NS3P1 Exam 1: Kidney Injury and Disease (AKI & CKD)

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  1. **Acute Kidney Injury Etiology and Pathophysiology
    Acute kidney injury (AKI), previously known as acute kidney failure, is the term used to encompass the entire range of the syndrome, including a very slight deterioration in kidney function to severe impairment.

    AKI is characterized by a rapid loss of kidney function. This loss is accompanied by a rise in serum creatinine level and/or a reduction in urine output. The severity of dysfunction can range from a small increase in serum creatinine or reduction in urine output to the development of azotemia (an accumulation of nitrogenous waste products [urea nitrogen, creatinine] in the blood).

    AKI can develop over hours or days with progressive elevations of blood urea nitrogen (BUN), creatinine, and potassium, with or without a reduction in urine output

    • onset: sudden
    • most common cause: Acute Tubular Necrosis
    • Diagnostic: acute reduction in urine output and/or elevantion in serum creatinine
    • Reversible
    • Primary cause of death: Infection!

    THREE TYPES: prerenal, intrarenal and post renal
  2. ** AKI Prerenal
    • Causes are factors external to the kidneys that reduce renal blood flow;
    • Severe dehydration, heart failure, ↓ CO
    • Decreases glomerular filtration rate
    • Causes oliguria
    • Autoregulatory mechanisms attempt to preserve blood flow
    • acute ischemia, but if prolonged it'll lead to intrarenal (the glomeruli will be damaged)

    -Know causes so treatments are different.

    • note: The oliguria is caused by a decrease in circulating blood volume (e.g., severe dehydration, heart failure, decreased cardiac output) and is readily reversible with appropriate treatment. It is important to distinguish prerenal oliguria from the oliguria of intrarenal AKI. In prerenal oliguria there is no damage to the kidney tissue (parenchyma).
    • -With a decrease in circulating blood volume, autoregulatory mechanisms that increase angiotensin II, aldosterone, norepinephrine, and antidiuretic hormone attempt to preserve blood flow to essential organs. Prerenal azotemia results in a reduction in the excretion of sodium (less than 20 mEq/L), increased salt and water retention, and decreased urine output.
    • -Prerenal conditions can lead to intrarenal disease if renal ischemia is prolonged. If decreased perfusion persists for an extended period of time, the kidneys lose their ability to compensate and damage to kidney parenchyma occurs (intrarenal damage).
    • Refer to Table 47-2 for common causes of acute kidney injury as we discuss prerenal, intrarenal, and postrenal causes.
  3. **Intrarenal
    • include conditions that cause direct damage to kidney tissue
    • => Results from Prolonged ischemia & Nephrotoxins are MOST common
    • Hemoglobin released from hemolyzed RBCs: REACTION TO BLOOD TRANSFUSIONS (incompatibilities
    • Myoglobin released from necrotic muscle cellsRHABDOMYOLOSIS: falling down, and AKI as a result.
    • Nephrotoxins: vanco, gentamycins, contrast Induced Nephropathy, NSAIDS, Statins "muscle aches, rhabdomyolosis which causes AKI"
    • Patients that overuse alcohol, fell down...crash victims: decreased circulation to muscles and ischemia, but when we do recover them, all the broken muscle and myoglobins now rush into the blood stream
    • Also autoimmune

    • *NOTE: Nephrotoxins can cause obstruction of intrarenal structures by crystallization or by causing damage to the epithelial cells of the tubules.
    • Hemoglobin and myoglobin can block the tubules and cause renal vasoconstriction.
    • Diseases of the kidney such as acute glomerulonephritis and systemic lupus erythematosus may also cause AKI.
  4. **Intrarenal & 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

    => NOTE: Acute tubular necrosis (ATN) is the most common cause of intrarenal AKI and is primarily the result of ischemia, nephrotoxins, or sepsis (Fig. 47-1)

    • Ischemic and nephrotoxic ATN are responsible for 90% of cases of intrarenal AKI.
    • Severe kidney ischemia causes a disruption in the basement membrane and patchy destruction of the tubular epithelium.
    • Nephrotoxic agents cause necrosis of tubular epithelial cells, which slough off and plug the tubules.
    • ATN is potentially reversible if the basement membrane is not destroyed and the tubular epithelium regenerates.
  5. **Acute Kidney Injury: Postrenal
    • Causes include
    • Benign prostatic hyperplasiaProstate cancerCalculiTraumaExtrarenal tumors

    So now urine is being backed up, so hydronephrosis due to pressure and damage of nephrons.

