12/1/23
KIDNEYS + URINARY
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KIDNEYS
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12/1/23
KIDNEY & URINARY ASSESSMENT
• What symptoms do patients present with?
• Pain, GI Upset, GU changes in voiding
• Health History
• What questions do we ask?
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PATHO
• Blood supply:
• Renal artery: takes fresh oxygenated blood that came from the heart to the kidney to be filtered.
• Renal vein: takes filtered blood back to the heart to be re-oxygenated and pumped to the body.
• The kidneys receive fresh blood from the heart via the renal artery and drains filtered blood back to the heart
via the renal vein.
• The Kidneys receive 20% to 25% of the total cardiac output
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KIDNEY FUNCTION
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URETERS, BLADDER & URETHRA
• The Urine formed in the nephrons in the kidneys flows through the renal
calyces and then into the ureters
• Each tubes connect each kidney to the bladder
• The usual capacity of the adult bladder is 400 to 500ml , it can distend
to hold a larger volume
• The healthy human body is composed of aprx 60% water,
water balance is regulated by the kidneys
and
results in the formulation of urine.
• Substances excreted in the Urine
are: Na, Cl, HCO3, K , Glucose, Urea,
Creatinine & Uric acid.
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URETERS, BLADDER & URETHRA
• Some of the substances we mentioned prior are reabsorbed into the blood.
• The rest are secreted into the filtrate and travel down the tubule to be excreted by
the urine.
• Amino Acids and glucose are usually filtered and reabsorbed so that neither is excreted in
the urine.
•
Normally glucose does not appear in the urine, however glycosuria (excretion of glucose in the
urine) occurs if the amount of glucose in the blood and glomerular filtrate exceeds the amount
that the tubules are able to reabsorb.
• This occurs when?
• In poorly controlled diabetes
• The blood glucose level exceeds the amount that
the kidneys can reabsorb.
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PHYSIOLOGY OF URINE FORMATION
•
1.
Filtration at the
glomerulus
2.
Absorption into
peritubular
capillaries
3.
Reabsorption into
tubule for excretion
into urine.
Filtration depends on adequate blood flow that maintains
a consistent pressure through the glomerulus
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EXCRETION OF WASTE PRODUCTS
• The kidneys eliminate the bodys metabolic waste products.
• The major waste products is urea.
• If the urea isn’t excreted through urine it will accumulate in the tissues.
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REGULATION OF WATER
EXCRETION
• Regulation of the amount of water excreted is an
important function of the kidney
• With high fluid intake, a large volume of dilute urine is
excreted.
• Conversely, with a low fluid intake, a small volume of
concentrated urine is expected
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ANTIDIURETIC HORMONE
• Also known as vasopressin
• Secreted by the posterior pituitary gland
• In response to changes in osmolality of the blood
• Decrease in water intake, blood osmolality tends to increase, which also stimulates
ADH.
• ADH acts on the kidney, increasing reabsorption of water and thereby returning the
osmolality of the blood to normal.
• What is Osmolality?
• Degree of dilution or concentration of the urine
• Number of moles of solute per kilogram of solvent
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REGULATION OF ELECTROLYTE EXCRETION
• When the kidneys are functioning normally, the volume of electrolytes excreted per day is equal to
the amount ingested.
• The regulation of Sodium Volume excreted all depends on aldosterone, a hormone synthesized and
released by the adrenal cortex.
• W/ increased aldosterone in the blood, less sodium is excreted in the Urine.
• Because aldosterone fosters renal reabsorption of Sodium
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AUTOREGULATION OF BP
• Specialized vessels of the kidney, constantly monitor blood pressure as blood begins
its passage into the kidney.
• When the kidneys detect a decrease in blood pressure, renin converts
angiotensinogen to angiotensin I which is then converted to angiotensin II (the
most powerful vasoconstrictor known) angiotensin II causes the blood pressure
to increase
• The adrenal cortex secretes aldosterone in response to stimulation by the
pituitary gland, which occurs in response to poor perfusion or serum osmolality.
• This result is an increase in blood pressure.
• When the BP is increased, renin secretion stops.
• Failure of this feedback mechanism is one of the primary causes
of hypertension.
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RENINANGIOTENSIN
SYSTEM
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REGULATION OF RBC PRODUCTION
• When the kidneys detect a decrease in O2, they release EPO (erythropoietin).
• What are some reasons for a decrease in oxygenation to the renal blood flow?
