NCM 112: NURSING CARE OF CLIENTS WITH URINARY TRACT  Excretion of Waste Products: The kidney functions as the

he kidney functions as the body’s

AND RENAL DISORDERS main excretory organ, eliminating the body’s metabolic waste
Ms. Marvie Joy Cabioc products. The major waste product of protein metabolism is
urea, of which about 25 to 30 g is produced and excreted daily.
Functions of Kidney: All of this urea must be excreted in the urine; otherwise it will
 Regulation of water excretion accumulate in body tissues. Other waste products of metabolism
 Regulation of electrolyte function that must be excreted are creatinine, phosphates, and sulfates.
 Regulation of acid-base balance - retain HCO3- and Uric acid, formed as a waste product of purine metabolism, is
excrete acid in urine also eliminated in the urine. The kidneys serve as the primary
 Regulation of blood pressure - RAAS mechanism for excreting drug metabolites.
 Regulation of RBCs
 Vitamin D synthesis So KIDNEY is a major body organ for excretion and NEPHRON is an
 Secretion of prostaglandin E and prostacyclin which important tissue of the kidney.
cause vasodilation, important in maintaining renal blood
flow Overview of Anatomy and Physiology:
 Excretion of waste products-body’s main excretory organ.  Functions of the urinary system
Urea, creatinine, phosphates, uric acid and sulfates. Drug  Excretion of waste products
metabolites.  Regulation of water (ADH), electrolytes,
and acid-base balance (pH of blood)
 Regulation of Water Excretion: Regulation of the amount of  Kidneys (two)
water excreted is also an important function of the kidney. With  Nephron: Functional unit of kidneys
high fluid intake, a large volume of dilute urine is excreted.  Urine composition and characteristics
Conversely, with a low fluid intake, a small volume of  95% water; remainder is nitrogenous
concentrated urine is excreted. A person normally ingests about wastes and salts
1 to 2 L of water per day, and normally all but 400 to 500 mL of  Urine abnormalities
this fluid is excreted in the urine. The remainder is lost from the  Albumin; glucose; erythrocytes; ketones;
skin, from the lungs during breathing, and in the feces. leukocytes
 Regulation of Electrolyte Function: When the kidneys are
functioning normally, the volume of electrolytes excreted per day As the body takes in nutrients to meet the body’s requirements to
is exactly equal to the amount ingested. Electrolyte excretion sustain life, the breakdown of these elements results in waste products.
includes sodium and potassium. The management of these waste products is handled by the urinary
 Regulation of Acid Base Balance: The catabolism, or system.
breakdown, of proteins results in the production of acid
compounds, in particular phosphoric and sulfuric acids. Unlike When there is something wrong in the laboratory, when there is
carbon dioxide (CO2), phosphoric and sulfuric acids are albumin, protein, high sugar, blood based on the urinalysis, it should
nonvolatile and cannot be eliminated by the lungs. Because give you a hint that there’s something wrong in the kidney.
accumulation of these acids in the blood would lower its pH
(making the blood more acidic) and inhibit cell function, they
must be excreted in the urine. A person with normal kidney
function excretes about 70 mEq of acid each day. The kidney is
able to excrete some of this acid directly into the urine until the
urine pH reaches 4.5, which is 1,000 times more acidic than
blood. More acid, however, usually needs to be eliminated from
the body than can be excreted directly as free acid in the urine.
These excess acids are bound to chemical buffers so they can
be excreted in the urine. Two important chemical buffers are
phosphate ions and ammonia (NH3). When buffered with acid,
ammonia becomes ammonium (NH4). Phosphate is present in
the glomerular filtrate, and ammonia is produced by the cells of
the renal tubules and secreted into the tubular fluid. Through the
buffering process, the kidney is able to excrete large quantities Coronal section through right kidney.
of acid in a bound form, without further lowering the pH of the (From Thibodeau, G.A., Patton, K.T. [2007]. Anatomy and physiology.
urine. [6th ed.]. St. Louis: Mosby.)