    • => NOTE: Postrenal causes of AKI involve mechanical obstruction in the outflow of urine. As the flow of urine is obstructed, urine refluxes into the renal pelvis, impairing kidney function.
    • Bilateral ureteral obstruction leads to hydronephrosis (kidney dilation), increase in hydrostatic pressure, and tubular blockage that results in a progressive decline in kidney function.
    • If bilateral obstruction is relieved within 48 hours of onset, complete recovery is likely. If it is not relieved after 12 weeks, recovery is unlikely.
  6. **Acute Kidney Injury Clinical ManifestationsRIFLE classificationloss (L) and end-stage kidney disease (E).
    Risk (R)Injury (I)Failure (F)Loss (L)End-stage kidney disease (E)

    => Clinically, AKI may progress through phases: oliguric, diuretic, and recovery. When a patient does not recover from AKI, then CKD may develop.

    The RIFLE classification is used to describe the stages of AKI (Table 47-3).

    RIFLE standardizes the diagnosis of acute kidney injury.

    Risk (R) is the first stage of AKI, followed by injury (I), which is the second stage, and then increases in severity to the final or third stage of failure (F). The two outcome variables are
  7. AKI Clinical Manifestations: Oliguric phase
    URINARY Changes
    • => Urinary changes
    • Urinary output less than 400 mL/dayOccurs within 1 to 7 days after injury
    • Lasts 10 to 14 days
    • Urinalysis may show casts, RBCs, WBCs
    • Specific gravity could be part of differential diaganois.: if intrarenal AKI, then glomerular are involved and lose the ability to concentrate to change the specific gravity, so it's FIXED specific gravity. 1.010. Loses ability to make it less or more concentrated.
    • -PRERENAL: body is trying to compensate for all the fluid and hold onto it, so the specific gravity is HIGH.

    *NOTE: Urinary changes: Oliguria is a reduction in urine output to less than 400 mL/day. Oliguria usually occurs within 1 to 7 days of the injury to the kidneys. If the cause is ischemia, oliguria will often occur within 24 hours. The duration of the oliguric phase lasts on average about 10 to 14 days but can last months in some cases. The longer the oliguric phase lasts, the poorer the prognosis for complete recovery of kidney function.A urinalysis may show casts, RBCs, and white blood cells (WBCs). The casts are formed from mucoprotein impressions of the necrotic renal tubular epithelial cells, which detach or slough into the tubules.
  8. AKI Clinical Manifestations: Oliguric phase
    => Fluid volume
    • Hypovolemia may exacerbate AKI
    • With decreased urine output, fluid retention occurs
    • -Neck veins distended-Bounding pulse-Edema-Hypertension
    • Fluid overload can lead to heart failure, pulmonary edema, and pericardial and pleural effusions
    • Retaining urine leads to fluid retention signs naturally.
    • NOTE: Fluid volume: Hypovolemia (volume depletion) has the potential to exacerbate all forms of AKI. The reversal of hypovolemia with fluid replacement is often sufficient to treat many forms of AKI, especially those with prerenal causes.When urinary output decreases, fluid retention occurs. The severity of the symptoms depends on the extent of the fluid overload. In the case of reduced urine output (anuria and oliguria), the neck veins may become distended with a bounding pulse. Edema and hypertension may develop. Fluid overload can eventually lead to heart failure, pulmonary edema, and pericardial and pleural effusions.
  9. AKI Clinical Manifestations: Oliguric phase=> Metabolic acidosis
    • Kidneys are responsible to get rid of H ions.
    • Serum bicarbonate level decreases

    • Severe acidosis develops: Kussmaul respirations
    • -Metabolic acidosis: In kidney failure, the kidneys cannot synthesize ammonia (needed for hydrogen ion excretion) or excrete acid products of metabolism.

    The serum bicarbonate level decreases because bicarbonate is depleted in buffering hydrogen ions.

    In addition, defective reabsorption and regeneration of bicarbonate occurs. With development of severe acidosis, the patient may develop Kussmaul respirations (rapid, deep respirations) in an effort to compensate by increasing the exhalation of carbon dioxide.
  10. AKI Clinical Manifestations: Oliguric phase=> Sodium balance
    Increased excretion of sodium

    Hyponatremia can lead to cerebral edema

    -Sodium balance: Damaged tubules cannot conserve sodium. Consequently, the urinary excretion of sodium may increase, resulting in normal or below-normal levels of serum sodium.

    Excessive intake of sodium should be avoided because it can lead to volume expansion, hypertension, and heart failure. Uncontrolled hyponatremia or water excess can lead to cerebral edema.
  11. AKI Clinical Manifestations: Oliguric phase=> Potassium excess
    • Usually asymptomatic
    • ECG changes
    • LETHAL: Dysrhythmias.

    • *NOTE:
    • Potassium excess: The kidneys normally excrete 80% to 90% of the body’s potassium. In AKI, the serum potassium level increases because the kidney’s normal ability to excrete potassium is impaired.

