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The nephron is the functional unit of the kidney. Each kidney contains approximately 1 million nephrons.  Each nephron is composed of the glomerulus, Bowman's capsule, and a tubular system.

The tubular system consists of the proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting tubules.

The glomerulus, Bowman's capsule, proximal tubule, and distal tubule are located in the cortex of the kidney.

The loop of Henle and collecting tubules are located in the medulla. Several collecting tubules join to form a single collecting duct. The collecting ducts eventually merge into a pyramid that empties via the papilla into a minor calyx.

Selective Filtration

Proximal tubule – Reabsorption of 80% of electrolytes and H2O, all glucose and amino acids, HCO3; secreation of H+ and creatinine

c

Loop of Henle– Ascending limb - Reabsorption of Na+ and Cl- ; descending loop – reabsorption of H2O; conceration of filtrate

Distal tubule – Secretion of K+, H+, ammonia; reabsorption of H2O (reulated by ADH); reabsorption of HCO2; regulation of Ca2+ and PO2/4 by parathyroid hormone, regulation of Na+ and K+ by aldosterone

c

Collecting duct -  Reaabsorption of water (ADH required)

What are the age related changes in the renal system?

Anatomic changes in the aging kidney include a 20% to 30% decrease in size and weight between ages 30 and 90 years. By the seventh decade of life, 30% to 50% of glomeruli have lost their function.Atherosclerosis accelerates the decrease of renal size with age. Despite these changes, older individuals maintain body fluid homeostasis unless they encounter diseases or other physiologic stressors.5

Physiologic changes in the aging kidney include decreased renal blood flow, due in part to atherosclerosis, resulting in a decreased GFR. Alterations in hormone levels including ADH, aldosterone, and ANP result in decreased urinary concentrating ability and alterations in the excretion of water, sodium, potassium, and acid. Under normal conditions, the aging kidney is able to maintain homeostasis. However, after abrupt changes in blood volume, acid load, or other insults, the kidney may not be able to function effectively because much of its renal reserve has been lost.

Kidney

¯Renal tissue

¯ # of nephrons and renal bld vessels; thickened basement mb of BC and Glomeruli

¯ Fnx of loop of Henle and Tubules

Assement findings:

Less palpable

¯Creatinine clearance

­ +BUN

­+Serum creatinine

Alterations in drug excretion

Nocuria

Loss of nrmal diurnal excretory patter due to ¯ability to concentrate urine

¯Urine vol

Ureter, Bladder, and Urethra

¯Elasticity and muscle tone

Weakening urinary sphincter

¯Bladder capacity and sensory receptors

Estrogen deviciency leading to thin, dry vaginal tissue

­+Prevalence of unstable

Prostataic enlargement

Assessment:

Palpable bladder after unrination due to retention

Streess incontinence (esp during Valsalva maneuver), dribbling urine after urination

Freq, urgency, nocturia, overflow incontinence

Stress of overactive bladder, dysuria (painful urination)

Overactive bladder

Hesitancy, freq, urgency, nocturia, straining to urinate, retention, dribbling

Assessment:

Palpable bladder after unrination due to retention

Streess incontinence (esp during Valsalva maneuver), dribbling urine after urination

Freq, urgency, nocturia, overflow incontinence

Stress of overactive bladder, dysuria (painful urination)

Overactive bladder

Hesitancy, freq, urgency, nocturia, straining to urinate, retention, dribbling

RENIN

Primary fnx: To increase BP and restore kidneys pressure perfusion

Secreted from juxtaglomerular cells

Released in response to decreased BV, BP or low renal Na+ (ATTEMPTS to increase BP)

Renin release causes production of Angiotensin II (a potent vaso-constrictor)

The renin-angiotensin-aldosterone system is a series of reactions designed to help regulate blood pressure.

1.When blood pressure falls (for systolic, to 100 mm Hg or lower), the kidneys release the enzyme renin into the bloodstream.

Renin is important in the regulation of blood pressure. Renin is produced and secreted by juxtaglomerular cells of the kidney (Fig. 45-4). 

The plasma protein angiotensinogen (from the liver) is activated to angiotensin I by renin. Angiotensin I is subsequently converted to angiotensin II by angiotensin-converting enzyme (ACE). ACE is located on the luminal surface of all blood vessels, with particularly high levels in the vessels of the lungs. Angiotensin II stimulates the release of aldosterone from the adrenal cortex, which causes Na+ and water retention, leading to an increased ECF volume. Angiotensin II also causes increased peripheral vasoconstriction. Release of renin is inhibited by an elevation in blood pressure brought about by increased ECF,vasoconstriction, and an increase in plasma sodium. Excessive renin production caused by impaired renal perfusion may be a contributing factor in the etiology of hypertension

Renin is released into the bloodstream in response to" decreased renal perfusion

decreased arterial blood pressure

decreased ECF

decreased serum Na+ concentration

increased urinary Na+ concentration.

What are the medications affecting BP regulation? What are the effects on kidney regulation?

• Thiazides and Thiazide-like diuretics
• Loop (high-ceiling diuretics)
• Osmotic diuretics
• Potassium-sparing diuretics
• Beta-blockers (a.k.a. Beta-adrenergic Blockers) “the –olols”
• ACE Inhibitors “the –prils”
• Calcium Channel Blockers

Thiazides and Thiazide-like diuretics

Thiazides and Thiazide-like diuretics- (HCTZ) Acts on the distal convoluted renal tubule, beyond the loop of Henle, to promote sodium, chloride, potassium, magnesium and water excretion. Used to tx HTN and peripheral edema. Used for clients with normal renal function.

Monitor for:

Hypercalcemia (b/c. Ca is reabsorbed),

Glucose tolerance.

Usually combined with other anti-HTN meds. MUST HAVE GOOD KIDNEY FNX

KNOW METABOLIC PANEL – ELECTROLYTES LEVEL BEFORE GIVING. Will have to replace if low.

