue
          • Prolonged ischemia, nephrotoxins
          • Hemoglobin released from hemolyzed RBCs
          • Myoglobin released from necrotic muscle cells
        • Acute tubular necrosis (ATN)
          • Results from ischemia, nephrotoxins, or sepsis
          • Severe ischemia causes disruption in basement membrane
          • Nephrotoxic agents cause necrosis of tubular epithelial cells
          • Potentially reversible
      • Postrenal
        • Causes include mechanical obstruction of outflow
          • Benign prostatic hyperplasia
          • Prostate cancer
          • Calculi
          • Trauma
          • Extrarenal tumors
          • Bilateral ureteral obstruction
Common Causes of Acute Kidney Injury
Prerenal Intrarenal Postrenal
Hypovolemia Nephrotoxic Injury
  • Dehydration
  • Hemorrhage
  • GI losses (diarrhea, vomiting)
  • Excessive diuresis
  • Hypoalbuminemia
  • Burns
  • Drugs: aminoglycosides (gentamicin, amikacin), amphotericin B
  • Contrast media
  • Hemolytic blood transfusion reaction
  • Severe crush injury
  • Chemical exposure: ethylene glycol, lead, arsenic, carbon tetrachloride
  • Benign prostatic hyperplasia
  • Bladder cancer
  • Calculi formation
  • Neuromuscular disorders
  • Prostate cancer
  • Spinal cord disease
  • Strictures
  • Trauma (back, pelvis, perineum)
Decreased Cardiac Output Interstitial Nephritis
  • Cardiac dysrhythmias
  • Cardiogenic shock
  • Heart failure
  • Myocardial infarction
  • Allergies: antibiotics (sulfonamides, rifampin), nonsteroidal anti-inflammatory drugs, ACE inhibitors
  • Infections: bacterial (acute pyelonephritis), viral (CMV), fungal (candidiasis)
Decreased Peripheral Vascular Resistance Other Causes
  • Anaphylaxis
  • Neurologic injury
  • Septic shock
  • Prolonged prerenal ischemia
  • Acute glomerulonephritis
  • Thrombotic disorders
  • Toxemia of pregnancy
  • Malignant hypertension
  • Systemic lupus erythematosus
Decreased Renovascular Blood Flow
  • Bilateral renal vein thrombosis
  • Embolism
  • Hepatorenal syndrome
  • Renal artery thrombosis

 

  • Clinical Manifestations
    • RIFLE classification
      • Risk (R)
      • Injury (I)
      • Failure (F)
      • Loss (L)
      • End-stage renal disease (E)
Stage GFR Criteria Urine Output Criteria Clinical Example
Risk Serum creatinine increased × 1.5

OR

GFR decreased by 25%

Urine output <0.5 mL/kg/hr for 6 hr 68-yr-old African American woman with type 2 diabetes, hypertension, CAD, and CKD.

Scheduled to undergo emergency coronary artery bypass graft.

Serum creatinine is 1.8 mg/dL (increased) and she weighs 60 kg.

Calculated GFR is 35 mL/min/1.73 m2.

She has Stage 3b CKD.

Injury Serum creatinine increased × 2

OR

GFR decreased by 50%

Urine output <0.5 mL/kg/hr for 12 hr During surgery, she experiences hypotension for a sustained period.

Acute tubular necrosis is diagnosed.

After surgery: Serum creatinine is 3.6 mg/dL and urine output is reduced to 28 mL/hr

Failure Serum creatinine increased × 3

OR

GFR decreased by 75%

OR

Serum creatinine >4 mg/dL with

acute rise ≥0.5 mg/dL

Urine output <0.3 mL/kg/hr for 24 hr (oliguria)

OR

Anuria for 12 hr

72 hours after surgery and in ICU develops ventilator-associated pneumonia and sepsis.

Serum creatinine rises to 5.2 mg/dL and urine output drops to 10 mL/hr.

BP remains low despite dopamine therapy.

Loss Persistent acute kidney failure.

Complete loss of kidney function >4 wk

Continuous venovenous hemodialysis is started.