    Patients with hyperkalemia usually have no symptoms. Acute and/or rapid development of hyperkalemia may result in clinical signs that are apparent on electrocardiogram (ECG). These changes include peaked T waves, widening of the QRS complex, and ST segment depression.
  12. **Acute Kidney Injury Collaborative care for Hyperkalemia
    • Is it permanent or temporry?
    • 1.QUICK & TEMP: Insulin OR sodium bicarbonate (which can also fix the metabolic acidosiis)
    • -insulin causes hypoglycemia so give glucose ALSO (IV bolus)
    • -Sodium bicarb causes storage of potassium given as bolus

    2. Calcium carbonate (changes threshold of cardiac cells, makes it less reactive to all these changes in potassium--third type of therapy)

    • 3. PERMANENT BUT TAKES TIME: Sodium polystyrene sulfonate (Kayexalate)
    • -Only sodium polystyrene sulfonate (Kayexalate) and dialysis actually remove potassium from the body.
    • Never give this drug to a patient with a paralytic ileus because bowel necrosis can occur
    • -very thick, brown, muddy, pt has to drink it. Liquid that can be given orally or as a retention enema-works on GI tract, so BS must be there! Ischemic collitis it not, as a complication.
    • -Pt must have ability to hold enema: must be fully continent b/c it has to work on the inteestines. BM shows it's working.. and evaluate with K labs and ECG tele

    4. Dialysis is a PERMANENT REMOVAL of potassium

    => Hyperkalemia is one of the most serious complications in AKI because it can cause life-threatening cardiac dysrhythmias.

    The various therapies used to treat elevated potassium levels are listed in Table 47-5. Both insulin and sodium bicarbonate serve as a temporary measure for treatment of hyperkalemia by promoting a shift of potassium into the cells, but potassium will eventually be released.

    Calcium gluconate raises the threshold at which dysrhythmias will occur, serving to temporarily stabilize the myocardium.
  13. AKI Clinical Manifestations: Oliguric phase=> Hematologic disorders

    -Hospital-acquired AKI often occurs in patients who have multiorgan failure. Leukocytosis is often present with AKI. The most common cause of death in AKI is infection. The most common sites of infection are the urinary and respiratory systems.
  14. AKI Clinical Manifestations: Oliguric phase=> Waste product accumulation
    Elevated BUN and serum creatinine levels

    • -The kidneys are the primary excretory organs for urea (an end product of protein metabolism) and creatinine (an end product of endogenous muscle metabolism). BUN and serum creatinine levels are elevated in kidney failure.
    • Low GFR.
  15. AKI Clinical Manifestations: Oliguric phase Neurologic disorders
    • Fatigue and difficulty concentrating
    • Seizures, stupor, coma; can be tied to electrolyte imbalances

    -Neurologic changes can occur as the nitrogenous waste products accumulate in the brain and other nervous tissue. The manifestations can be as mild as fatigue and difficulty concentrating and then escalate to seizures, stupor, and coma.
  16. **AKI Clinical Manifestations: DIURETIC PHASE
    Daily urine output is 1 to 3 LMay reach 5 L or more

    Monitor for hyponatremia, hypokalemia, and dehydration

    Hypovolemia: not enough volume (pre-renal risks), looking for signs of losing the electrolytes: low potassium --cause dystrhymias, ekg.

    -Diuretic phase: During the diuretic phase of AKI, daily urine output usually is approximately 1 to 3 L but may reach 5 L or more. The high urine volume is caused by osmotic diuresis from the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine. The kidneys have recovered their ability to excrete wastes but not to concentrate urine.

    -Because of the large losses of fluid and electrolytes, the patient must be monitored for hyponatremia, hypokalemia, and dehydration. The diuretic phase may last 1 to 3 weeks. Near the end of this phase, the patient’s acid-base, electrolyte, and waste product (BUN, creatinine) values begin to normalize.
  17. **AKI Clinical Manifestations: RECOVERY PHASE
    May take up to 12 months for kidney function to stabilize

    -The recovery phase begins when the GFR increases, allowing the BUN and serum creatinine levels to plateau and then decrease. Although the major improvements occur in the first 1 to 2 weeks of this phase, kidney function may take up to 12 months to stabilize.

    -The outcome of AKI is influenced by the patient’s overall health, the severity of kidney failure, and the number and type of complications.
  18. Acute Kidney Injury Diagnostic studies
    -thorough history is essential for diagnosing the etiology of AKI. Consider prerenal causes when there is a history of dehydration, blood loss, or severe heart disease, drugs they were taking.

    -An increase in serum creatinine may not be evident until there is a loss of more than 50% of kidney function.

    -Urinalysis is an important diagnostic test. The urine osmolality, sodium content, and specific gravity are measured, and urine sediment, hematuria, pyuria, and crystals may be seen.

    -Kidney ultrasonography is often the first test done because it provides imaging without exposure to potentially nephrotoxic contrast agents.

    -A renal scan can help assess abnormalities in kidney blood flow, tubular function, and the collecting system.

    -A computed tomographic (CT) scan can identify lesions and masses, as well as obstructions and vascular anomalies. RISK: contrast!