1.     Decrease hypertension (lower blood pressure) and to

2.     Decrease edema (peripheral and pulmonary) in heart failure (CHF) and renal or liver disorders

Loop (high-ceiling diuretics)- acts on the ascending loop of Henle by inhibiting chloride transport of sodium into the circulation. Sodium and water are lost, together with potassium, calcium, and magnesium. Have little effect on the blood sugar. Uric acid level increases. More potent that thiazides as diuretics. Increases renal blood flow up to 40% (Lasix, Furosemide, Bumex, Torsemide) 

MBP – Metabolic panel.  Only wan to get rid of excess fluid. CREATINE CLEARANCE

Osmotic diuretics (Mannitol, Urea)-increases the osmolality (concentration) of the plasma and fluid in the renal tubules. Na, Cl, K, and water are excreted. Used to prevent renal failure, decrease ICP, IOP. INTRACRANIAL PRESSURE OR INTRAOCULAR PRESSURE

Potassium-sparing diuretics-

Potassium-sparing diuretics- weaker than thiazides and loop diuretic. Monitor for Hyperkalemia. (Aldactone, Aldosterone, Amiloride, Triamterene. Usually used with a diuretic.Never used with ACE inhibitors 

KEEPS POTASSIUM- RISK FOR HYPERKALEMIA

Beta-blockers (a.k.a. Beta-adrenergic Blockers)-reduces renin (enzyme) release. (Acebutolol, Atenolol, Betaxolol,

Metoprolol, all the suffix –olol)

CAN MASK S/S of  HYPOGLYCEMIa

ACE Inhibitors

ACE Inhibitors- tx HTN and CHF, blocks Angiotensin II and inhibits formation of Aldosterone (Benazepril, Captopril, Lisinopril, etc.) PRILS

HTN and CHF

c

Calcium Channel Blockers- decreases Calcium levels to promote vasodilation

Serum pH

↑↓

↑Alkalosis

↓Acidosis

135-145 mEq/L

↑Impaired Renal fnx

↓Diabetic ketoacidosis, diuretic therapy, water intoxication

Main extracellular electrolyte determining blood volume. Usually values stay within normal range until late stages of renal failure.

3.5-5.0

↑Renal failure, Addison's disease, diabetic ketosis, massive tissue destruction

↓Cushing syndrome, diarrhea
(severe), diuretic therapy,
gastrointestinal fi stula,
pyloric obstruction,
starvation, vomiting

Kidneys are responsible for excreting majority of body's potassium. In renal disease, K+ determinations are critical because K+ is one of the first electrolytes to become abnormal. Elevated K+ levels of >6 mEq/L can lead to muscle weakness and cardiac dysrhythmias.

6-20 mg/dl

↑Renal disease, increase in protein catabolism
(fever, stress),
urinary tract infection

↓Malnutrition, severe liver
damage

Blood urea nitrogen or BUN test is primarily used, along with the creatinine test, to evaluate kidney function in a wide range of circumstances, to help diagnose kidney disease, and to monitor patients with acute or chronic kidney dysfunction or failure. It also may be used to evaluate a person’s general health status when ordered as part of a basic metabolic panel

Creatinine Clearance

Creatinine urine

Creatinine serum

Serum Creatinine 0.2-1.0

Creatinine urine 6.0-2.0g/day

Creatinine clearance 59-137 ml/min/1.73m2

urin creatinine mg/ml x urine vol ml/min ÷Serum Creatinine mg/ml

Creatinine is a waste product of protein breakdown (primarily body muscle mass). Clearance of creatinine by kidney approximates the GFR.

Na

↑↓

135-145 mEq/L

Main extracellular electrolyte determining blood volume. Usually values stay within normal range until late stages of renal failure.

↑impaired renal fnx

↓Diabetic ketoacidosis, diuretic therapy water intoxication

1.5-2.5 mEq/L

↑Addison’s disease, hypothyroidism, absence of reflexes, resp failure and renal failure

↓Chronic alcoholism, severe
malabsorption

Magnesium is primarily excreted by the kidneys. Hypermagnesemia is generally not a problem unless the patient is ingesting magnesium (e.g., milk of magnesia, magnesium citrate, antacids containing magnesium). Clinical manifestations of hypermagnesemia can include absence of reflexes, decreased mental status, cardiac dysrhythmias, hypotension, and respiratory failure, People with kidney disease may not be able to excrete excess amounts of magnesium

22-26 mEq/L

Most patients in renal failure have metabolic acidosis and low serum HCO3– levels.

­ ↑Resp Acidosis, metabolic alkalosis

↓Resp alkalosis, metabolic acidosis

The anemia is due to decreased production of the hormone erythropoietin by the kidneys. Erythropoietin normally stimulates precursor cells in the bone marrow to produce RBCs (erythropoiesis). 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. Blood loss due to dialysis can be a contributing factor too

Homeostasis

Fluid regulation

Acid-base balance

Blood pressure control

Renin production (enzyme)

Erythropoietin production

Vitamin D activation

Filtration and excretion

Kidney Acid Base Balance

Secrete hydrogen ions

Reabsorb sodium and bicarbonate ions

Acidify phosphate salts

Produce ammonia

Acidosis pH < 7.35 (metabolic acidosis)

Alkalosis pH > 7.45 (metabolic alkalosis)

K. Na, P

 Sodium and salt should not be equated because the sodium content in 1 g of sodium chloride is equivalent to 400 mg of sodium.

Potassium restriction depends on the ability of the kidneys to excrete potassium. Most salt substitutes should be avoided if patients have been instructed to restrict potassium because they contain potassium chloride.

As kidney function deteriorates, phosphate elimination by the kidneys is diminished and the patient begins to develop hyperphosphatemia. Limit 1g/day

Monitor respiratory pattern for symptoms of respiratory difficulty (e.g., dyspnea, tachypnea, and shortness of breath) that are indicators of fluid excess.

Weigh patient daily and monitor trends to evaluate interventions.

Monitor intake and output to determine effect of treatment on kidney function.

Provide appropriate diet to help control edema and hypertension.