 Regulation of Blood Pressure: Regulation of blood pressure is
also a function of the kidney. Specialized vessels of the kidney The kidneys are dark red, bean-shaped organs. They are located, one
called the vasa recta constantly monitor blood pressure as blood on each side, toward the back of the body, just below the diaphragm.
begins its passage into the kidney. When the vasa recta detect a
decrease in blood pressure, specialized juxtaglomerular cells The kidney has the hilum, a concave portion of each kidney. Each hilum
near the afferent arteriole, distal tubule, and efferent arteriole is penetrated with blood cells, nerves, and the ureter. So the kidney is
secrete the hormone renin. Renin converts angiotensinogen to located in the body from the twelfth thoracic vertebra to the third lumbar
angiotensin I, which is then converted to angiotensin II, the most vertebra. An aton kidneys ada hiya just above the lower quadrant of the
powerful vasoconstrictor known. The vasoconstriction causes stomach and around 3-4 inches after the xiphoid process.
the blood pressure to increase. The adrenal cortex secretes
aldosterone in response to stimulation by the pituitary gland, There are 1 million nephrons that is a major linkage to have an
which in turn is in response to poor perfusion or increasing adequate renal function. So kun an imo nephrons dysfunctional, an imo
serum osmolality. The result is an increase in blood pressure. liwat renal function, naguba. We have two types of nephrons, the
When the vasa recta recognize the increase in blood pressure, cortical and juxtamedullary nephrons. Cortical nephrons is 80-85% of
renin secretion stops. Failure of this feedback mechanism is one the entire nephron and juxtamedullary nephrons is 15-20%.
of the primary causes of hypertension.
 Regulation of RBCs: When the kidneys sense a decrease in the
oxygen tension in renal blood flow, they release erythropoietin.
Erythropoietin stimulates the bone marrow to produce red blood
cells (RBCs), thereby increasing the amount of hemoglobin
available to carry oxygen.
 Vitamin D Synthesis: The kidneys are also responsible for the
final conversion of inactive vitamin D to its active form, 1-25
dihydroxycholecalciferol. Vitamin D is necessary for maintaining
normal calcium balance in the body.
 Secretion of Prostaglandins: The kidneys also produce
prostaglandin E (PGE) and prostacyclin (PGI), which have a
vasodilatory effect and are important in maintaining renal blood
flow.
  Urinalysis (most common urologic study)
 Blood urea nitrogen (BUN)
 Blood creatinine
 Creatinine clearance
 Prostate-specific antigen (PSA)
 Osmolality
 Kidney-ureter-bladder radiography (KUB)
 Intravenous pyelogram (IVP)
 Retrograde pyelography
 Voiding cystourethrography
 Endoscopic procedures
 Renal angiography
 Renal venogram
 Computed tomography (CT)
 Magnetic resonance imaging (MRI)
 Renal scan
The nephron unit.  Ultrasonography
(From Thibodeau, G.A., Patton, K.T. [2007]. Anatomy and physiology.  Transrectal ultrasound
[6 ed.]. St. Louis: Mosby.)
th
 Renal biopsy
Always remember that the red color, which is the arteries, carries  Urodynamic studies
oxygenated blood while the blue color which is the veins, carries the
deoxygenated blood. When attempting to diagnose a disorder of the urinary system, the first
line of testing involves the urine. The urine provides clues into many
Everything that we drink is filtered in the kidney. So if you imagine, yung disorders. Collection of the specimen will vary by test.
nephron hindi lang siya tissue eh. It is a unit with several parts that
makes it functional. So sometimes kun magdidialysis ka na, what acts In addition to analyzing the urine, detecting disorders of the urinary
as a nephron unit is the dialysis machine. Hiya na yan nagfifilter lalo na system can also include scanning or biopsy procedures.
kun zero function na it imo kidney.