    -Renal biopsy is considered the best method for confirming intrarenal causes of AKI: glomerulnephritis! (autommune), and also for suspected cancer
  19. Acute Kidney Injury: CONTRAINDICATED Diagnostic studies
    • Magnetic resonance imaging (MRI)
    • Magnetic resonance angiography (MRA) with gadolinium contrast medium --contraindictated due to CIN
    • Nephrogenic systemic fibrosis Contrast-induced nephropathy (CIN)

    • => Administration of gadolinium has been associated with the development of a devastating and potentially lethal disorder, nephrogenic systemic fibrosis, in patients with kidney failure.
    • In patients with kidney failure, contrast-induced nephropathy (CIN) can occur when contrast medium for diagnostic studies causes nephrotoxic injury.
  20. **AKI Collaborative care & Primary goals
    • Eliminate the cause
    • Manage signs and symptoms
    • Prevent complications while the kidneys recover :)
    • Eliminate the cause-Intrarenal: damage to tissues, NSAIDS, remove it.
    • -Blood transfusion reactions: stop the traansfusions, and push the fluids and getting rid of it.
    • -rhabdomyolosis: push fluids at high rate: 250 ml but also look at all signs of fluid overload-

    • => 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
    • *If AKI is already established, forcing fluids and diuretics will not be effective and may, in fact, be harmful.
    • Closely monitor fluid intake during the oliguric phase of AKI. The general rule for calculating the fluid restriction is to add all losses for the previous 24 hours (e.g., urine, diarrhea, emesis, blood) plus 600 mL for insensible losses (e.g., respiration, diaphoresis, stool, sweating).
  21. **Indications for renal replacement therapy (RRT)
    • Volume overload
    • Elevated serum potassium level
    • Metabolic acidosis BUN level higher than 120 mg/dL (43 mmol/L)
    • Significant change in mental status
    • Pericarditis, pericardial effusion, or cardiac tamponade

    -The most common indications for RRT in AKI are (1) volume overload, resulting in compromised cardiac and/or pulmonary status; (2) elevated serum potassium level; (3) metabolic acidosis (serum bicarbonate level less than 15 mEq/L [15 mmol/L]); (4) BUN level greater than 120 mg/dL (43 mmol/L); (5) significant change in mental status; and (6) pericarditis, pericardial effusion, or cardiac tamponade.

    Peritoneal dialysis (PD): not used for acutee needs, pt needs to go for surgery

    Intermittent hemodialysis (HD): helps for accute; started in a short time

    • Continuous renal replacement therapy (CRRT)Cannulation of artery and vein
    • -There is no consensus regarding the best approach to renal relacement therapy (RRT).

    • Even though peritoneal dialysis (PD) is considered a viable option for RRT, it is not frequently used.
    • Intermittent hemodialysis (HD) (e.g., at intervals of 4 hours either daily, every other day, or three to four times per week) is the method of choice when rapid changes are required in a short period of time.

    Continuous renal replacement therapy (CRRT) has been used effectively and involves cannulation of an artery and a vein.
  22. **Acute Kidney Injury: Collaborative care DIET
    • Maintain adequate caloric intake
    • Restrict sodium and possibly K and phosphate
    • Increase dietary fat
    • Enteral nutrition
    • restrict protein

    => The challenge of nutritional management in AKI is to provide adequate calories to prevent catabolism despite the restrictions necessary to prevent electrolyte disorders, fluid disorders, and azotemia.

    A primary nutritional goal in AKI is to maintain adequate caloric intake (providing 30 to 35 kcal/kg and 0.8 to 1.0 g of protein per kilogram of desired body weight) to prevent the further breakdown of body protein for energy purposes.

    Adequate energy should be primarily from carbohydrate and fat sources to prevent ketosis from endogenous fat breakdown and gluconeogenesis from muscle protein breakdown. Supplementation of essential amino acids can be given for amino acid replacement.

    Sodium is restricted as needed to prevent edema, hypertension, and heart failure.

    Dietary fat intake is increased so that the patient receives at least 30% to 40% of total calories from fat. Fat emulsion IV infusions given as a nutritional supplement provide a good source of nonprotein calories (see Chapter 40).

    If a patient cannot maintain adequate oral intake, enteral nutrition is the preferred route for nutritional support (see Chapter 40).

