ppt

1. By Linda Self

2.  Regulation of water excretion
 Regulation of electrolyte function
 Regulation of acid-base balance—retain
HCO3- and excrete acid in urine
 Regulation of blood pressure--RAAS
 Regulation of RBCs
 Vitamin D synthesis

3.  Secretion of prostaglandin E and prostacyclin
which cause vasodilation, important in
maintaining renal blood flow
 Excretion of waste products-body’s main
excretory organ. Urea, creatinine, phosphates,
uric acid and sulfates. Drug metabolites.

4. Stimuli for Renin Excretion
Angiotensinogen in liver
Renin release
Angiotensin I
Converting enzyme in lungs
Angiotensin II
Renal autoregulation
Increased BP, increased circulating volume

5.  Renin—raises BP
 Bradykinins—increase blood flow and vascular
permeability
 Erythropoietin
 ADH
 Aldosterone—promotes sodium reabsorption
and potassium excretion
 Natriuretic hormones—released from the
cardiac atria and brain.

6. 1. Hypertension
2. Diabetes mellitus
3. Immobilization
4. Parkinson’s disease
5. SLE
6. Gout
7. Sickle cell anemia, multiple myeloma
8. BPH
9. Pregnancy
10. SCI

7.  GFR decreases following 40 years with a yearly
decline of about 1 mL/min
 Renal reserve declines
 Multiple medications can result in toxic
metabolites
 Diminished osmotic stimulation of thirst
 Incomplete emptying of bladder
 Urinary incontinence

9.  Sp. Gravity—1.005-1.020
 Microscopic examination for protein, RBCs,
ketones, glycosuria, presence of bacteria,
general appearance and odor
 Leukocyte esterase—enzyme found in WBCs
 Nitrites –bacteria convert nitrates to nitrites
 Osmolality—accurate measurement of the
kidney’s ability to concentrate urine. Normal
range is 500-1200 mOsm/kg.
 Culture important in ‘Id’ing pathogen

10.  Albuminuria—albumin in urine not
measurable by dipstick
 Normal values in freshly voided sample should
range between 2.0-20 for men and 2.8-28 for
women. Higher levels indicate
microalbuminuria.
 Can also be determined by 24h specimen

11.  Urine osmolality—indication of concentrating
ability, changes seen early in disease processes
 Creatinine clearance—tests clearance of
creatinine in one min. Reflects GFR.
 Serum creatinine—measures effectiveness of
renal function. 0.6 to 1.2 mg/dL
 Urea nitrogen—also indicator of renal function.
7-18 mg/dL. Measures renal excretion of urea
nitirogen, a byproduct of protein metabolism.
Is not always elevated with kidney disease. Not
best indicator of renal function.

12.  Liver must function properly to produce urea
nitrogen. BUN levels indicate the extent of
renal clearance of this nitrogenous waste
product.
 May see elevation of BUN with bleeding into
tissues or from rapid cell destruction from
infection/steroids

13.  Ratio of BUN to creatinine distinguishes
between renal and non-renal factors causing
elevations
 Dehydration can affect the BUN
 When blood volume is down, or BP is low,
BUN level rises more rapidly than creatinine
level.

14.  Volume of fluid filtered from renal glomerular
capillaries into Bowman’s capsule per unit of
time
 Generally expressed in ml/minute
 Normal GFR generally is 125mL/minute

15.  Cockcraft-Gault formula
 Modification of Diet in Renal Disease Study
Group formula (MDRD)
 Schwartz formula
 Starling equation

17.  No common pathologic condition, other than
renal disease, increases the serum creatinine
level
 Serum creatinine does not increase until at least
50% of renal function is lost

18.  Is a calculated measure of glomerular filtration
rate. Is best indicator of overall kidney
function.
 Based on 24 hour urine collection
 Midway will obtain serum creatinine. Serum
creatinine levels vary with age, gender and
body muscle mass
 Calculate: (Volume of urine X urine creatinine)
Divided by serume creatinine

19.  KUB
 Ultrasonography
 CT
 MRI
 Nuclear scans
 IV urography—IVP. NPO before. Bowel prep.
Nephrotoxic agent. Metformin.
 VCUG

20.  Cystoscopy
 Ureteral brush biopsy
 Kidney biopsy
 Urodynamic tests—cystometrogram. Measures
detrusor muscle function.