• Anemia, arterial hypoxia or inadequate blood flow
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REGULATION OF ACID-BASE BALANCE
• Normal ph is 7.35-7.45
• The Kidney performs major functions to assist in this balance
• One function is to reabsorb and return to the body’s circulation any bicarb from the urinary filtrate
• Another function is to excrete or reabsorb acid, synthesize ammonia and excrete
ammonium chloride.
• The body’s acid production is a result of catabolism or breakdown of proteins which
produces acid compounds.
• The accumulation of these acids in the blood lowers ph (making the blood more
acidic) and inhibits cellular function.
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ABG ANALYSIS
• Normal values —In general, normal values for acidity (pH), the partial
pressure of carbon dioxide (PaCO2) and bicarbonate concentration (HCO3) are
as follows:
• pH – 7.35 to 7.45
• PaCO2 – 35 to 45 mmHg HCO3 – 21 to 27 mEq/L
• it is reasonable to consider a resting PaO2 >80 mmHg
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RESPIRATORY IMBALANCES
• Respiratory acidosis is a disturbance in acid-base balance usually due to
alveolar hypoventilation that can be acute or chronic. It is characterized by
an increased PaCO2 >45 mmHg (hypercapnia) and a reduction in pH (pH
<7.35)
• Respiratory alkalosis is usually due to alveolar hyperventilation which leads
to a decrease in PaCO2 (hypocapnia) and an increase in the pH. It can also be
acute or chronic. In acute respiratory alkalosis, the PaCO2 level is below the
lower limit of normal (<35 mmHg or 4.7 kPa) and the serum pH is
appropriately alkalemic (>7.45)
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METABOLIC IMBALANCES
• Metabolic acidosis is defined as a pathologic process that, when unopposed,
increases the concentration of hydrogen ions in the body and reduces the
HCO3 concentration. Acidemia (as opposed to acidosis) is defined as a low
arterial pH (<7.35), which can result from a metabolic acidosis, respiratory
acidosis, or both
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METABOLIC ALKALOSIS
• Metabolic alkalosis is primary increase in bicarbonate (HCO3−) with or without
compensatory increase in carbon dioxide partial pressure (Pco2); pH may be high or
nearly normal.
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RENAL CLEARANCE
• What is the primary test of renal clearance?
• A 24 hour urine collection
• Creatinine is an endogenous waste product and is excreted in the urine. Creatinine clearance
is a good measure of GFR.
• What is GFR?
• GFR is the amount of plasma filtered through the glomeruli per unit of time.
• Creatinine clearance is the best approximation of renal function.
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AKI
• AKI is a reversible clinical syndrome in which there is a sudden and almost complete loss of kidney function
over a period of hours to days, with failure to excrete nitrogenous waste products and to maintain fluid and
•
electrolyte homeostasis.
Which drugs are affected by kidney disease?
o NSAIDS’
§ Reduction of renal blood flow will damage kidneys.
o ACE’s
§ Higher risk of Hyperkalemia
o Warfarin
§ Higher incidence of over coagulation
o Lithium
§ Increased risk of kidney injury
• Lithium affects sodium.
o Accurate results when measured 12 hours post last dose.
o K-sparing diuretics
§ Higher risk of Hyperkalemia
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CAUSES OF ACUTE KIDNEY FAILURE
• Hypovolemia
• Hypotension
• Reduced cardiac output and heart failure
• Obstruction of the kidney or lower urinary tract
• Obstruction of renal arteries or veins
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3 TYPES OF AKI
• Prerenal
• Intrarenal
• Post renal
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PRERENAL
COMMON REASONS FOR PRE-RENAL AKI
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INTRARENAL AKI
NEPHROTOXICITY OR DAMAGE TO THE NEPHRONS
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POST RENAL
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CLINICAL FEATURES OF AKI
• 3 stages
• 1st stage – Initial stage subtle symptoms but can still urinate
•
Look at Bun/creatinine levels (initial rise in serum BUN and creatinine)
nd
• 2 oliguric or anuric phase
• Low urine output <500ml/24
• Progressive increase in Bun/creatinine
• Increase in serum urea levels
• Uremia: can cause symptoms of anorexia, n/v and pruritus
• Metabolic acidosis : kussmal respirations
• Hypervolemia – hypertension – pulmonary and peripheral edema
• Increase in electrolyte levels
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CLINICAL FEATURES OF AKI
• Stage 3
• Diuretic phase