    When the gastrointestinal (GI) tract is not functional, parenteral nutrition is necessary to provide adequate nutrition. The patient treated with parenteral nutrition may need daily HD or CRRT to remove the excess fluid. Concentrated formulas of parenteral nutrition are available to minimize fluid volume.
  23. **AKI Nursing Management
    • Measure vital signs
    • Measure fluid intake and output
    • Examine urine
    • Assess general appearance
    • Observe dialysis access site

    => Daily monitoring of a patient’s urine output is essential because this information provides prognostic implications and is crucial in determining therapy and daily fluid volume replacement.Examine the urine for color, specific gravity, glucose, protein, blood, and sediment. Assess the patient’s general appearance, including skin color, edema, neck vein distention, and bruises.If a patient is receiving dialysis, observe the access site for signs of inflammation and exudate. Evaluate the patient’s mental status and level of consciousness. Examine the oral mucosa for dryness and inflammation. Auscultate the lungs for crackles and rhonchi or diminished breath sounds. Monitor the heart for the presence of an S3 gallop, murmurs, or a pericardial friction rub. Assess ECG readings for the presence or development of dysrhythmias. Review laboratory values and diagnostic test results.
  24. AKI Planning and Health Promotion
    • **AKI Planning
    • The patient with AKI will
    • Completely recover without any loss of kidney function
    • Maintain normal fluid and electrolyte balance
    • Have decreased anxiety
    • Comply with and understand the need for careful follow-up care

    • **AKI Health promotion
    • Identify and monitor populations at high risk Control exposure to nephrotoxic drugs and industrial chemicals
    • Prevent prolonged episodes of hypotension and hypovolemia

    • In the hospital, the factors that increase the risk for developing AKI are the presence of preexisting CKD, older age, massive trauma, major surgical procedures, extensive burns, cardiac failure, sepsis, and obstetric complications.
    • Careful monitoring of intake and output, fluid balance, and electrolyte balance is essential.
    • Assess and record extrarenal losses of fluid from vomiting, diarrhea, hemorrhage, and increased insensible losses.
    • Prompt replacement of significant fluid losses will help prevent ischemic tubular damage associated with trauma, burns, and extensive surgery.
    • Intake and output records and the patient’s weight provide valuable indicators of fluid volume status.
    • Aggressive diuretic therapy for the patient with fluid overload resulting from any cause can lead to a reduction in renal blood flow.
    • Nephrotoxic drugs should be used sparingly in a patient at high risk. When these drugs must be used, they should be given in the smallest effective doses for the shortest possible periods.

    Angiotensin-converting enzyme (ACE) inhibitors can also decrease perfusion pressure and cause hyperkalemia.

    other nephro: vanco, nsaid, statin, digoxin tox, ace inhibitors (take off during renal insufficiency), metformin-hold vitamins until AFTER dialysisA
  25. **Chronic Kidney Disease (CKD)
    • Involves progressive, irreversible loss of kidney function
    • Kidneys can accomodate for loss hence live kidney donations; 20% left and you can still be functioning.

    • -Creatinine clearance is same as GFR. Normal 125 Defined as one of the following:
    • => Kidney damage
    • Pathologic abnormalities
    • Markers of damage Blood, urine, imaging tests

    • =>Low glomerular filtration rate (GFR) <60 mL/min for 3 months or longer
    • Disease staging based on decrease in GFR
    • Normal GFR: 125 mL/min, which is reflected by urine creatinine clearance
    • Last stage of kidney failure: End-stage kidney disease (ESKD) occurs when GFR <15 mL/min
  26. **Chronic Kidney Disease
    Up to 80% of GFR may be lost without much change in functioning of body

    Remaining nephrons hypertrophy to compensate

    End result is a systemic disease involving every organ

    • Over 26 million Americans have CKD
    • Mortality rates are 19% to 24% for patients with stage 5 CKD on dialysis (Primary due to CV disease)

    • =>Leading causes of ESKD
    • Diabetes
    • Hypertension
    • Others: autoimmune (systemic lupus) that also affect kidneys, Glomeularnephritis, chronic pyelonephritis

    • =>Clinical Manifestations
    • Result of retained substancesUreaCreatininePhenolsHormonesElectrolytes: potassiumWater
    • Other substances

    Changes ability to metabolize hormones and insulin (so pts may require less insulin b/c lose ability to metabolize insulin, risk is hyperglycemia.)
  27. **CKD Manifestations:
    • =>Uremia
    • Syndrome that incorporates all signs and symptoms seen in various systems throughout the body Often occurs when the GFR is 10 mL/min or lower

    • =>Oliguria
    • Occurs as CKD worsens ; common sign but not necessarily

    • =>Anuria
    • Urine output lower than 40 mL per 24 hours (don't assume this with ESKD or Dialysis pts)

    • =>Metabolic Disturbances:
    • -NOTE: Serum creatinine clearance determinations (calculated glomerular filtration rate) are considered more accurate indicators of kidney function than BUN or creatinine values.
    • -Waste product accumulation: As GFR ↓, BUN and serum creatinine levels ↑=>BUN level ↑ Not only from kidney failure but also from protein intake, fever, corticosteroids, and catabolismN/V, lethargy, fatigue, impaired thought processes, and headaches occur

    • =>Altered carbohydrate metabolism
    • Caused by impaired glucose metabolism
    • From cellular insensitivity to normal action of insulin
    • Defective carbohydrate metabolism
    • Patients with diabetes who develop uremia may require less insulin after onset of CKD
    • Excretion of insulin dependent on kidneys

    • NOTES: 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. Insulin and glucose metabolism may improve (but not to normal values) after the initiation of dialysis.
    • As a result, a number of patients on dialysis who required insulin before starting dialysis will be able to discontinue insulin therapy with kidney disease progression.