21.  Antigen-antibody complexes form in blood and
become trapped in glomerular capillaries
 Induce an inflammatory response
 Manifested by proteinuria, hematuria,
decreased GFR and alteration in excretion of
sodium
 Acute and chronic glomerulonephritis
 Nephrotic syndrome

22. Antigen (group A strep)
Antigen-antibody product
Deposition of antigen-antibody complex in glomerulus
Increased production of epithelial cells lining the glomerulus
Leukocyte infultration of the glomerulus
Thickening of the glomerular filtration membrane
Scarring and loss of glomerular filtration membrane
Decreased GFR

23.  Staph, klebsiella, CMV, mono, hep B,
mycoplasma, group A beta-hemolytic strep

24.  Hematuria
 Edema
 Azotemia-accumulation of nitrogenous wastes
 Urine appearance may be cola colored
 Hypertension
 Hypoalbuminemia
 Hyperlipidemia
 Rising BUN and creatinine

25.  Hypertensive encephalopathy
 Heart failure
 Rapid decline in renal function can occur to
ESRD

26.  Treat s/s such as elevated BP
 Check GFR by 24h urine for creatinine clearance
 ANA
 Treat streptococcal infection with antibiotics,
preferably PCN
 Corticosteroids
 Immunosuppressants
 Limit dietary protein, increase CHO
 Restrict sodium
 May progress to chronic glomerulonephritis, will
treat as in CKD

27.  Is not a specific glomerular disease
 Is a syndrome with a cluster of findings that
include:
 Marked increase in protein in urine (especially
albumin)
 Hypoalbuminemia
 Edema
 High serum cholesterol and LDL

28.  A condition of increased glomerular permeability
 Results in massive protein loss
 Often linked genetically or r/t
immune/inflammatory process
 Caused by chronic glomerulonephritis, diabetes
mellitus with glomerulosclerosis, amyloidosis,
lupus, multiple myeloma and renal vein
thrombosis
 Major manifestation is edema
 Hallmark is albuminuria exceeding 3.5g/day

29. Damaged glomerular
cap. membrane
Loss of plasma
protein (albumin)
Stimulates synthesis
of lipoproteins
hyperlipidemia

30. Damaged glomerular capillary
membrane
Loss of plasma proteins
hypoalbuminemia
Decreased oncotic pressure
Generalized edema>RAAS>sodium
retention>>>>edema

31.  Massive proteinuria
 Hypoalbuminemia
 Edema
 Lipiduria
 Hyperlipidemia
 Increased coagulation
 Renal insufficiency

32.  Renal biopsy to determine specific cause
 Steroids
 Immunosuppressive agents
 ACEIs can decrease proteinuria
 Cholesterol lowering agents
 Heparin to reduce coagulability
 Limit sodium intake

33.  Reversible clinical syndrome whereby there is
sudden and pronounced loss of kidney
function
 Occurs over hours to days
 Results in kidneys failure to excrete
nitrogenous wastes

34. Intrarenal actual parenchymal damage
 Prolonged renal ischemia from myoglobinuria
(rhabdo, trauma, burns), hemoglobinuria
(transfusion reaction, hemolytic anemia)
 Nephrotoxic agents like aminoglycosides,
radiopaque contrast, heavy metals, solvents,
NSAIDs, ACEIs, acute glomerulonephritis

35. Prerenal 60-70% of cases
 Volume depletion as seen in hemorrhage, renal
losses from diuretics, GI losses from vomiting,
diarrhea
 Impaired cardiac output 2ndary to MI, heart
failure, dysrhythmias, cardiogenic shock
 Vasodilation from sepsis, anaphylaxis,
antihypertensive meds