Instruct patient and/or caregivers on measures instituted to treat the hypervolemia (e.g., daily weights, fluid restrictions) to help monitor and control fluid overload and related hypertension

Color

      Dark hematuria

      Colorless  Excessive fluid, renal disease, or diabetes insipidus

Protein

      Persistent proteinuria – acute and cronic renal disease, esp involving glomeruli; heart failure

Glucose

      Glycosuria (excretion of glu in urine) – DM, low renal threshold for glu reabsorp

Ketones

      Prestent – Altered carb and fat metab in DM; dehydration

Specific gravity 1.003-1.030

            Low Dilute urine, excessive diuresis; diabetes insipidus

            High -  dehydration, glycosuria

Osmolality 300-1300 mOsm/kg

<300 Tubular dysfunction; kidney lost ability to concentrate or dilute urine (not part of routine urinalysis)

pH (urine) 4.0-8.0 (avg 6.0)  

            <4 Resp or metabolic acidosis

RBC 0.4/hpf

      >4 glomerulonephritis, kidney biopsy

WBC 0-5/hpf

      >5 UTI or inflammation

Urinalysis - General examination of urine to establish baseline information or provide data to establish a tentative diagnosis and determine whether further studies are to be ordered

Try to obtain first urinated morning specimen. Ensure specimen is examined within 1 hr of urinating. Wash perineal area if soiled with menses or fecal material.

59-137 ml/min/1.73m2

Creatinine is a waste product of protein breakdown (primarily body muscle mass). Clearance of creatinine by kidney approximates the GFR

Collect 24-hr urine specimen. Discard first urination when test is started. Save urine from all subsequent urinations for 24 hr. Instruct patient to urinate at end of 24 hr and add specimen to collection. Ensure that serum creatinine is determined during 24-hr period.

Reference interval: ≤50 mL urine (increases with age)

Residual - Determines amount of urine left in bladder after urinating. Finding may be abnormal in problems with bladder innervation, sphincter impairment, BPH, or urethral strictures.

If residual urine test is ordered, catheterize patient immediately after urinating or use bladder ultrasound equipment. If a large amount of residual urine is obtained, health care provider may want catheter left in bladder.

Urea nitrogen (BUN)

Used to identify presence of renal problems. Concentration of urea in blood is regulated by rate at which kidney excretes urea.

Reference interval: 6-20 mg/dL (2.1-7.1 mmol/L).

Be aware that when interpreting BUN, nonrenal factors may cause increase (e.g., rapid cell destruction from infections, fever, GI bleeding, trauma, athletic activity and excessive muscle breakdown, corticosteroid therapy).

Creatinine

More reliable than BUN as a determinant of renal function. Creatinine is end product of muscle and protein metabolism and is liberated at a constant rate.

Reference interval: 0.6-1.3 mg/dL (53-115 µmol/L).

Explain test and watch for postpuncture bleeding.

BUN/creatinine ratio

Reference interval: 12:1 to 20:1.

Uric Acid see Uric acid card

Fatigue
Headaches
Blurred vision
Elevated blood pressure
Anorexia
Nausea and vomiting
Chills
Itching
Excessive thirst
Change in body weight
Cognitive changes

Edema

acial (periorbital)
Ankle
Ascites
Anasarca
Sacral
Dysuria

Pain
Flank or costovertebral angle
Groin
Suprapubic

Female: 2.3-6.6 mg/dL (137-393 µmol/L)

Male: 4.4-7.6 mg/dL (262-452 µmol/L)

Higher than normal uric acid levels in the blood is called hyperuricemia and can be caused by the over-production of uric acid in the body or the inability of the kidneys to clear out enough uric acid

Used as screening test primarily for disorders of purine metabolism but can also indicate kidney disease. Values depend on renal function, rate of purine metabolism, and dietary intake of food rich in purines

Explain test and watch for postpuncture bleeding.

VITAMIN D

Activated in liver and kidneys

Activated Vitamin D is essential for absorption of calcium in GI tract

Renal failure can lead to alteration in Calcium and Phosphate balance

Radiology procedures
KUB, IVP, Retrograde pyelogram, renal angiogram, renal ultrasound, CT scan, etc.
Renal biopsy

Cystoscopy

KUB- to detect kidney stones
IVP- use contrast dye (nephrotoxic); check lesions obstructions
Renal US- check for masses
Bladder scan- check for residual urine
CT scan- use IV contrast.
Renal angiography- check renal vessels; use contrast
Renal biopsy- complication: hemorrhage

Prerenal

Intrarenal

Postrenal

Prerenal - heart/aorta

Intrarenal- Kidneys

Postrenal - Ureters/bladder

What are infections of the UT?

Upper and lower?

Lower UTI - cystitis (bladder inflammation) and erethritis (urethra)

Upper UTI - pylonephritis (kidney infection)

Most common UTI pathogen?

Counts indicating signifant UTI?

Minimal indicative count?

Patients at risk
Are immunosuppressed
Have diabetes
Have undergone multiple antibiotic courses
Have traveled to certain Third World countries

Hospital aquired UTI account for what %?

Cause of HA UTI?

Hospital-acquired UTI accounts for 31% of all nosocomial infections.
Causes
Often: E. coli
Seldom: Pseudomonas
Catheter-acquired UTIs
Bacterial biofilms develop on inner surface of catheter.

Urine for culture and sensitivity (if indicated)

Clean-catch sample preferred
Specimen by catheterization or suprapubic needle aspiration more accurate
Determine susceptibility of bacteria to antibiotics

Imaging studies
IVP or abdominal CT when obstruction suspected
Renal ultrasound for recurrent UTIs

Antibiotics
Selected on empiric therapy or results of sensitivity testing
Uncomplicated cystitis
Short-term course (1 to 3 days)
Complicated UTIs
Require long-term treatment (7 to 14 days)

Nitrofurantoin (Macrodantin)
Given 3 or 4 times a day
Long-term use
Pulmonary fibrosis
Neuropathies
Fluoroquinolones
Treat complicated UTIs
Example: Ciprofloxacin (Cipro)
Trimethoprim/sulfamethoxazole (TMP/SMX)
Used to treat uncomplicated or initial
Inexpensive
Taken twice a day
E. coli resistance to TMP-SMX ↑

What are two urinary analgesics?

What effect do they have?

Pyridium
Used in combination with antibiotics
Provides soothing effect on urinary tract mucosa
Stains urine reddish orange
Can be mistaken for blood and may stain underclothing
OTC

Urised
Used in combination with antibiotics
Used to relieve UTI symptoms
Preparations with methylene blue tint urine blue or green.