    • =>Elevated triglyceride levels
    • Hyperinsulinemia stimulates hepatic production of triglycerides
    • Altered lipid metabolism ↓ Levels of enzyme lipoprotein lipase: Important in breakdown of lipoproteins

    Note: Almost all patients with uremia develop dyslipidemia, with elevated levels of very-low-density lipoproteins (VLDLs), normal or decreased levels of low-density lipoproteins (LDLs), and decreased levels of high-density lipoproteins (HDLs). Elevated glucose levels lead to increased insulin levels, and insulin stimulates hepatic production of triglycerides. Most patients with CKD die from cardiovascular disease.
  28. CKD Electrolyte/Acid-Base Imbalances
    Calcium and Phosphate
    Metabolic Acidosis results from?
    • Potassium: Hyperkalemia
    • Most serious electrolyte disorder in kidney disease
    • Fatal dysrhythmiasmain prevention: diet restrictions; Fatal dysrhythmias can occur when the serum potassium level reaches 7 to 8 mEq/L (7 to 8 mmol/L).
    • Hyperkalemia results from the decreased excretion of potassium by the kidneys, the breakdown of cellular protein, bleeding, and metabolic acidosis. Potassium may also come from the food consumed, dietary supplements, drugs, and IV infusions.

    • =>Sodium
    • May be elevated, normal, or low
    • Because of impaired excretion, sodium is retained so reduce sodium in their diet. DON"T USE SALT SUBS B/C THEY HAVE POTASSIUM!!Water is retained
    • EdemaHypertensionCHF

    note: Sodium intake must be individually determined but is generally restricted to 2 g/day.

    => Calcium and phosphate alterations Magnesium alterations: can cause dysrhythmias, OTC meds have: maalox, antacids, milk of magnesia (so reinforce) Clinical manifestations of hypermagnesemia can include absence of reflexes, decreased mental status, cardiac dysrhythmias, hypotension, and respiratory failure.Lower calcium while they hyperphosphatemia.

    • How to correct phosphate: Can't give dairy because they have phosphate which we need to limit So dairy isn't good for these pts
    • Calcium supplements PLUS normalizing of phosphate by using BINDERS (bind into the foods and reduces phosphate of that food)-You must give binders with food
    • -Fleet enemas: phosphate?

    • => Metabolic acidosis
    • Results from Inability of kidneys to excrete acid load (primary ammonia)
    • Defective reabsorption/regeneration of bicarbonate
    • The average adult produces 80 to 90 mEq of acid per day. This acid is normally buffered by bicarbonate. In kidney failure, plasma bicarbonate level, which is an indirect measure of acidosis, usually falls to a new steady state at approximately 16 to 20 mEq/L (16 to 20 mmol/L).
  29. HYPERKALEMIA Drug Therapy for CKD
    • => Hyperkalemia
    • IV insulin; IV glucose to manage hypoglycemia
    • IV 10% calcium gluconate
    • Sodium polystyrene sulfonate (Kayexalate)
    • -Cation-exchange resin
    • -Resin in bowel exchanges potassium for sodium

    NOTE: Sodium polystyrene sulfonate (Kayexalate) is commonly used to lower potassium levels in stage 4 and can be administered on an outpatient basis. Tell the patient to expect some diarrhea because this preparation contains sorbitol, a sugar alcohol that has an osmotic laxative action and ensures evacuation of the potassium from the bowel. Never give Kayexalate to a patient with a hypoactive bowel (paralytic ileus) because fluid shifts could lead to bowel necrosis.
  30. Care for Dyslipidemia
    • Goal
    • Lowering LDL level below 100 mg/dL
    • Lowering triglyceride level below 200 mg/dL

    • =>StatinsHMG-CoA reductase inhibitors
    • Most effective for lowering LDL level

    • **Collaborative Care:
    • Drug therapy ComplicationsDrug toxicityDigoxinAntibiotics Pain medication (meperidine [Demerol], NSAIDs)
  31. **Clinical Manifestations Hematologic system
    • =>Anemia
    • Due to ↓ production of erythropoietin that stimulates RBCs so hemoglobin low
    • From ↓ of functioning renal tubular cells
    • -give epogoen: SubQ or IV, can be done at dialysis center, monitor: H&H (takes 2 weeks to stimulate): goal is 12 for hemoglobin

    • =>Bleeding tendencies
    • Defect in platelet function
    • NOTE: Other factors contributing to anemia are nutritional deficiencies, decreased RBC life span, increased hemolysis of RBCs, frequent blood samplings, and bleeding from the GI tract. Defect in platelet function is caused by impaired platelet aggregation and impaired release of platelet factor III.