Medication Considerations:
Urine Formation:  Diuretics to enhance urinary output
 3 Phases of Urine Formation  Thiazide diuretics
 Filtration  Loop (or high-ceiling) diuretics
 Of water and blood products occurs  Potassium-sparing diuretics
in glomerulus of Bowman’s capsule  Osmotic diuretics
 Reabsorption  Carbonic anhydrase inhibitor diuretics
 Water, glucose, and necessary ions  Medications for urinary tract infections
back into blood (primarily done in  Quinolone
proximal/distal convoluted tubules and  Nitrofurantoin
Henle’s loop)  Methenamine
 Secretion  Fluoroquinolone
 Certain ions, nitrogenous waste and
drugs (primarily distal convoluted tubule); Diuretics’ method of action is accomplished by increasing the kidney’s
this is the reverse of reabsorption; filtration of elements.
substances move from blood to filtrate
Hormonal Influence: Maintaining Adequate Urinary Drainage:
 Increased fluid loss (hemorrhage, vomiting, diarrhea, etc.  Types of catheters
=hypotension)  Coudé catheter
 Decreases amount of filtrate produced by kidneys  Foley catheter
 Posterior pituitary releases ADH  Malecot, Pezzer, or mushroom catheters
 ADH causes nephrons to increase rate of water  Robinson catheter
reabsorption  Ureteral catheters
 This causes water to return to bloodstream thus raising  Whistle-tip catheter
BP and urine to be concentrated  Cystostomy, vesicostomy, or suprapubic
catheter
Overview of Anatomy and Physiology:  External (Texas or condom) catheter
 Ureters (two)
 Passageway for urine from the kidneys to
the urinary bladder
 Urinary bladder (one)
 Temporary storage pouch for urine
 Urethra (one)
 Carries urine by peristalsis from the urinary
bladder out to its external opening

Different types of commonly used catheters.

(From Lewis, S.M., Heitkemper, M.M., Dirksen, S.R. [2007]. Medical-
surgical nursing: assessment and management of clinical problems. [7th
ed.]. St. Louis: Mosby.)

Catheters are indicated when a patient’s condition does not allow

successful elimination of urine.

Physiology of Renin-Angiotensin System:

The male urinary bladder, cut to show the interior.
(From Thibodeau, G.A., Patton, K.T. [2007]. Anatomy and physiology.
[6th ed.]. St. Louis: Mosby.)

Laboratory and Diagnostic Examinations:

 Glomerular Filtration Rate is the amount of plasma filtered through the
glomeruli per unit of time.

Diagnostic Evaluation:
Urinalysis and Culture
 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
Renin excretion is prompted by decreased renal perfusion and/or
Specific Gravity is the expression of urine concentration.
decreased salt delivery to kidney tubules, e.g. hemorrhage, heart
failure, loop diuretics
Urine Tests
 Albuminuria - albumin in urine not measurable by dipstick
Increased BP - vasoconstriction, increased myocardial contractility,
 Normal values in freshly voided sample should range
prostaglandin release
between 2.0-20 for men and 2.8-28 for women. Higher
levels indicate microalbuminuria.
Increased circulating volume - aldosterone release, sodium and water
 Can also be determined by 24h specimen
reabsorption, potassium excretion, ADH release
Microalbuminuria not measurable by dipstick
Hormones influencing Renal Function:
 Renin - raises BP
Renal Function Tests
 Bradykinins - increase blood flow and vascular
 Urine osmolality - indication of concentrating ability,
permeability
changes seen early in disease processes
 Erythropoietin
 Creatinine clearance - tests clearance of creatinine in one
 ADH
min. Reflects GFR.
 Aldosterone - promotes sodium reabsorption and
 Serum creatinine - measures effectiveness of renal
potassium excretion
function. 0.6 to 1.2 mg/dL
 Natriuretic hormones - released from the cardiac atria and
 Urea nitrogen - also indicator of renal function. 7-18
brain
mg/dL. Measures renal excretion of urea nitirogen, a
byproduct of protein metabolism. Is not always elevated
 Renin - secondary to angiotensin and aldosterone with kidney disease. Not best indicator of renal function.
 Bradykinins - increase blood flow and vascular permeability  Liver must function properly to produce urea nitrogen.
 ADH - from Posterior Pituitary; maximizes reabsorption of water BUN levels indicate the extent of renal clearance of this
in the kidney and produces a concentrated urine. nitrogenous waste product.