Inflammation of the bladder
ASSESSMENT FINDINGS:
Dysuria
Urinary frequency
Urinary urgency
Hematuria
Fever and chills
Increasing flank pain
Elevated WBC

Antibiotics Septra, Pyridium
Antipyretics
Antispasmodic
Force fluids
Proper hygiene
Bedrest
Treat underlying cause
Hospitalization- if acute

Infection/Inflammation of the urethra
ASSESSMENT FINDINGS:
Manifestations: same as cystitis, urethra tender, discharge present

Often associated with STD’s in men (gonorrhea), in women (chlamydia, trichomonas, monolilial).

Monitor VS, I/O
Increase fluid intake
 Collect sample
Antibiotics: Bactrim, Flagyl (trichomonas), Diflucan (monilial)

What are urinary Tract Calcul?

Risk factors?

Kidney stones

Metabolic
Abnormalities that result in increased urine levels of calcium, oxaluric acid, uric acid, or citric acid
Climate
Warm climates that cause increased fluid loss, low urine volume, and increased solute concentration in urine
Diet
Large intake of dietary proteins that increases uric acid excretion
Excessive amounts of tea or fruit juices that elevate urinary oxalate level
Large intake of calcium and oxalate
Low fluid intake that increases urinary concentration
Genetic Factors
Family history of stone formation, cystinuria, gout, or renal acidosis
Lifestyle
Sedentary occupation, immobility

The overall goals are that the patient with urinary tract calculi will have

(1) relief of pain

(2) no urinary tract obstruction

(3) knowledge of ways to prevent further recurrence of stones. (lo purines, oxalate, calcium.)

What is pyelonephritis?

Pathophysiology?

Pyelonephritis is an inflammation of the renal parenchyma (in renal medulla) and collecting system (including the renal pelvis). The most common cause is bacterial infection, but fungi, protozoa, or viruses sometimes infect the kidneys. Usually begins with colonization and infection of the lower urinary tract via the ascending urethral route

Infection spread by ascending microorganisms along the ureters or by way of bloodstream

Fever

chills

flank or low back pain
nausea, and vomiting

headache

malaise

painful urination

CVA tenderness

Diagnostic tests: CBC, WBC, STD’s testing, CT scan to detect abscess, US, KUB to check for tumor or cysts, IVP, UA/CS
Antibiotics
Anti-pyretics
Increase water intake
Treat underlying cause
Relieve obstruction if present

What is urinary incontinence?

Interventions?

uncontrolled leakage of urine. Among young adult to middle-aged women, the prevalence is 30% to 40% and it increases to 30% to 50% in older women

NOT a natural cause of aging

Interventions

Pelvic floor exercises and biofeedback with lifestyle modifications can help prevent or reverse incontinence

SIS R UFO

Stress Sudden increase in intraabdominal pressure causes involuntary passage of urine. (giving birth, lo estrogen, prostate surgery)

Incontinence after surgery and trauma - Vesicovaginal or urethrovaginal fistula may occur in women. (Fistulas)

Reflex -  occurs when no warning or stress precedes periodic involuntary urination. Spinal cord lesion above S2

Urge -involuntary urination is preceded by urinary urgency. Overactivity of detrusor muscle - CNS diseases

Functional - Loss of urine resulting from cognitive, functional, or environmental factors (elderly due to problems w/mobility and balance)

Overflow - when the pressure of urine in overfull

bladder overcomes sphincter control, obstruction or detrouser caused by myogenic or neurogenic factors (DM)

What is IVP?

Pre and post procedure care

Visualizes urinary tract after IV injection of contrast media.

Presence, position, size, and shape of kidneys, ureters, and bladder can be evaluated.

Cysts, tumors, lesions, and obstructions cause a distortion in normal appearance of these structures. Patient with significantly decreased renal function should not have IVP, because contrast media can be nephrotoxic and worsen renal function.*

Post care

Evening before procedure, give cathartic or enema to empty colon of feces and gas.

Assess for iodine sensitivity

Inform patient that procedure involves lying on table and having serial x-rays taken.

Advise patient that warmth, a flushed face, and a salty taste during injection of contrast material may occur.

Post procedure

Force fluids (if permitted) to flush out contrast media.

What is a renal biopsy?

pre and post procedure

Obtains renal tissue for examination to determine type of renal disease or to follow progress of renal disease. Technique is usually done as a skin (percutaneous) biopsy through needle insertion into lower lobe of kidney. Can be performed with CT or ultrasound guidance. Absolute contraindications are bleeding disorders, single kidney, and uncontrolled hypertension. Relative contraindications include suspected renal

infection, hydronephrosis, and possible vascular lesions.

Type and crossmatch patient for blood. Ensure consent form is signed.

Pre pocedure

Type and crossmatch patient for blood. Ensure Consent form

Ascertain coagulation status through patient history, medication history, CBC, hematocrit, prothrombin time, and bleeding and clotting time.

Discontinue anticoagulants

After procedure: Apply pressure dressing and keep on affected side for 30-60 min; bed rest for 24 hr.

Vital signs every 5-10 min,first hour.

Assess for flank pain, hypotension, decreasing hematocrit, ↑ temperature, chills, urinary frequency, dysuria, and serial urine specimens (gross/microscopic hematuria).

Urine dipstick can be used to test for bleeding in urine. Inspect biopsy site for bleeding. Instruct patient to avoid lifting heavy objects for 5-7 days and to not take anticoagulant drugs until allowed by health care provider.

What is a renal scan?

Pre and post procedure

valuates anatomic structures, perfusion, and function of kidneys. Radioactive isotopes are injected IV. Radiation detector probes are placed over kidney, and scintillation counter monitors radioactive material in kidney. Radioisotope distribution in kidney is scanned and mapped. Shows location, size, and shape of kidney and, in general, assesses blood flow, glomerular filtration, tubular function, and urinary excretion. Abscesses, cysts, and tumors may appear as cold spots because of presence of nonfunctioning tissue. Also used to monitor function of a transplanted kidney.

Requires no dietary or activity restriction. Inform patient that no pain or discomfort should be felt during test.