After 3 wk of therapy she has a cardiopulmonary arrest and does not survive.

End-Stage

Renal Disease

Complete loss of kidney function >3 mo

 

  • Oliguric phase
    • Urinary changes- oliguria
      • Urinary output less than 400 mL/day
      • Occurs within 1 to 7 days after injury
      • Lasts 10 to 14 days
      • Urinalysis may show casts, RBCs, WBCs
    • Fluid volume
      • Hypovolemia may exacerbate AKI
      • Decreased urine output leads fluid retention
        • Neck veins distended
        • Bounding pulse
        • Edema
        • Hypertension
      • Fluid overload can lead to heart failure, pulmonary edema, and pericardial and pleural effusions
    • Metabolic acidosis
      • Impaired kidney cannot excrete hydrogen ions
      • Serum bicarbonate production is decreased
      • Severe acidosis develops
        • Kussmaul respirations
    • Sodium balance
      • Increased excretion of sodium
      • Hyponatremia can lead to cerebral edema
    • Potassium excess
      • Impaired ability of kidneys to excrete potassium
      • Increased risk with massive tissue trauma
      • Usually asymptomatic
      • ECG changes
    • Hematologic disorders
      • Leukocytosis
    • Waste product accumulation
      • Elevated BUN and serum creatinine levels
    • Neurologic disorders
      • Fatigue and difficulty concentrating
      • Seizures, stupor, coma
  • Diuretic phase
    • Daily urine output is 1 to 3 L
    • May reach 5 L or more
    • Monitor for hyponatremia, hypokalemia, and dehydration
  • Recovery phase
    • May take up to 12 months for kidney function to stabilize
  • Diagnostic studies 
    • Thorough history and physical examination
    • Identification of precipitating cause
    • Serum creatinine and BUN levels
    • Serum electrolytes
    • Urinalysis
    • Kidney ultrasonography
    • Renal scan
    • CT scan
    • Renal biopsy
    • Contraindicated
      • MRI with gadolinium contrast medium
      • Magnetic resonance angiography (MRA) with gadolinium contrast medium
        • Nephrogenic systemic fibrosis 
        • Contrast-induced nephropathy (CIN)
  • Management
    • Treatment of precipitating cause
    • Fluid restriction (600 mL plus previous 24-hr fluid loss)
    • Nutritional therapy
    • Adequate protein intake (0.6-2 g/kg/day) depending on degree of catabolism
    • Enteral nutrition
    • Parenteral nutrition
    • Dietary restrictions (potassium, phosphate, sodium)
    • Measures to lower potassium (if elevated) 
      • Therapies for Elevated Potassium levels
        • Regular Insulin IV
          • Potassium moves into cells when insulin is given.
          • IV glucose is given concurrently to prevent hypoglycemia.
          • When effects of insulin diminish, potassium shifts back out of cells.
        • Sodium Bicarbonate
          • Therapy can correct acidosis and cause a shift of potassium into cells.
        • Calcium Gluconate IV
          • Generally used in advanced cardiac toxicity (with evidence of hyperkalemic ECG changes).
          • Calcium raises the threshold for excitation, resulting in dysrhythmias.
        • Hemodialysis
          • Most effective therapy to remove potassium.
          • Works within a short time.
        • Sodium Polystyrene Sulfonate (Kayexalate)
          • Cation-exchange resin is administered by mouth or retention enema.
          • When resin is in the bowel, potassium is exchanged for sodium.
          • Therapy removes 1 mEq of potassium per gram of drug.
          • It is mixed in water with sorbitol to produce osmotic diarrhea, allowing for evacuation of potassium-rich stool from body.
        • Dietary Restriction
          • Potassium intake is limited to 40 mEq/day.
          • Primarily used to prevent recurrent elevation. Not used for acute elevation.
        • Patiromer (Veltassa)
          • Oral suspension that binds potassium in GI tract.
          • It is used to treat chronic kidney disease.
          • It should not be used as an emergency drug for life-threatening hyperkalemia.
    • It has a delayed onset of action.
    • Calcium supplements or phosphate-binding agents
    • Initiation of dialysis (if necessary)
    • Continuous renal replacement therapy (if necessary)
  • Interprofessional Care 
    • Primary goals
      • Eliminate cause 
      • Manage signs and symptoms
      • Prevent complications
    • Ensure adequate intravascular volume and cardiac output
      • Force fluids
      • Loop diuretics (e.g., furosemide [Lasix])
      • Osmotic diuretics (e.g., mannitol)
    • Closely monitor fluid intake during oliguric phase
    • Hyperkalemia
      • Insulin and sodium bicarbonate
      • Calcium carbonate
      • Sodium polystyrene sulfonate (Kayexalate)
    • Indications for renal replacement therapy (RRT)
      • Volume overload
      • Elevated serum potassium level
      • Metabolic acidosis 
      • BUN level > 120 mg/dL (43 mmol/L)
      • Significant change in mental status
      • Pericarditis, pericardial effusion, or cardiac tamponade
    • Renal replacement therapy (RRT)
      • Peritoneal dialysis (PD)
        • Not frequently used
      • Intermittent hemodialysis (HD)
      • Continuous renal replacement therapy (CRRT)
        • Cannulation of artery and vein
    • Nutritional therapy
      • Maintain adequate caloric intake
        • Primarily carbohydrates and fat
        • Limited protein
      • Restrict sodium
      • Increase dietary fat
      • Enteral nutrition