    • =>Infection
    • Changes in WBC function
    • Altered immune response and function
    • Diminished inflammatory response
  32. Anemia CKD Drug Therapies.
    • Erythropoietin
    • Epoetin alfa (Epogen, Procrit)Administered IV or subcutaneously
    • Increased hemoglobin and hematocrit in 2 to 3 weeks
    • Side effect: hypertension

    • =>Iron supplements b/c they lose blood druing dialysis
    • If plasma ferritin level is less than 100 ng/mL
    • Side effects: gastric irritation, constipationMay make stool dark in color

    • =>Folic acid supplements
    • Needed for RBC formation Removed by dialysis

    • Avoid blood transfusions because of fluid overload!! Extra volume that the body has to deal with, Undesirable effects of transfusions are the suppression of erythropoiesis as a result of a decrease in the hypoxic stimulus and the possibility of iron overload because each unit of blood contains about 250 mg of iron.
    • -Transplant donors: HLA compatibilities because the more exposure to other blood products, the more chances for you to develop antibodies to all those antigens, so more difficult to find a perfect kidney donor ):
  33. Clinical Manifestations Cardiovascular system
    • Hypertension
    • Heart failure
    • Left ventricular hypertrophy
    • Peripheral edema: fluid overloads
    • Dysrhythmias: electrolytes: K and Mg
    • Uremic pericarditis: urea starts depositiing on pericardium.
  34. Clinical Manifestations Respiratory system
    Kussmaul respirationsDyspnea may occur withFluid overloadPulmonary edemaUremic pleuritis Respiratory infections
  35. **Clinical Manifestations Gastrointestinal system
    Every part of GI system is affected

    • Cause: excessive urea depositing on GI mucous
    • Mucosal ulcerations

    Stomatitis (Stomatitis with exudates and ulcerations, a metallic taste in the mouth, and uremic fetor (a urinous odor of the breath) are commonly found in CKD. )

    Uremic fetor (urinous odor of breath)

    GI bleeding (GI bleeding is also a risk because of mucosal irritation and the platelet defect. Constipation may be due to the ingestion of iron salts and/or calcium-containing phosphate binders.)

    Anorexia, nausea, vomiting: becomes worse as CKD progress, and not treated by dialysis

  36. **Clinical Manifestations Neurologic system
    Expected as renal failure progresses

    Attributed to ↑ Nitrogenous waste products

    Electrolyte imbalancesMetabolic acidosisAtrophy Demyelination of nerve fibersRestless legs syndromeMuscle twitchingIrritabilityDecreased ability to concentratePeripheral neuropathy

    Altered mental ability: The treatment for neurologic problems is dialysis or kidney transplantation. Altered mental status is a late manifestation of CKD stage 5, is rarely seen unless the patient has chosen to forgo renal replacement therapy.

    Seizures (Seizures and coma may result from a rapidly increasing BUN level and hypertensive encephalopathy.)ComaDialysis encephalopathy: An aluminum toxicity from dialysate water sources containing aluminum; also can occur from ingestion of aluminum-containing antacids (phosphate binders). This is not a common occurrence.

    • HD removing blood so drop in BP, hypoperfusion, dysequilibrum syndrome (water in brain)
    • -A rapid change in the composition of the extracellular fluid occurs during hemodialysis.
    • b. Solutes are removed from the blood faster than from the cerebrospinal fluid and brain; fluid is pulled into the brain, causing cerebral edema.
    • c. Occurs more frequently in a new client duringthe initial onset of hemodialysis.
  37. Clinical Manifestations Musculoskeletal system: CKD
    -Mechanisms of CKD-MBD
    • CKD mineral and bone disorder
    • Systemic disorder of mineral and bone metabolism
    • Results in Skeletal complications (osteomalacia, ostetis fibrosa) Extraskeletal (vascular calcifications)
    • -develop secondary parathyroid hormone (background: try to balance out the calcium, so it incease PTH to compensate for low calcium, but this comes from the bone--> Osteomalacia.)
    • -so you MUST normalize calcium and give supplements .

    **Mechanisms of CKD-MBD: As kidney function deteriorates, less vitamin D is converted to its active form, resulting in decreased serum levels. Activated vitamin D is necessary to optimize absorption of calcium from the GI tract. Thus low levels of active vitamin D results in decreased serum calcium levels. Normally, serum calcium levels are tightly regulated. Parathyroid hormone (PTH) is the primary regulator of serum calcium levels. When hypocalcemia occurs, the parathyroid gland secretes PTH, which stimulates bone demineralization, thereby releasing calcium from the bones. Phosphate is released as well, which leads to elevated serum phosphate levels. Hyperphosphatemia also results from decreased phosphate excretion by the kidneys.

    Hyperphosphatemia decreases serum calcium levels and further reduces the ability of the kidneys to activate vitamin D.