What is a KUB?

pre and post procedure

Involves x-ray examination of abdomen and pelvis and delineates size, shape, and position of kidneys. Radiopaque stones and foreign bodies can be seen.

Perform bowel preparation (if ordered).

What is an antegrade pyelogram (nephrostogram)

pre and post procedure

What is a renal arteriogram?

pre andpost procedure?

Visualizes renal blood vessels. Can assist in diagnosing renal artery stenosis additional or missing renal blood vessels, and renovascular hypertension. Can assist in differentiating between a renal cyst and a renal tumor. Also included in workup of a potential renal transplant donor. A catheter is inserted into the femoral artery and passed up the aorta to the level of the renal arteries (Fig. 45-9). Contrast media is injected to outline the renal blood supply.*

Before procedure: Prepare patient the prior evening by giving cathartic or enema. Before injection of contrast material, test for iodine sensitivity. The patient may experience a transient warm feeling along the course of the blood vessel when contrast media is injected. After procedure: Place a pressure dressing over femoral artery injection site. Observe site for bleeding. Have patient maintain bed rest with affected leg straight. Take peripheral pulses in the involved leg every 30-60 min to detect occlusion of blood flow caused by a thrombus. Observe for complications including thrombus, embolus, local inflammation, and hematoma.

Med for chronic renal failure

Epogen

Procrit

Man-made epoetin alfa called colony-stimulating factor to stimulate cells in the bone marrow to multiply and produce RBC

 Target patient with HGB 10-12

The erythropoietin that is used for therapy, called epoetin alfa, is man-made. It is a product of the genetic engineering of ovarian cells of the Chinese hamster and is produced through recombinant DNA technology in bacteria. It does not cure the underlying cause of the anemia, and unless the underlying cause can be reversed, treatment with epoetin alfa must be continued indefinitely. Epoetin alfa belongs to a class of drugs called colony-stimulating factors because of their ability to stimulate cells in the bone marrow to multiply and form colonies of identical cells

Natriuretic Hormone: The right atrium of the heart releases this in response to increased volume and stretch (preload bld load in ventricle at end of diastole)

Inhibits ADH secretion so that the collecting tubules in the kidney are less porous and a larger amount of urine is thus produced (decreasing preload)

Increase aldosterone= decrease in urine output

Post- surgery: Increased ADH release=increase in water reabsorption= decrease in urine output

Anesthesia and/or narcotics= decrease bladder fullness sensation

More water reabsorbed less excreated

Cytoscopy?

Pre and postcare?

Inspects interior of bladder with a tubular lighted scope (cystoscope) Can be used to insert ureteral catheters, remove calculi, obtain biopsy specimens of bladder lesions, and treat bleeding lesions. Lithotomy position is used. Procedure may be done using local or general anesthesia, depending on needs and condition of patient. Complications include urinary retention, urinary tract hemorrhage, bladder infection, and perforation of the bladder

Before procedure: Force fluids or give IV fluids if general anesthesia is to be used. Ensure consent form is signed. Explain procedure to patient. Give preoperative medication.

Prepocedure

Force fluids or give IV fluids if general anesthesia is to be used. Ensure consent form is signed. Explain procedure to patient. Give preoperative medication.

Postprocedure

Explain that burning on urination, pink-tinged urine, and urinary frequency are expected effects. Observe for bright red bleeding which is not normal. Do not let patient walk alone immediately after procedure because orthostatic hypotension may occur. Offer warm sitz baths, heat, mild analgesics to relieve discomfort.

Renal CT?

Pre and postprocedure?

Visualization of kidneys.

Size

Tumors

Abscesses

Suprarenal masses (e.g., adrenal tumors, pheochromocytomas)

Obstructions

Advantage of CT over ultrasound is its ability to distinguish subtle differences in density.

Use of IV-administered contrast media during CT accentuates density of renal tissue and helps differentiate masses

Preprocedure 

Iodine sensitivity.

Lie very still during the procedure while the machine takes precise transaxial images.

Sedation may be required if patient is unable to cooperate.

No postprocedure

Acute Kidney injury (AKI)/

Acute Kidney Failure

• A rapid rise in serum creatinine and/or < urine output. (Severity may range from mild to aztemia - accumulation of nitrogenous wate products in the blood may warrant renal replacement)
• Usually develops over hrs or days with progressive > in BUN, creatinine and K w or w/o < urine output.
• < perfusion of kidney that results in:
• Damaged nephrons
• May develop into:

• severe prolonge HYPOtension or hypovolemia or exposure to a nephrotoxic agent.
• 60% of ICU pts (70-80% mortality)

• Factors that reduce systemic circulation causing a < in renal bld flow and lead to < glomerular perfusion and filtration fo kidnesy.
• Glomerular and renal tubular vnx are preseverd, but glomerular filtration is < as a result of < perfusion.

• No damage to kideny tissue (parenchyma).
• Cuased by < in circulating bld voume (severe dehydration, < cardiac output, burns) and is usually REVERSIBLE.
• >angiotension II, aldosterone, NE, and ADH attempt to presever bld flow to organs.
• Can lead to intrarenal disease if ischemia is prolonged.

• Conditions that cause direct damage to the kidney tissue, resulting in impaired nephron fnx.
• Usually results from prolonged ischemia, nephrotoxins (e.g., aminoglycoside antibiotics, contrast media), hemoglobin released from hemolyzed red blood cells (RBCs), or myoglobin released from necrotic muscle cells.
• Acute glomerulonephritis
• Systemic lupus erythematosus
• ATN - acute tubular necrosis - most common cuase 90% - result of ischemia, nephrotoxins or sepsis.  REVERSIBLE IF basement mb is not destroyed and tubular epithelium regenerates. - risks - major surgery, shock, sepsis, bld transfusion rx, muscle injury from trauma, prolonged hypotension and nephrotoxic agents.

• Mechanical obstrution in the outflow of urine.
• Urine refluxes into renal pelvis, impairing kidney fnx.
• Common cuases:   Benign prostatic hyperplasia, prostate cancer, calculi, trauma, extrarenal tumors.
• Bilateral ureteral obstruction leads to hydronephrosis (kidney dilation), > hydrostatic pressure, and tubular blockage resulting in progressive < in kidney fnx.
• Unilateral obstructioon rarely results in azotemia and if bilateral is relieved w/in 48 hrs. > 12 wks unlikely.