• Bun and creatinine levels start to decrease
• Near Normal or normal kidney function resumes gradually
• Heavy diuresis and fluid volume loss . 4-5L per day
• Fluid and electrolyte losses leading to hypovolemia and hypokalemia
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INTERVENTIONS
• Fix the underlying cause
• Iv fluids – hypovolemia
• Medication dosage adjustments
• Strict Is and Os / Daily weights
• Avoid nephrotoxic medications
• Monitor lung sounds (crackles) and hypertension
• Potassium restricted diet
• Temporary hemodialysis
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NEPHROLITHIASIS
(KIDNEY STONE)
• Stone or calculi formation within the
urinary tract
• Salts within the urine crystalize which form
solid deposits
• Form primarily within the Kidney and
travels through the GU system
• Types of Stones
•
Calcium (most common)
•
•
Hypercalcemia patient will increase
risk for stones
Uric Acid
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KIDNEY STONES
• Risk Factors for Renal Calculi
• Hypercalcemia from any cause
• Dehydration
• Family History
• Immobilization
• Gout – high serum uric acid
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KIDNEY STONES
• Severe flank pain/radiating to groin
• Called referred pain
• Intense pain can cause N/V
• Hematuria
• Dysuria and urinary urgency
• Diagnosis
• Ultrasound
• CT scan
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KIDNEY STONE COMPLICATIONS
• Urinary obstruction can lead to a backflow of urine itself leading to hydronephrosis – can
lead to AKI
• Urinary Stasis- can lead to infection
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NURSING INTERVENTIONS
• Concentrated Urine can lead to formation of Kidney stones – Treat with Fluids
• Pain management
• Ambulation
• Antiemetics
• Lithotripsy (shockwave therapy) – NPO procedure , can have flank pain post
• Complications
• Pyelonephritis (monitor for infections)
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UTI’S
• Urinary tract infections (UTIs) include cystitis (infection of the bladder/lower
urinary tract) and pyelonephritis (infection of the kidney/upper urinary
tract).
• Pyelonephritis develops when pathogens ascend to the kidneys via the
ureters.
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UTI’S
•
What are the types of UTI’s?
o Lower (cystitis) vs upper (pyelonephritis)
§ They can share the same clinical features
• Dysuria, suprapubic pressure, and hematuria
o How do you differentiate between upper & lower UTI?
§ The presence of WBC casts on a urinalysis will differentiate and confirm.
• WBC casts are found only on pyelonephritis.
o Nitrofurantoin provides excellent coverage for uncomplicated urinary tract infections.
§ Pyelonephritis
• N/V, fever & chills & flank pain
o We can give Bactrim or oral cipro for pyelonephritis.
§ Cystitis
• Burning on urination/frequency/urgency
o Interstitial cystitis
• Chronic pelvic pain, most associated w/ bladder filing, urinary urgency, and frequency
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SIMPLE VS COMPLICATED UTI
ACUTE SIMPLE CYSTITIS*
• Acute UTI that is presumed to be confined to
the bladder
• There are no signs or symptoms that suggest
an upper tract or systemic infection
• Symptoms and signs of cystitis include
• dysuria, urinary frequency and urgency,
suprapubic pain, and hematuria. .
ACUTE COMPLICATED UTI
• Acute UTI accompanied by signs or symptoms
that suggest extension of infection beyond the
bladder:
•
Fever (>99.9°F/37.7°C)¶
•
•
Chills, rigors, significant fatigue or malaise
beyond baseline, or other features of systemic
illness
Flank pain
•
Costovertebral angle tenderness
•
Pelvic or perineal pain in men
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ACUTE PYELONEPHRITIS
• Infection of the kidney usually caused by an infection from the bladder
• What will we see?
• Chills, fever, vomiting, flank pain and costovertebral tenderness
• What are these patients at risk for?
• Sepsis
• What should we do for patients at risk for sepsis?
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COMPLICATIONS
• Patients with acute complicated UTI can also present with bacteremia,
sepsis, multiple organ system dysfunction, shock, and/or acute renal failure.
This is more likely to occur in patients with urinary tract obstruction, recent
urinary tract instrumentation, or other urinary tract abnormalities, and in
patients who are older adults or have diabetes mellitus.
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GLOMERULONEPHRITIS
• Glomerulonephritis
• Direct inflammation and destruction of the glomerulus
• The more glomeruli damaged the worse the kidney function is
o This can occur from what?