 Aldosterone - from Adrenal Cortex; promotes sodium  May see elevation of BUN with bleeding into tissues or
reabsorption and potassium secretion in distal collecting tubules; from rapid cell destruction from infection/steroids
water and chloride follow sodium  Ratio of BUN to creatinine distinguishes between renal
 Natriuretic hormones - cause tubular secretion of sodium; and non-renal factors causing elevations
release from cardiac atria and brain  Dehydration can affect the BUN
 When blood volume is down, or BP is low, BUN level rises
Risk Factors for Renal or Urologic Disorders: more rapidly than creatinine level
1. Hypertension
2. Diabetes mellitus Creatinine is end product of muscle energy metabolism. Usually
3. Immobilization remains constant.
4. Parkinson’s disease
5. Systemic Lupus Erythematosus (SLE) Glomerular Filtration Rate (GFR)
6. Gout  Volume of fluid filtered from renal glomerular capillaries
7. Sickle cell anemia, multiple myeloma into Bowman’s capsule per unit of time
8. Benign Prostatic Hyperplasia (BPH)  Generally expressed in ml/minute
9. Pregnancy  Normal GFR generally is 125mL/minute
10. Spinal Cord Injury (SCI)
Calculation of GRF – Complex and Differing Formulas:
Possible Renal or Urologic Disorder:  Cockcraft-Gault formula
1. Hypertension - Renal insufficiency, chronic renal failure  Modification of Diet in Renal Disease Study
2. Diabetes mellitus - Chronic renal failure, neurogenic bladder  Group formula (MDRD)
3. Immobilization - Kidney stone formation  Schwartz formula
4. Parkinson’s disease - Incomplete emptying of bladder, leading to  Starling equation
urinary tract infection
5. Systemic Lupus Erythematosus (SLE) - Nephritis, chronic renal Creatinine Level
failure  No common pathologic condition, other than renal
6. Gout - Kidney stone formation disease, increases the serum creatinine level
7. Sickle cell anemia, multiple myeloma - Chronic renal failure  Serum creatinine does not increase until at least 50% of
8. Benign Prostatic Hyperplasia (BPH) - Obstruction to urine flow, renal function is lost
leading to frequency, oliguria, anuria
9. Pregnancy - Incontinence Creatinine Clearance
10. Spinal Cord Injury (SCI) - Neurogenic bladder, urinary tract  Is a calculated measure of glomerular filtration rate. Is
infection, incontinence best indicator of overall kidney function.
 Based on 24 hour urine collection
Gerontological Considerations:  Midway will obtain serum creatinine. Serum creatinine
 GFR decreases following 40 years with a yearly decline of levels vary with age, gender and body muscle mass
about 1 mL/min  Calculate: (Volume of urine X urine creatinine) Divided by
 Renal reserve declines serume creatinine
 Multiple medications can result in toxic metabolites
 Diminished osmotic stimulation of thirst Imaging Studies
 Incomplete emptying of bladder  KUB
 Urinary incontinence  Ultrasonography
 CT
  MRI
 Nuclear scans
 IV urography—IVP. NPO before. Bowel prep. Nephrotoxic
agent. Metformin.
 VCUG
Kidney, Ureter, and Bladder Studies
An x-ray study of the abdomen or kidney, ureters, and bladder (KUB)
may be performed to delineate the size, shape, and position of the
kidneys and to reveal any abnormalities, such as calculi (stones) in the
kidneys or urinary tract, hydronephrosis (distention of the pelvis of the
kidney), cysts, tumors, or kidney displacement by abnormalities in
surrounding tissues.
Bladder Ultrasonography
Bladder ultrasonography is a noninvasive method of measuring urine
volume in the bladder. It may be indicated for urinary frequency, inability
to void after removal of an indwelling urinary catheter, measurement of
postvoiding residual urine volume, inability to void postoperatively, or
assessment of the need for catheterization during the initial stages of an
intermittent catheterization training program.
Computed Tomography and Magnetic Resonance Imaging
Computed tomography (CT) and magnetic resonance imaging (MRI)
are noninvasive techniques that provide excellent crosssectional views
of the kidney and urinary tract. They are used in evaluating
genitourinary masses, nephrolithiasis, chronic renal infections, renal or
urinary tract trauma, metastatic disease, and soft tissue abnormalities.
Nuclear Scans
Nuclear scans require injection of a radioisotope (technetium-99m–
labeled compound or iodine-131 hippurate) into the circulatory system;
the isotope is then monitored as it moves through the blood vessels of
the kidneys. Nuclear scans are used to evaluate acute and chronic
renal failure, renal masses, and blood flow before and after kidney
transplantation.