Prerenal

Causes

Hypovolemia
•    Dehydration
•    Hemorrhage
•    GI losses (diarrhea, vomiting)
•    Excessive diuresis
•    Hypoalbuminemia
•    Burns
Decreased Cardiac Output
•    Cardiac dysrhythmias
•    Cardiogenic shock
•    Heart failure
•    Myocardial infarction
Decreased Peripheral Vascular Resistance
•    Anaphylaxis
•    Neurologic injury
•    Septic shock
Decreased Renovascular Blood Flow
•    Bilateral renal vein thrombosis
•    Embolism
•    Hepatorenal syndrome
•    Renal artery thrombosis

Intrarenal

Causes

Nephrotoxic Injury
•    Drugs (aminoglycosides [gentamicin, amikacin], amphotericin B)
•    Radiocontrast agents
•    Hemolytic blood transfusion reaction
•    Severe crush injury
•    Chemical exposure (ethylene glycol, lead, arsenic, carbon tetrachloride)
Interstitial Nephritis
•    Allergies (antibiotics [sulfonamides, rifampin], nonsteroidal antiinflammatory drugs, ACE inhibitors)
•    Infections (bacterial [acute pyelonephritis], viral [CMV], fungal [candidiasis])
Other Causes
•    Prolonged prerenal ischemia
•    Acute glomerulonephritis
•    Thrombotic disorders
•    Toxemia of pregnancy
•    Malignant hypertension
•    Systemic lupus erythematosus

Postrenal

Causes

•    Benign prostatic hyperplasia
•    Bladder cancer
•    Calculi formation
•    Neuromuscular disorders
•    Prostate cancer
•    Spinal cord disease
•    Strictures
•    Trauma (back, pelvis, perineum)

AKI may progress through phases: oliguric, diuretic, and recovery. In some situations, the patient does not recover from AKI, and CKD results, eventually requiring dialysis or a kidney transplant

RIFLE

Staging of AKI

• Risk - creatinine > x 1.5 or GFR < by 25%/Urine output < 0.5 ml/dk/hr for 6 hr
• Injury - creatinine x 2 or GFR < by 50%/Urine output < 0.5 ml/kg/hr for 12 hr
• Failure - creatinine increased x 3 or GFR < by 75% or creatinine > mg/dl w/ acute rise >= 0.5 mg/dl - Urine output < 0.3 ml/kg/hr for 24 hr (OLIGURIA)
• Loss - Persistent acute kidney failure; complete loss of kidney fnx > 4 wk
• End-stage kidney disease - Complete loss of fnx > 3 mo

• Most common initial manifestation of AKI
• < 400 ml/day urine output
• Occurs within 1-7 days of injury (24 hrs with injury/1 wk with nephrotoxicity)
• Commonly seen w/prerenal
• Urinalysis may show RBCs, WBC and a specific gravity around 1.010 and urine osmolality about 300 may have proteinuria
• Begins when first signs of renal failure is apparent.
• Most common sign is oliguria non-responsive to fluid challenges or diuretics
• > BUN and creatinine may be present

• Ammonia coannot be synthesized
• HCO3 <, resabsorption <
• Kassmaul resp.

• Damaged tubules cannot conserve Na
• Urinary excretion of Na may > = low Na
• AVOID excessive Na intake -> volume expansion, HTN and HF
• Uncontrolled Hyponatremia or water excess can lead to cerebral edema.

• K+ > kidney cannot excrete
• If tissue trauma caused AKI - damaged cells release K+ into ECF
• Bleedng and bld transfusions may destroy cells -> K+ into ECF
• Acidosis worsens hyper K -> H+ ions drive K+ into ECF
• Mostly asymptomatic
• ECG

• Marked by restoration of kidney fnx
• Leveling off of BUN, creatinine and electrolytes
• Lasts approx. 10 days (1-3 wks) and ends when serum levels return to normal
• Can result in an output of 10L/day to dilute urine.
• Kidneys have recovered ability to excrete wastes, but no concentrate urine.

Chronic Kidney Disease (CKD)

Diagnostics

Stages

• A progressive loss of nephron fnx which ultimately causes the kidneys to lose their ability to filter waste and mntn homeostasis
• The presence of kidney damage or a < GFR < than 60 ml/min/1.73 m2 for longer than 3 months
• Stage 1:
• >= 90 or > GFR
• Action - diagnosis and treatment -CVD risk reduction, slow progression
• Stage 2
• Kidney damage with mile < 60-89 GFR
• Action - estimating progression
• Stage 3
• Moderate < GFR 30-59
• Action - evaluating and treating complicatons
• Stage 4
• Severe < GFR 15-29
• Action - preparation for kidney replacement therapy
• Stage 5
• Kidney failure - (ESRD) - GFR < 15 (or dialysis)
• Action - Kidney replacement (if uremia present and pt desires treatment)

• DM 2/3
• HTN 1/3
• More common than AKI
• 1 in 9 Americans
• HF
• Ureteral or prostatic obstruction

Uremia

• A syndrome in which kidney fnx declines to the point that symptoms develop in multiple body systems. 
• Most often when GFR is <= 10 mL/min.

CKD

Urinary changes

• Usually no change in urine output - Polyuria may be present since DM is primary cause of CKD.
• As the CKD progresses, pts will have increasing difficulty with fluid retention and require diuretic therapy.
• Once on dialysis and after a while on dialysis, pt may develp anuria.

•    Early detection and treatment are the primary methods for reducing chronic kidney disease.
•    Monitor blood pressure to detect elevations so treatment can be started early.
•    Ensure proper diagnosis and treatment of diabetes mellitus as it is the leading cause of chronic kidney disease.
•    Treat hypertension appropriately and aggressively as it is the second leading cause of chronic kidney disease.