§ Mostly caused from immune mediated infections
§ Strep infections or SLE or vasculitis
§ What is an expected presentation of Glomerulonephritis?
o Oliguria
o Hematuria (rust color or dark) Proteinuria
o Periorbital edema in particular (flood loves migrating there)
o Peripheral edema
o Hypertension as well as notable remarkable findings on the urinalysis
such as red blood cell casts and protein.
o GFR will decrease
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DIAGNOSTIC STUDIES WILL SHOW
• Evidence of a streptococcal infection
• Elevated BUN & Creatinine
• Urinalysis
• Presence of RBC/ Protein
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COMPLICATIONS
• N/V Headache leading into seizures
• AKI
• Fluid overload (systemically)
• Listen to lung sounds – rales
• Hypertensive encephalopathy
• Due to hypertensive state
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CKD
• is an umbrella term that describes kidney damage or a decrease in GFR lasting 3 or
more months.
• Is a progressive irreversible deterioration in renal function
• Untreated CKD can result in ESRD which is the final stage of CKD.
• Risk Factors include CVD, diabetes, hypertension and obesity.
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CAUSES OF CHRONIC KIDNEY FAILURE
• Diabetes mellitus
• Hypertension
• Chronic glomerulonephritis
• Pyelonephritis or other infections
• Obstruction of urinary tract
• Hereditary lesions
• Vascular disorders
• Medications or toxic agents
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SYMPTOMS
• CKD can cause retention of fluid, potassium and phosphate.
• How do we treat this?
• Diet adjustments limiting foods high in Na, K , P
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CKD STAGES
NORMAL GFR IS >120ML/MIN
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RENAL FUNCTION TESTS
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DIAGNOSTIC IMAGING
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KIDNEY FAILURE
• Results when the kidneys cannot remove wastes or perform regulatory functions
• A systemic disorder that results from many different causes
• Acute kidney injury is a reversible syndrome that results in decreased glomerular
filtration rate and oliguria
• Chronic renal failure (ESRD) is a progressive, irreversible deterioration of renal function
that results in azotemia
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NURSING PROCESS: THE CARE OF PATIENTS WITH CHRONIC
KIDNEY DISEASE AND ACUTE KIDNEY INJURY—ASSESSMENT
• Fluid status
• Nutritional status
• Patient knowledge
• Activity tolerance
• Self-esteem
• Potential complications
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NURSING PROCESS: THE CARE OF PATIENTS WITH CHRONIC
KIDNEY DISEASE AND ACUTE KIDNEY INJURY—DIAGNOSIS
• Excess fluid volume
• Imbalanced nutrition
• Deficient knowledge
• Risk for situational low self-esteem
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COLLABORATIVE PROBLEMS AND COMPLICATIONS
• Hyperkalemia
• Pericarditis
• Pericardial effusion
• Pericardial tamponade
• Hypertension
• Anemia
• Bone disease and metastatic calcifications
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NURSING PROCESS: THE CARE OF PATIENTS WITH CHRONIC
KIDNEY DISEASE AND ACUTE KIDNEY INJURY—PLANNING
• Goals may include:
• Maintaining IBW without excess fluid
• Maintenance of adequate nutritional intake
• Increased knowledge
• Participation of activity within tolerance
• Improved self-esteem
• Absence of complications
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EXCESS FLUID VOLUME
• Assess for s/s of fluid volume excess, keep accurate I&O, and daily weights
• Limit fluid to prescribed amounts
• Identify sources of fluid
• Explain to patient and family the rationale for fluid restrictions
• Assist patient to cope with the fluid restrictions
• Provide or encourage frequent oral hygiene
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HEMODIALYSIS
• Mimics the kidneys to filter the
blood
• Graft vs fistula
• Graft is synthetic
• Fistula is own vessels
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DIALYSIS TREATMENT
• Prior to treatment of dialysis, the
nurse should assess what?
• What is the patient on dialysis at
risk for?
• What should we do with medication
administration prior to dialysis
treatment?
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IMAGING
• Most patients with acute complicated UTI do not warrant imaging studies for diagnosis or
management
• Imaging is generally reserved for those who are severely ill, have persistent clinical
symptoms despite 48 to 72 hours of appropriate antimicrobial therapy, or have suspected
urinary tract obstruction (eg, if the renal function has declined below baseline or if there is
a precipitous decline in the urinary output).
• Imaging is also appropriate in patients who have recurrent symptoms within a few weeks
of treatment.
• CT Scan/ Renal Ultrasound/MRI
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MANAGEMENT
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MANAGEMENT
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MANAGEMENT
• Empiric antimicrobial therapy should be initiated promptly, taking into
account risk factors for drug resistance, including previous antimicrobial use
and results of recent urine cultures,
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