Nursing Management

  • Nursing Assessment
    • Measure vital signs
    • Measure fluid intake and output
    • Examine urine
    • Assess general appearance
    • Observe dialysis access site
    • Mental status/level of consciousness
    • Oral mucosa
    • Lung sounds
    • Heart rhythm
    • Laboratory values
    • Diagnostic test results
  • Nursing Diagnoses
    • Risk for infection related to invasive lines, uremic toxins, and altered immune responses secondary to kidney injury
    • Excess fluid volume related to kidney injury and fluid retention
    • Fatigue related to anemia, metabolic acidosis, and uremic toxins
    • Anxiety related to disease processes, therapeutic interventions, and uncertainty of prognosis
    • Potential complication: dysrhythmias related to electrolyte imbalances
  • Nursing Planning
    • The patient with AKI will
      • Completely recover without any loss of kidney function
      • Maintain normal fluid and electrolyte balance
      • Have decreased anxiety
      • Adhere to and understand need for careful follow-up care
  • Nursing Implementation
    • Health Promotion
      • Identify and monitor populations at high risk 
      • Control exposure to nephrotoxic drugs and industrial chemicals
      • Prevent prolonged episodes of hypotension and hypovolemia
      • Measure daily weight
      • Monitor intake and output
      • Monitor electrolyte balance
      • Replace significant fluid losses
      • Provide aggressive diuretic therapy for fluid overload
      • Use nephrotoxic drugs sparingly
    • Acute Care
      • Accurate intake and output 
      • Daily weights
      • Assess for signs of hypervolemia or hypovolemia
      • Assess for potassium and sodium disturbances
      • Meticulous aseptic technique
      • Careful use of nephrotoxic drugs
      • Skin care measures/mouth care
    • Ambulatory Care
      • Regulate protein and potassium intake
      • Follow-up care
      • Teaching the patient the signs and symptoms of recurrent kidney disease
      • Appropriate referrals for counseling
        • If the kidneys do not recover, the patient will need to transition to life on chronic dialysis or possible future transplantation
    • Evaluation
      • The expected outcomes are that the patient with AKI will
        • Regain and maintain normal fluid and electrolyte balance
        • Adhere to the treatment regimen
        • Experience no complications
        • Have complete recovery
  • Gerontologic considerations
    • More susceptible to AKI
      • Dehydration
        • Polypharmacy- diuretics, laxatives
        • Illness and immobility
    • Hypotension
    • Diuretic therapy
    • Aminoglycoside therapy
    • Obstructive disorders
    • Surgery
    • Infection

 