CKD

Wate product accumulation

• < GFR
• > creatinine
• >BUN (kidney failure, protein intake, fever, corticosteroids, and catabolism) as BUN > increases, nausea, vomiting, lethargy, fatigue, impaired thought processes, and headaches become common as a result of the effects of waste products on the central nervous and GI system

CKD

Altered Carb Metabolism

• caused by impaired glucose use resulting from cellular insensitivity to the normal action of insulin. 
• Moderate hyperglycemia and hyperinsulinemia
• May improve after dialysis
• Patients with diabetes who become uremic may require less insulin than before the onset of CKD  or may stop as disease progresses(kidney excretes insulin - it remains in system longer)

CKD

Elevated Triglycerides

• Hyperinsulinemia stimulates hepatic production of triglycerides.
• Almost al pts w/uremia develp dyslipidemia with elevated VLDLs, normal or < LDL and < HDLs.
• Altered lipid metabolism r/t < levels of enzyme lipoprotein lipase -> breaks down lipids

CKD

Electrolyte/acid-base

• Hyperkalemia - < exretion, breakdown of cellular protien, bleeding and metabolic acidosis.
• Na - may be normal or low in kidney failure.  - Impaired exretion along with water is retained. If water is retained, dilutional hyponatremia can occur.  - Contributes to HF, edema, HTN. Restrict to 2 g/day.
• Ca and PO3/4 see musculoskeletal
• Mg - Hyper magnesemia usually NOT a problem - = absent DTR, < LOC, cardiac dysrhythmias, Hypotn, resp failure.
• Metabolic Acidosis - Failure of kidnesy to excrete acid load (ammonia) and deffectiv reabsorption and regeneration of bicarbonate.

CKD

Anemia

• due to decreased production of the hormone erythropoietin by the kidneys
• < RBC life span
• > hemolysis of RBCs
• Frequent bld samplings
• GI bleed
• HD bld loss
• > levels of parathyroid hormone PTH can inhibit erythropoiesis
• Iron deficiency

CKD

Bleeding

• The most common cause of bleeding in uremia is a qualitative defect in platelet function
• impaired platelet aggregation and impaired release of platelet factor III.
• alterations in the coagulation system with increased concentrations of both factor VIII and fibrinogen are found in the serum of these patients.
• HD or PD can usually correct

CKD

Infection

• caused by changes in leukocyte function and altered immune response and function.
• hyperglycemia and external trauma (e.g., catheters, needle insertions into vascular access sites).

CKD

Cardio system

• Most common cause of death is CV disease t/r vascular calcification and arterial stiffness
• HTN - Na retention and > ECF
• > renin in some
• DM comorbitity and HTN , > triglyceride levels
• Cardiac dysrhythmias - hyperkalemia and < coronary artery perfusion
• Uremic pericarditis (friction rub, chest pain and low-grade fever) -> pericardial effusion and cardiac tamponade.
• HTN -> retinopathy, encephalopathy, and nephropathy.

CKD

Respiratory Changes

• Kussmaul breathing - metabolic acidosis
• Dyspnea from fluid overload
• Pulmonary edema, uremic pleuritis (pleurisy), pleural effusion, and predisposition to respiratory infx r/t < pulmonary macrophage activity.

CKD

GI changes

• Stomatitis w/exudates and ulcerations
• Metallic tast in mouth
• Uremic fetor (urinous odor of breath - urea in bld)
• Anorexia, N/V if CKD -> ESRD and is not treated w/dialysis
• Weight loss and malmutrition
• Delayed gastric emptying -> malnutrition for DM
• GI bleeding r/t mucosal irritation and platelet defect.
• Constipation - ingestion of iron salts and/or Ca containing phosphate binders, fluid limit and physical inactivity.

CKD

Neurologic changes

• The result of increased nitrogenous waste products, electrolyte imbalances, metabolic acidosis, and axonal atrophy and demyelination of nerve fibers.
• CNS depression - lethargy, apathy, decreased ability to concentrate, fatigue, irritability, and altered mental ability.
• Seizures and coma may result from a rapidly increasing BUN and hypertensive encephalopathy.
• Peripheral neuropathy is initially manifested by a slowing of nerve conduction to the extremities. - restless legs syndrom - bugs crawling
• Paresthesias - most often in feet and legs - may be a burning sensation
• Bilateral footdrop
• Muscular weakness and atrophy
• Loss of DTR
• Muscle twitching, jerking, asterixix and nocturnal leg cramps.
• The treatment for neurologic problems is dialysis or transplantation

CKD

Musculoskeletal changes

• CKD mineral and bone disorder (CKD-MBD) develops as a systemic disorder of mineral and bone metabolism due to progressive deterioration in kidney function
• less vitamin D is converted to its active form -> hypocalcemia
• When hypocalcemia occurs, the parathyroid gland secretes parathyroid hormone (PTH), which stimulates bone demineralization, thereby releasing calcium and phosphorus from the bones.
• Hyperphosphatemia also results from decreased phosphate excretion by the kidneys.
• Relase of PTH -> accelerated rate of bone remodeling -> weakened bone matrix - > risk for fractures.
• Hypocalcemia is usually asympomatic.
• Osteomalacia - r/t demineralization from slow bone turnover and defective mineralization of new bone
• Osteitis fibrosa - decalcification of bone and replacement of bone tissue w/fibrous tissue
• “Uremic red eye” is caused by the irritation from deposits in the eye.
• Intracardiac calcifications can disrupt the conduction system and cause cardiac arrest.

CKD

Integumentary changes

• pruritus is multifactorial due to dry skin, calcium-phosphate deposition in the skin, and sensory neuropathy.
• Uremic frost is a rare condition in which urea crystallizes on the skin and is usually seen only when BUN levels are extremely high.