Intravenous Urography
Intravenous urography includes various tests such as excretory
urography, intravenous pyelography (IVP), and infusion drip
pyelography. Intravenous urography may be used as the initial
assessment of any suspected urologic problem, especially lesions in
the kidneys and ureters.
Voiding Cystourethrography
Voiding cystourethrography uses fluoroscopy to visualize the lower
urinary tract and assess urine storage in the bladder. It is commonly
used as a diagnostic tool to identify vesicoureteral reflux (between
bladder and ureter).
Urologic Endoscopic Procedures
 Cystoscopy
 Ureteral brush biopsy
 Kidney biopsy
 Urodynamic tests - cystometrogram. Measures detrusor
muscle function.
Cytoscopy
The cystoscopic examination is used to directly visualize the urethra
and bladder. The cystoscope, which is inserted through the urethra into
the bladder, has a self-contained optical lens system that provides a
magnified, illuminated view of the bladder.
Ureteral Brush Biopsy
Brush biopsy techniques provide specific information when abnormal x-
ray findings of the ureter or renal pelvis raise questions about whether
the defect is a tumor, a stone, a blood clot, or an artifact.
Kidney Biopsy
Biopsy of the kidney is used in diagnosing and evaluating the extent of
kidney disease. Indications for biopsy include unexplained acute renal
failure, persistent proteinuria or hematuria, transplant rejection, and
glomerulopathies.
Urodynamic Tests
Urodynamic tests provide an accurate evaluation of voiding problems,
thus assisting in diagnosis. Urodynamic studies are useful in evaluating
changes in bladder filling and bladder emptying.
Definition of Terms:
 aldosterone: hormone synthesized and released by the adrenal
cortex; causes the kidneys to reabsorb sodium
 antidiuretic hormone (ADH): hormone secreted by the posterior
pituitary gland; causes the kidneys to reabsorb more water
 anuria: total urine output less than 50 mL in 24 hours
 bacteriuria: bacteria in the urine; bacterial count higher than
100,000 colonies/mL
 clearance: volume of plasma that the kidneys can clear of a
specific solute (eg, creatinine); expressed in millilitres per
minute
 creatinine: endogenous waste product of muscle energy
metabolism
 dysuria: painful or difficult urination
 frequency: voiding more frequently than every 3 hours
 glomerulus: tuft of capillaries forming part of the nephron
through which filtration occurs
 glomerular filtration rate (GFR): volume of plasma filtered at the
glomerulus into the kidney tubules each minute; normal rate is
approximately 120 mL/min
 hematuria: red blood cells in the urine
 micturition: urination or voiding
 nephron: structural and functional unit of the kidney responsible
for urine formation
 nocturia: awakening at night to urinate
 oliguria: total urine output less than 400 mL in 24 hours
 osmolality: number of particles dissolved per kilogram of urine;
expression of the degree of concentration of the urine
 proteinuria: protein in the urine
 pyuria: pus in the urine
 specific gravity: reflects the weight of particles dissolved in the
urine; expression of the degree of concentration of the urine
 tubular reabsorption: movement of a substance from the kidney
tubule into the blood in the peritubular capillaries or vasa recta
 tubular secretion: movement of a substance from the blood in
the peritubular capillaries or vasa recta into the kidney tubule
 urea nitrogen: nitrogenous end product of protein metabolism
 urinary incontinence: involuntary loss of urine
 Valsalva leak-point pressure (VLPP): amount of abdominal
pressure against the bladder that causes the urethra to open
and leak urine
 vesicoureteral reflux: backflow of urine from the bladder into
the ureters
 acute tubular necrosis: type of acute renal failure in which there
is actual damage to the kidney tubules
 bacteriuria: more than 105 colonies of bacteria per milliliter of
urine continent urinary diversion (Koch, Indiana, Charleston
pouch): transplantation of the ureters to a segment of bowel
with construction of an effective continence mechanism or
valve
 cutaneous ureterostomy: procedure in which the distal ureter is
detached from the bladder, brought through the abdominal
wall, and attached to an opening in the skin
 cystectomy: removal of the urinary bladder
 cystitis: inflammation of the urinary bladder