36. Postrenal
Urinary tract obstruction by calculi, tumors, BPH,
blood clots

37. 1. Initiation occurs with the insult
2. Oliguria with urinary output less than
400ml/24h . rising potassium, BUN, Cr. Not
responsive to fluid challenges.
3. Diuresis period— gradual increase in urinary
output. Beginning recovery. Renal function
gradually improves
4. Recovery—may take 3-12 months. May have
permanent reduction in functioning of 1%-3%.

38.  Prerenal-hypotension, tachycardia, decreased
CO, decreased urinary output, lethargy
 intrarenal and postrenal—oliguria or anuria,
hypertension, tachycardia, SOB, orthopnea,
n/v, generalized edema and weight gain,
lethargy, confusion

39.  Nonoliguric form also exists. Phases are
similar.

40.  Elevated BUN and creatinine
 Sodium retention but may be deceptive due to
water retention
 Potassium increased
 Phosphorus increased
 Calcium decreased
 H&H decreased
 Sp. Gravity decreased and fixed

41.  Objectives : Restore normal
chemical balance and prevent complications
until restoration of renal function
 Identify and treat underlying cause
 Maintain fluid balance—wts, serial CVP
readings, BP, strict I&O
 May give Mannitol, Lasix or Edecrin
 May need temporary dialysis

42.  If prerenal, fluid challenges and diuretics to
enhance renal blood flow
 Oliguric renal failure, low dose dopamine.
Calcium channel blockers may be used to
prevent influx of calcium into kidney cells,
maintains cell integrity and increase GFR

43.  Hyperkalemia—closely monitor electrolytes
 Kayexalate/Sorbitol—may need Flexiseal
 IV dextrose, insulin and calcium may help shift
K+
 Cautious administration of any medication that
can be nephrotoxic
 Monitor ABGs and acid-base balance
 Monitor phosphate levels

44.  Azotemia and uremia are directly related to the
rate of protein breakdown
 Dietary proteins are individualized to each
patient. Is a catabolic state and if insufficient
intake, patient may lose up to 0.5-1 pounds
daily. Encourage high CHO. Protein needs for
non-dialysis patients need 0.6g/kg of body
weight
 Dialysis patients will need 1-1.5g/kg
 Fluid restriction=urine volume plus 500ml

45.  Monitor fluid and electrolyte balance
 Reduce metabolic demands
 Promote pulmonary function
 Prevent infection
 Provide skin care
 Provide support

46.  Progressive, irreversibe deterioration in renal
function
 Causation: #1 diabetes mellitus, hypertension,
glomerulonephritis, pyelonephritis, polycystic
kidney disease, vascular disorders, others
 Uremia---collection of nitrogenous wastes
normally excreted by the kidneys. S/S include:
HA, seizures, coma, dry skin, rapid pulse,
elevated BP, scanty urine, labored breathing

47.  Nephrons hypertrophy and work harder until
70-80% of renal function is lost
 Nephrons could only compensate by
decreasing water reabsorption thus:
 Hyposthenuria—loss of urine concentrating
ability occurs
 Polyuria—increased urine output
 Then isosthenuria—fixed osmolality
 Gradual decline in urinary output

48. 1. GFR greater than or equal to 90mL/min/1.73
m2. Kidney damage w/normal or increased
GFR
2. GFR = 60-89, mild decrease in GFR
3. GFR = 30-59, moderate decrease in GFR
4. GFR = 15-29. severe decrease in GFR
5. GFR < 15. Kidney failure

49.  Every body system is affected
 CV—hypertension (RAAS), heart failure,
pulmonary edema, pericarditis, MI
 Pulm.—crackles, Kussmaul, pleuritic pain
 Derm—severe pruritus, uremic frost (urea
crystals)
 GI—n/v, anorexia, uremic fetor (ammonia
odor to breath), constipation or diarrhea
 Neurologic—LOC changes, confusion, seizures,
agitation, neuropathies, RLS