  • Chronic Kidney Disease
    • Progressive, irreversible loss of kidney function
    • Mortality rates are as high as 19% to 24% for individuals with ESRD on dialysis
    • Many different causes, the leading causes are 
      • Diabetes (about 50%) 
      • Hypertension (about 25%).
    • Less common etiologies include glomerulonephritis, cystic diseases, and urologic diseases.
  • Stages of Chronic Kidney Disease
Description GFR (mL/min/1.73 m2)  Clinical Action Plan
Stage 1

Kidney damage with normal or increased GFR

≥90  Diagnosis and treatment

CVD risk reduction

Slow progression

Stage 2

Kidney damage with mild decreased GFR

60-89  Estimation of progression
Stage 3a

Moderate decreased GFR

45-59 Evaluation and treatment of complications
Stage 3b

Moderate decreased GFR

30-44  More aggressive treatment of complications
Stage 4

Severe decreased GFR

15-29 Preparation for renal replacement therapy (dialysis, kidney transplant)
Stage 5

Kidney failure

<15 (or dialysis) Renal replacement therapy (if uremia present and patient desires treatment)

 

  • Clinical Manifestations
    • Result of retained 
      • Urea
      • Creatinine
      • Phenols
      • Hormones
      • Electrolytes
      • Water
    • Uremia is a syndrome in which kidney function declines to the point that symptoms may develop in multiple body systems
    • Manifestations of uremia vary among patients according to the cause of the kidney disease, co-morbid conditions, age, and degree of adherence to the prescribed medical regimen
    • Cultural and ethnic health disparities
      • Chronic kidney disease (CKD) has a high incidence in minority populations, especially African Americans and Native Americans.
      • Hypertension and diabetes mellitus are also more common in African Americans and Native Americans.
        • African Americans 
          • The risk of CKD as a complication of hypertension is significantly increased in African Americans.
          • African Americans have the highest rate of CKD, nearly four times that of whites.
        • Native Americans
          • Native Americans have a rate of CKD twice that of whites.
          • The rate of CKD is six times higher among Native Americans with diabetes than among other ethnic groups with diabetes.
        • Hispanics
          • The rate of CKD in Hispanics is 1.5 times higher than in non-Hispanic whites.
    • Urinary system
      • In the early stages of CKD, patients usually do not report any change in urine output
      • Since diabetes is the primary cause of CKD, polyuria may be present, but not necessarily as a consequence of kidney disease
      • As CKD progresses, patients have increasing difficulty with fluid retention and require diuretic therapy
      • Anuria may develop after a period on dialysis
    • Metabolic Disturbances
      • Waste Product Accumulation. 
        • As the GFR decreases, the BUN and serum creatinine levels increase. 
        • The BUN is increased not only by kidney disease but also by protein intake, fever, corticosteroids, and catabolism. 
        • For this reason, serum creatinine clearance determinations (calculated GFR) are considered more accurate indicators of kidney function than BUN or creatinine. 
        • Significant elevations in BUN contribute to development of nausea, vomiting, lethargy, fatigue, impaired thought processes, and headaches.
      • Altered Carbohydrate Metabolism. 
        • Defective carbohydrate metabolism is caused by impaired glucose metabolism, resulting from cellular insensitivity to the normal action of insulin.
      • Mild to moderate hyperglycemia and hyperinsulinemia may occur.
    • Possible clinical manifestations of chronic kidney disease
Body System Manifestations
  1. Psychologic
  • Anxiety
  • Depression
  1. Neurologic
  • Fatigue
  • Headache
  • Sleep disturbances
  • Encephalopathy
  1. Ocular
  • Hypertensive retinopathy
  1. Cardiovascular
  • Hypertension
  • Heart failure
  • Coronary artery disease
  • Pericarditis
  • Peripheral artery disease
  1. Pulmonary
  • Pulmonary edema
  • Uremic pleuritis
  • Pneumonia
  1. Gastrointestinal
  • Anorexia
  • Nausea
  • Vomiting
  • Gastrointestinal bleeding
  • Gastritis
  1. Endocrine/Reproductive
  • Hyperparathyroidism
  • Thyroid abnormalities
  • Amenorrhea
  • Erectile dysfunction
  1. Integumentary
  • Pruritus
  • Ecchymosis
  • Dry, scaly skin
  1. Musculoskeletal
  • Vascular and soft tissue calcifications
  • Osteomalacia
  • Osteitis fibrosa
  1. Metabolic
  • Carbohydrate intolerance
  • Hyperlipidemia
  1. Hematologic
  • Anemia
  • Bleeding
  • Infection
  1. Peripheral neuropathy
  • Paresthesias
  • Restless legs syndrome