 end-stage renal disease (ESRD): progressive, irreversible
deterioration in renal function that results in retention of uremic
waste products
 glomerulonephritis: inflammation of the glomerular capillaries
 ileal conduit: transplantation of the ureters to an isolated
section of the terminal ileum, with one end of the ureters
brought to the abdominal wall
 interstitial cystitis: inflammation of the bladder wall that
eventually causes disintegration of the lining and loss of
bladder elasticity
 interstitial nephritis: inflammation of the renal interstitial tissue,
often due to use of medications or exposure to chemicals
 nephrosclerosis: hardening, or sclerosis, of the arteries of the
kidney due to prolonged hypertension
 nephrotic syndrome: disorder characterized
by proteinuria, edema, hypoalbuminuria, and hyperlipidemia
 prostatitis: inflammation of the prostate gland
 pyelonephritis: inflammation of the renal pelvis
 pyuria: white blood cells in the urine
 urethritis: inflammation of the urethra
 ureterosigmoidostomy: transplantation of the ureters into the
sigmoid colon, allowing urine to flow through the colon and out
the rectum
 ureterovesical or vesicoureteral reflux: backward flow of urine
from the bladder into one or both ureters
 urethrovesical reflux: backward flow of urine from the urethra into
the bladder
 urinary casts: protein plugs secreted by damaged kidney tubules

NURSING CARE OF CLIENTS WITH URINARY DISORDERS
LOWER URINARY TRACT INFECTIONS
 Cystitis
 Ureterovesical reflux
 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
Risk factors
 Inability or failure to empty the bladder completely
 Obstructed urinary flow, from congenital anomalies,
urethral strictures, contracture of the bladder neck,
bladder tumors, calculi (stones) in the ureters or kidneys,
compression of the ureters, and neurologic abnormalities
 Decreased natural host defenses or immunosuppression
 Instrumentation of the urinary tract (eg, catheterization,
cystoscopic procedures)
 Inflammation or abrasion of the urethral mucosa
 Contributing conditions (certain populations of patients
are more prone to UTIs than others), including those with:
Diabetes mellitus (increased urinary glucose levels create
an infection-prone environment in the urinary tract),
pregnancy, neurologic disorders, gout, and other altered
states characterized by incomplete emptying of the
bladder and urinary stasis
Routes of Infection
 up the urethra (ascending infection),
 through the bloodstream, (hematogenous spread),
 or by means of a fistula from the intestine (direct
extension)
 (transurethral) most common route of infection, which
bacteria (often from fecal contamination) colonize the
periurethral area and subsequently enter the bladder by
means of the urethra
Clinical Manifestations
 frequent pain and burning on urination, frequency,
urgency, nocturia, incontinence, and suprapubic or pelvic
pain. Hematuria and back pain may also be present.
Assessment and diagnostics findings
 colony counts, cellular studies, and urine cultures
Factors contributing to urinary tract infections
 Obstruction
 Stones
 Diabetes mellitus
 Gender
 Age—anticholinergics, neuromuscular conditions,
hypoestrogenism
 Sexual activity
 Alkalotic urine
 Vesicoureteral reflux
 Most common organism is E. coli
 Other causative organisms are: S. saprophyticus, K.
pneumoniae, Proteus and Enterobacter
Treatment
 Bactrim, Macrodantin, Cipro,Levaquin
 Fluids, avoid urinary irritants
 Hygiene
 Prevention
UPPER URINARY TRACT INFECTIONS
ACUTE PYELONEPHRITIS
 bacterial infection of the renal pelvis, tubules, and
interstitial tissue of one or both kidneys
 are associated with the antibody coating of the bacteria in
the urine. (This occurs in the renal medulla; when the
bacteria are excreted in the urine, the immunofluorescent
test can detect the antibody coating.)
 Bacteria reach the bladder by means of the urethra and
ascend to the kidney.
 Although the kidneys receive 20% to 25% of the cardiac
output, bacteria rarely reach the kidneys from the blood:
fewer than 3% of cases are due to hematogenous spread.
 enlarged kidneys with interstitial infiltrations of
inflammatory cells
 Abscesses may be noted on the renal capsule and at the
corticomedullary junction.
 Eventually, atrophy and destruction of tubules and the
glomeruli may result.