CKD

Reproductive changes

• INfertility and < libido
• Women - decreased levels of estrogen, progesterone, and luteinizing hormone, causing anovulation and menstrual changes (usually amenorrhea - may return with dialysis).
• Men experience loss of testicular consistency, decreased testosterone levels, and low sperm counts. 
• Sexual dysfnx r/t anemia = < libido

CKD

Psychologic changes

• Emotional lability
• WD
• Depression
• Anxiety
• < mental ability
• Changes in body image

Kidney

Fnx

 •Prerenal

AKD

ND

AKD

Interventions

• Fluid restrictions/challenges as ordered
• Diuretics and meds as prescribe
• KNOW route of med excretion - may > 1/2 life
• Sodium bicarb precautions (can give too much)
• K and PO3/4 restrictions as ordered
• Dialysis
• O2 therapy - exchanged < as resp > - Need to support the lungs
• Meticulous sterile technique > risk of infection (suctioning, Foley)

AKD

Evaluation

• Effectiveness - labs, weight
• Nutritional statis (needs 10,000 cal)
• Continual eval and mntn of shunt or fistula
• Evaluate Thrill and Bruit
• Provide continual emotional support
• Pt and family teaching

Stages of CKD

(class)

• < renal reserve
• Renal insufficiency - 75% of nephrons tops fnxing (nocturia complaints)
• Renal failure
• End stage disease - 90% or > of nephrons are non-fnx
• FEW SYMPTOMS SEEN UNTIL 75% of GFR is lost

• A catheter is inserted into the peritoneum (membranes of the abdomen) clean blood w/o removing from body. 
• A catheter will be surgically implanted creating a port in which it will enter and leave the abdomen. 
  
• It is filled with dialysate for a specified period of time. 
  
• The waste products and dialysate will filter through and into a bag to be tossed out. 

• Treat AKI or to remove drugs or posions from the body.  
• Immediate initiation in alsomt any hospital. 
• Less complicated than hemodialysis.
• Fewer dietary restrictions. 
• Short training time. 
• Usuable for patients with vascular access problems. 
• Less cardiovascular stress.
• Perferable for DM

• Bacterial or chemical peritonitis
• Protein loss into dialysate
• Exit site and tunnel infx
• Self-image problems w/catheter placement
• Hyperglycemia
• CONTRAINDICATED in pt with multiple abdominal surgieries, trauma, unrepaired hernia
• Catheter can migrate

• Metabolic acidosis – Kidneys cannot regulate acid/base and cannot produce and reabsorb bicarbonate.

• High, Low, No - High cal, Low protein, No added salt
  
• Low-protein, low-phosphorus, low-potassium, low-sodium (2-4 g/day)  Fluid-restriction.  Vitamin D and Ca are nutrients of concern.
• K is dependent on lab values
• Na and fluid are determined by BP, weight, serum electrolytes and urine output.
• Protein needs to increase once dialysis hads begun.  50% should be from biologic sources (eggs, milk, meat, fish, poultry, soy.
• 35kcal/kg
• Phosphate binders must be taken with all meals and snacks.
• Lack of Vit D alters metabolism of Ca, P and Mg
• Hyper P, Mg
• Hypo Ca,

•       Extract wastes from the blood

•       Regulate salt and water

•       Endocrine

–      Renin

–      Erythropoietin – stimulates bone marrow to produce RBC

•       Regulate production of bicarb

•       Controls levels of bicarb

•       Activation of vitamin D

What is erythropoietin?

What does it doe?

Drugs?

• The kidney produces erythropoietin in the interstitial fibroblasts. – a glycoprotein hormone that controls RBC production.
• .  Erythropoietin stimulates precursor cells in the bone marrow to produce RBCs – lack of will cause anemia

Eoptine alfa (Epogen, Procrit) – IV or subQ.  Usually 2-3 x per week.

Darbepoetin alfa (Aranesp) is longer acting and can be administered weekly or biweekly.

Rise in Hgb/Hct not seen for 2-3 weeks. Should improve cardiac performace and exercise tolerance  and enhance quality of life.  Should have a targe Hbg of 10-12 g/dl or it could result in thromboembolic event.  If it > than 12 g/dl they should lower the does.

 Side fx:  HTN (contraindication). iron deficiency resulting from the increased demand for iron to support erythropoiesis

Iron supplements should be given. Do NOT take with phosphate binders – Ca will bind to iron preventing absorption.

• Oligaric-anuretic – Low and no urine output and > BUN and creatinine
• Diuresis – urine output returns, 1-3 L/day may reach up to 10 L/day because the kidneys can’t necessarily filter.  1-3 wks.  High urine volume is caused by osmotic diuresis from high urea concentration in glomerular filtrate and inability of tubules to concentrate urine.  They can excrete waste, but not concentrate. Hypovolemia and hypotension can occure.
• Recovery – BUN and creatinine levels and GFR return to normal levels. Can take up to 12 months for kidneys to stabilize.

Lab values

Acute Renal Failure

• Decrease:
• pH
• Ca
• Increased
• BUN
• Creatinine
• K
• Sodium then <
• P

• Lo protein diet
• Essential amino acid proteins
• High calorie diet
• Na, and K restrictions
• Monitor VS, weight, I/O
• Diuretics
• P binding antacids

Acute kidney failure

ND

Fluid volum excess

Activity intolerance

Risk for impaired skin integrity

Risk for infection

Deficient knowledge

Acute kidney failure

Order of interventions

***few symptoms seen until 75% GFR lost

CKF

Cardio changes

CKF

Neuro changes

CKF

GI changes

CKF

Integ changes

    stages)

CKF

Musculoskeletal

Changes

CKF

Endocrine changes

CKF

Hema changes

CKF

ND

CKD

ND

Potential complications

CKD/CKF

Drugs for CKD

1. Erythropoietin
2. IV glucose and insulin
3. Nifedipine
4. Sevelamer
5. Sodium polystyrene sulfonate
6. Furosemide
7. Calcium acetate
8. 10% calcium gluconate IV

1. Anemia
2. Hyper K
3. HTN
4. Hyper P
5. Hyper K
6. HTN
7. Hyper P
8. HYper K

• Arterial venous graft - 2-4 wks to heal. May lead to distal ischemia
• Arterial venous fistula -  Least likely to thrombose. - 4-6 wks to heal
• External AV shunt - Most prone to infection.  Temorary access.
• Silastic catheter tunneled subQ into the jugular - Temp while waiting for replacement graft or fistual (if throbus requires removal).

What activates

1. Erythropoitin
2. Renin-angiotension-aldosterone sys.
3. Aldosterone

1.  Lo oxygen tension of renal blood supply  -> production of RBC in bone marron
2. HYPOtension- (or other factors causing reduction in blood supple to kidneys) causes activation as well as release of ADH
3. Hyperkalemia stimulates aldosterone from the adrenal cortex

• Fluid overload does NOT directly stimulate factors fx the kidney.