 

  • Diagnostic studies
    • History and physical examination
    • Identification of reversible kidney disease
    • Renal ultrasound, renal scan, CT scan
    • Renal biopsy
    • BUN, serum creatinine, and creatinine clearance levels
    • Serum electrolytes
    • Lipid profile
    • Urinalysis
    • Protein-to-creatinine ratio in first morning voided specimen
    • Hematocrit and hemoglobin levels
  • Management
    • Correction of extracellular fluid volume overload or deficit
    • Renal replacement therapy (dialysis, kidney transplant)
    • Nutritional therapy 
    • Measures to lower potassium 
  • Drug Therapy
    • Calcium supplementation, phosphate binders, or both
    • Antihypertensive therapy
    • Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs)
    • Erythropoietin therapy
    • Lipid-lowering drugs
    • Adjustment of drug dosages to degree of renal function
  • Risk factors for Chronic Kidney Disease
Risk Factors Prevention and Management
Diabetes Achieve optimal glycemic control.
Hypertension Maintain BP in normal range with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs).
Age >60 yr. Prevent insult or injury to kidneys.
Cardiovascular disease Institute aggressive risk factor reduction.
Family history of CKD Teach about increased risk and assist with appropriate screening (BP measurement, urinalysis).
Exposure to nephrotoxic drugs Limit exposure and give sodium bicarbonate as treatment.
Ethnic minority (e.g., African American, Native American) Teach about increased risk and assist with appropriate screening (BP measurement, urinalysis).

 

  • Nutritional therapy
    • Protein restrictions
      • Calorie-protein malnutrition is a potential and serious problem that results from altered metabolism, anemia, proteinuria, anorexia, and nausea
      • Additional factors leading to malnutrition include depression and complex diets that restrict protein, phosphorus, potassium, and sodium.
      • Frequent monitoring of laboratory parameters, especially serum albumin, prealbumin (may be a better indicator of recent or current nutritional status than albumin), and ferritin, and anthropometric measurements are necessary to evaluate nutritional status
    • Fluid restrictions
      • Water and any other fluids are not routinely restricted in patients with CKD stages 1 to 5 who are not receiving HD
      • Use of diuretics to reduce fluid retention
      • Patients on HD are on more restriction and depends on daily urine output
    • Sodium and Potassium restrictions
      • Sodium-restricted diets may vary from 2 to 4 g/day.
      • Instruct the patient to avoid high-sodium foods, such as cured meats, pickled foods, canned soups and stews, frankfurters, cold cuts, soy sauce, and salad dressings
      • Potassium restriction depends on the kidneys’ ability to excrete potassium. 
      • Salt substitutes should be avoided in potassium-restricted diets because they contain potassium chloride.
      • High-Potassium foods
Fruits Vegetables Other Foods
  • Apricot, raw (medium)
  • Avocado ( 114 whole)
  • Banana ( 114 whole)
  • Cantaloupe
  • Dried fruits
  • Grapefruit juice
  • Honeydew
  • Orange (medium)
  • Orange juice
  • Prunes
  • Raisins
  • Baked beans
  • Butternut squash
  • Refried beans
  • Black beans
  • Broccoli, cooked
  • Carrots, raw
  • Greens, except kale
  • Mushrooms, canned
  • Potatoes, white and sweet
  • Spinach, cooked
  • Tomatoes or tomato products
  • Vegetable juices
  • Bran or bran products
  • Chocolate (1.5-2 oz)
  • Granola
  • Milk, all types (1 cup)
  • Nutritional supplements (use only under the direction of physician or dietitian)
  • Nuts and seeds (1 oz)
  • Peanut butter (2 Tbsp)
  • Salt substitutes, Lite Salt
  • Salt-free broth
  • Yogurt