50.  Hematologic—anemia, thrombocytopenia
 Musculoskeletal—muscle cramps, renal
osteodystrophy, bone pain, bone fractures
 Metabolic changes—urea and creatinine,
sodium, potassium, acid-base, calcium and
phosphorus

51.  Calcium and phosphorus binders—Calcium
carbonate, calcium acetate
 Antihypertensives
 Antiseizure—valium or dilantin
 Erythropoietin
 Iron supplements
 Diet—CHO and fat, vitamins, restrict protein

52. Indications:
1. Uremia
2. Persistent hyperkalemia
3. Uncompensated metabolic acidosis
4. Fluid volume excess
5. Uremic encephalopathy
6. Remove toxic substances

53.  Based on principles of diffusion, osmosis and
ultrafiltration
 Diffusion—removal of toxins and wastes.
Move from blood to dialysate.
 Osmosis—excess water is removed. Goes from
area of higher solute concentration (blood) to
lower concentration (dialysate)
 Ultrafiltration—water moves from high
pressure area to lower pressure. Applied by
negative pressure, more efficient than just by
osmosis

54.  ASHD
 Disturbances of lipids worsened by dialysis
 Anemia and fatigue
 Gastric ulcers
 Renal osteodystrophy
 Sleep problems
 Hypotension
 Muscle cramps
 Dysrhythmias
 Dialysis equilibrium from cerebral fluid shifts

55.  Caused by rapid decrease in fluid volume and
blood urea nitrogen levels during HD
 Change in urea levels can cause cerebral edema
and increased ICP
 Neurologic complications include: HA,
vomiting, restlessness, decreased LOC,
seizures, coma or death
 Can be prevented by starting HD for short
periods and low blood flows

56.  Hemodialysis
 In ICUs where patient is too unstable to have
hemodialysis, can have CRRT
 Peritoneal dialysis

57.  More successful if done before dialysis
 HLA and ABO compatibility
 Donor kidney placed in iliac fossa
 Patient must be free from infection
 Similar care for patient post-op as any surgery

58.  Post-op—assess for s/s of rejection such as
oliguria, edema, fever, increasing blood
pressure, weight gain and swelling or
tenderness over transplanted area
 Monitor creatinine level, in those on
cyclosporine, may be the only s/s
 Monitor WBCs
 Monitor urinary output, may need
hemodialysis temporarily (2-3 weeks may
initially have ATN)

59.  Occurs in types 1 and 2
 Severity of diabetic renal disease is related to
extent, duration and effects of atherosclerosis,
htn and neuropathy.

60.  Microvascular complication of diabetes
 First manifestation is persistent albuminuria
 Diabetic patients are always considered to be at
risk for renal failure
 Avoid nephrotoxic agents and dehydration

61.  Stage 1—at time of diagnosis of diabetes.
Kidney size and GFR are increased. Blood
sugar control can reverse the changes.
 Stage 2, 2-3 years after diagnosis. Basement
membrane changes result in loss of filtration
surface area and scar formation. These changes
are called glomerulosclerosis.

62.  Stage 3, 7-15 years after diagnosis.
Microalbuminuria is present. GRF may be
normal or increased.
 Stage 4, albuminuria is detectable by dipstick.
GRF decreased. BP is increased. Retinopathy is
present.
 Stage V, GFR decreases at an average rate of
10ml/min./year

63.  Cystitis
 Ureterovesical reflux

64.  If bacteriuria, following should have cultures done:
 All men
 All children
 Patients with diabetics
 Those with recent instrumentation
 Those hospitalized or who live in long term care
 Pregnant women
 Sexually active
 Postmenopausal

65.  Obstruction
 Stones
 Diabetes mellitus
 Gender
 Age—anticholinergics, neuromuscular
conditions, hypoestrogenism
 Sexual activity
 Alkalotic urine
 Vesicoureteral reflux