    • =>Phosphate intake restricted to less than 1000 mg/day
    • =>Phosphate binders
    • Calcium acetate (PhosLo)
    • Calcium carbonate (Caltrate): Bind phosphate in bowel and in excretement
    • Sevelamer hydrochloride (Renagel): Lowers cholesterol and LDL levels DON"T GIVE FOR NPO pts
    • Bind phosphate to bowels and excretes

    Phosphate binders Should be administered with each meal; Side effect: constipation

    • =>Supplementing vitamin D
    • Calcitriol (Rocaltrol)
    • Serum phosphate level must be lowered before calcium or vitamin D is administered

    =>Controlling secondary hyperparathyroidism

    • Calcimimetic agents-Cinacalcet (Sensipar)-↑ Sensitivity of calcium receptors in parathyroid glands
    • Subtotal parathyroidectomy

    • NOTE: especially during dialysis b/c they lose those vitamins. GIVE MULITVIT AFTER DIALYSIS
  38. **Clinical Manifestations Integumentary system

    Uremic frost: gray colored skin?The cause of pruritus is multifactoral: dry skin, calcium-phosphate deposition in the skin, and sensory neuropathy. The itching may be so intense that it can lead to bleeding or infection secondary to scratching. Uremic frost is an extremely rare condition in which urea crystallizes on the skin and is usually seen only when BUN levels are extremely elevated (e.g., over 200 mg/dL).
  39. **Clinical Manifestations Reproductive system
    Infertility Experienced by both sexes

    • Decreased libido
    • Low sperm counts
    • Sexual dysfunction

    Women usually have decreased levels of estrogen, progesterone, and luteinizing hormone, which causes anovulation and menstrual changes (usually amenorrhea).

    Men experience loss of testicular consistency, decreased testosterone levels, and low sperm counts.

    Sexual function may improve with maintenance dialysis and may become normal with successful kidney transplantation.
  40. **CKD **Diagnostic Studies
    • History and physical examination
    • Dipstick evaluation
    • Albumin-to-creatinine ratio (first morning void)
    • GFR
    • Renal ultrasonography
    • Renal scan
    • CT scan
    • Renal biopsy
    • A person with persistent proteinuria (1+ protein on standard dipstick testing two or more times over a 3-month period) should have further assessment of risk factors and a diagnostic workup with blood and urine tests. The two equations used most frequently to estimate GFR are the Cockcroft-Gault formula and the Modification of Diet in Renal Disease (MDRD) Study equation (see Table 47-8).

    An ultrasound study of the kidneys is usually done to detect any obstructions and to determine the size of the kidneys.

    Other diagnostic studies (Table 47-7) help establish the diagnosis and cause of CKD. Kidney biopsy may be necessary to provide a definitive diagnosis.
  41. **Collaborative Care Overall goals
    Preserve existing kidney function, slow down the ratee!control the risk (DM better)

    Reduce the risks of CV disease

    Prevent complications

    Provide for the patient’s comfort

    • => Collaborative Care
    • Conservative therapy
    • Correction of extracellular fluid volume overload or deficit
    • Nutritional therapy
    • Erythropoietin therapy
    • Calcium supplementation, phosphate binders
    • Antihypertensive therapy
    • Measures to lower potassium
    • Adjustment of drug dosages to degree of renal function
  42. CDK DIET:
    • =>Protein restriction
    • Benefits are being studied
    • Monitor laboratory parameters

    =>Water restriction Intake depends on daily urine output

    • =>Sodium restriction
    • Diets vary from 2 to 4 g, depending on degree of edema and hypertension
    • Sodium and salt should not be equated Salt substitutes should not be used because they contain potassium chloride

    • =>Potassium restriction
    • Limit: 2 to 3 g
    • High-potassium foods should be avoided

    • =>Phosphate restriction
    • Limit: 1000 mg/day
    • Foods high in phosphate
    • Dairy products Most foods high in phosphate are also high in protein
  43. Nursing Implementation, Acute Interventions,  & Ambulatory and Home care
    **Nursing Implementation=> Health promotionIdentify individuals at risk for CKDHistory of renal diseaseHypertensionDiabetes mellitusRepeated urinary tract infectionRegular checkups and changes in urinary appearance, frequency, and volume should be reported

    • =>Acute intervention
    • Daily weight
    • Daily BPs
    • Identify signs and symptoms of fluid overload
    • Identify signs and symptoms of hyperkalemia
    • Strict dietary adherence

    =>Ambulatory and home care

    • When conservative therapy is no longer effective, HD, PD, and transplantation are treatment options
    • Patient and family need clear explanation of dialysis and transplantation
    • Acute intervention
    • Medication teaching
    • Motivate patients in management of their disease

    **Nursing Management Evaluation

    =>The patient with CKD will maintain Fluid and electrolyte levels within normal ranges An acceptable weight with no more than a 10% weight loss
Card Set:
NS3P1 Exam 1: Kidney Injury and Disease (AKI & CKD)
2015-08-28 20:08:36
NS3 NS3P1 Kidney Renal Olga

AKI CKD Dialysis?
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