 

  • Phosphate restrictions
    • As kidney function deteriorates, phosphate elimination by the kidneys is diminished and the patient begins to develop hyperphosphatemia.
    • Foods that are high in phosphate include meat, dairy products (e.g., milk, ice cream, cheese, yogurt), and foods containing dairy products (e.g., pudding).
    • Many foods that are high in phosphate are also high in protein.
    • Patients on dialysis are encouraged to eat a diet containing protein, phosphate binders are essential to control the phosphate level.

 

Nursing Management

  • Nursing Assessment
    • History and Past family medical history
    • Current and past use of prescriptions and over-the-counter drugs and herbal preparations
      • Many drugs are potentially nephrotoxic
    • Assess the patient’s dietary habits
    • Assess the patient’s support system
  • Nursing Diagnoses
    • Excess fluid volume related to impaired kidney function
    • Risk for electrolyte imbalance related to impaired kidney function resulting in hyperkalemia, hypocalcemia, hyperphosphatemia, and altered vitamin D metabolism
    • Imbalanced nutrition: less than body requirements related to restricted intake of nutrients (especially protein), nausea, vomiting, anorexia, and stomatitis
  • Nursing Planning
    • The overall goals are that a patient with CKD will 
      • Demonstrate knowledge of and ability to comply with the therapeutic regimen
      • Participate in decision making for the plan of care and future treatment modality
      • Demonstrate effective coping strategies
      • Continue with activities of daily living within physiologic limitations.
  • Nursing implementation
    • Health promotion
      • Individuals should have regular checkups that include a routine urinalysis and calculation of the estimated GFR
        • Diabetes or hypertension
        • People with a history (or a family history) of kidney disease 
        • Repeated urinary tract infections
      • People with diabetes need to have their urine checked for albuminuria if routine urinalysis is negative for protein.
        • Report any changes in urine appearance (color, odor), frequency, or volume to HCP
      • Monitor kidney function with serum creatinine and BUN and GFR if are on potentially nephrotoxic medications
      • Prevention and detection of chronic kidney disease
        • Early detection and treatment are the primary methods for reducing chronic kidney disease.
        • Monitor BP to detect elevations so that treatment can be started early.
        • Treat hypertension appropriately and aggressively, since it is the second leading cause of chronic kidney disease.
        • Ensure proper diagnosis and treatment of diabetes mellitus, since it is the leading cause of chronic kidney disease.
      • Glycemic control for patients with diabetes
    • Acute care
      • In-hospital care is required for management of complications and for kidney transplantation (if applicable)
    • Ambulatory care
      • Encourage the patients to participate in their care
        • Include the following information in the teaching plan for the patient and caregiver.
          • Dietary (protein, sodium, potassium, phosphate) and fluid restrictions.
          • Difficulties in modifying diet and fluid intake.
          • Signs and symptoms of electrolyte imbalance, especially high potassium.
          • Alternative ways of reducing thirst, such as sucking on ice cubes, lemon, or hard candy.
          • Rationales for prescribed drugs and common side effects.
            • Examples:
  • Phosphate binders (including calcium supplements used as phosphate barriers) should be taken with meals.
  • Calcium supplements prescribed to treat hypocalcemia should be taken on an empty stomach (but not at the same time as iron supplements).
  • Iron supplements should be taken between meals.
  • The importance of reporting any of the following:
    • Weight gain >4 lb (2 kg)
    • Increasing BP
    • Shortness of breath
    • Edema
    • Increasing fatigue or weakness
    • Confusion or lethargy
  • Need for support and encouragement. Share concerns about lifestyle changes, living with a chronic illness, and decisions about type of dialysis or transplantation.
  • The expected outcomes are that the patient with CKD will maintain
    • Fluid and electrolyte levels within normal ranges
    • An acceptable weight with no more than a 10% weight loss

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