66.  Most common organism is E. coli
 Other causative organisms are: S. saprophyticus,
K. pneumoniae, Proteus and Enterobacter

67.  Bactrim, Macrodantin, Cipro,Levaquin
 Fluids, avoid urinary irritants
 Hygiene
 Prevention

68. Acute pyelonephritis
 Will have fever, chills, leukocytosis, bacteriuria
and pyuria
 CVA tenderness
 US or CT to r/o any obstruction
 Urine C&S

69.  Tx:
 Hydration
 Antiemetics
 Two week course of antibiotics such as
Bactrim, Cipro, gentamycin w/or w/o
ampicillin, 3rd generation cephalosporin
 Pregnant women hospitalized for 2-3 days
 f/u culture in two weeks

70.  Stress incontinence—invol. loss of urine w/
activities that increase intraabdominal pressure
 Urge incontinence—unable to suppress signal
from bladder to brain
 Overflow incontinence-when bladder is distended,
will have small amount of incont.
 Functional incontinence as seen in Alzheimer’s
 Reflex incontinence as seen in SCI patients
 Mixed-stress and urge
 Neurogenic bladder—lesion of ns leads to urinary
incontinence

71.  May be caused by MS, SCI, HNP, spinal tumor,
spina bifida, diabetes
 Spastic—upper motor neuron lesion
 Flaccid—lower motor neuron lesion. Fills then
have overflow incontinence
 Assess by checking residuals, I&O, UA,
assessing sensory awareness
 Tx-urecholine, surgery, intermittent caths, S/P
caths

72.  Diuretics
 CNS depressants which affect LOC
 CVAs
 Parkinson’s
 Depression and altered self-esteem
 Inability to ambulate safely
 Assistance products cost prohibitive for patient
 UTI

73.  TCAs
 Anticholinergics—Sudafed, Detrol, Ditropan
 Estrogen in women

74.  Weight loss in obese
 Fluid management
 Transvaginal or transrectal electrical
stimulation
 Inflatable cuff
 Vaginal cone retention exercises
 Urinary catheterization
 Scheduled toileting
 Pelvic muscle exercises

75.  Presence of calculi in urinary tract
 Cause pain as they pass
 Nephrolithiasis is formation of stones in the
kidney

76.  Involves three conditions:
1. Slow urine flow resulting in supersaturation of
the urine with the particular element
2. Damage to the lining of the urinary tract
3. Decreased inhibitor substances in the urine
that would otherwise prevent supersaturation
and crystal aggregation

77.  Metabolic risk factors such as hyperuricemia,
hyperoxaluria or hypercalcemia
 High dietary calcium not contributive unless
metabolic or renal tubular defect exists
 Immobilization
 Urinary stasis, dehydration and urinary
retention mamy be causative

78.  Evaluate for bladder obstruction
 UA will reveal RBCs, odor, turbidity, WBCs
 MRI, KUB, CT
 Noncontrast helical CT has highest sensitivity
 IV urography will show obstruction

79.  Analgesia
 Avoid NSAIDs if to have lithotripsy (affect
platelets)
 Hydration
 Urine straining
 Lithotripsy (monitor ECG and sedate patient)
 Minimally invasive surgical procedures (MIS)
such as stenting, nephrolithotomy

80.  Antibiotics
 Thiazide diuretics for hypercalciuria
 Allopurinol and vitamin B6 for oxalate
containing stones
 Uric acid stone—allopurinol and alkalinizing
the urine. Sodium bicarbonate or potassium
citrate helpful.
 Cystine –captopril and
alphamercaptopropionylglycine w/ hydration
and alkalinazation of urine

81.  Urothelial
 Tx with BCG
 Radiation
 chemotherapy

82.  Ureterostomy
 Conduits—to intestine and stoma
 Sigmoidostomies-divert urine to large intestine
so no stoma
 Ileal reservoir—surgically created pouch