 When pyelonephritis becomes chronic, the kidneys
become scarred, contracted, and nonfunctioning.
Clinical manifestations
 acutely ill with chills and fever, leukocytosis, bacteriuria
and pyuria, flank pain, and CVA tenderness. In addition,
symptoms of lower urinary tract involvement, such as
dysuria and frequency, are common.
Assessment and Diagnostics findings
 ultrasound
 CT scan
 Radionuclide imaging with gallium citrate and indium-111
(In111)–labeled WBCs
 Urine culture and sensitivity tests
Therapy
 2-week course of antibiotics
 TMP-SMZ, ciprofloxacin, gentamicin with or without
ampicillin, or a third-generation cephalosporin
CHRONIC PYELONEPHRITIS
 decreasing as a common cause of end-stage renal
disease (ESRD), while renovascular disease is increasing
as one of the most common causes for ESRD.
Clinical Manifestations
 no symptoms of infection unless an acute exacerbation
occurs
 Noticeable signs and symptoms may include fatigue,
headache, poor appetite, polyuria, excessive thirst, and
weight loss. Persistent and recur ring infection may
produce progressive scarring of the kidney, with renal
failure the end result.
Assessment and Diagnostics findings
 The extent of the disease is assessed by an intravenous
urogram and measurements of creatinine clearance and
BUN and creatinine levels. Bacteria, if detected in the
urine, are eradicated if possible.
Complications
 Complications of chronic pyelonephritis include ESRD
(from progressive loss of nephrons secondary to chronic
inflammation and scarring), hypertension, and formation
of kidney stones (from chronic infection with urea-splitting
organisms)
Nursing Management
 The patient may require hospitalization or may be treated
as an outpatient. When the patient is hospitalized, fluid
intake and output are carefully measured and recorded.
Unless contraindicated, fluids are encouraged (3 to 4
L/day) to dilute the urine, decrease burning on urination,
and prevent dehydration. The nurse assesses the
patient’s temperature every 4 hours and administers
antipyretic and antibiotic agents as prescribed. Often the
patient is more comfortable on bed rest during the acute
phase of the illness.
 Patient teaching focuses on prevention of UTIs by
consuming adequate fluids, emptying the bladder
regularly, and performing recommended perineal hygiene.
The importance of taking antimicrobial medications
 exactly as prescribed is stressed to the patient, as is the
need for keeping follow-up appointments.
URINARY INCONTINENCE
 Urinary incontinence is the unplanned loss of urine that is
sufficient to be considered a problem. Urinary continence
relies on intact urinary, neurologic, and musculoskeletal
systems. Continence is maintained via a complex
communication system of suprasacral, sacral, and local
nerve-mediated loops of information, all of which must be
functioning efficiently and synergistically
Risk factors
 Pregnancy: vaginal delivery, episiotomy
 Menopause
 Genitourinary surgery
 Pelvic muscle weakness
 Incompetent urethra due to trauma or sphincter relaxation
 Immobility
 High-impact exercise
 Diabetes mellitus
 Stroke
 Age-related changes in the urinary tract
 Morbid obesity
 Cognitive disturbances: dementia, Parkinson’s disease
 Medications: diuretics, sedatives, hypnotics, opioids
 Caregiver or toilet unavailable
 CNS depressants which affect LOC
 CVAs
 Depression and altered self-esteem
 Inability to ambulate safely
 Assistance products cost prohibitive for patient
 UTI
Types of Incontinence
1. Stress Incontinence
 involuntary loss of urine through an intact urethra
as a result of a sudden increase in intra-abdominal
pressure (sneezing, coughing, or changing
position).
 It predominately affects women who have had
vaginal deliveries and is
thought to be the result of decreasing ligament and
pelvic floor support of the urethra and decreasing
or absent estrogen levels within the urethral walls
and bladder base.
 In men, stress incontinence is often experienced
after a radical prostatectomy for
prostate cancer because of the loss of urethral
compression that the prostate had supplied before
the surgery, and possibly bladder wall irritability.
2. Urge incontinence
 involuntary loss of urine associated with a strong
urge to void that cannot be suppressed. The
patient is aware of the need to void but is unable to
reach a toilet in time.
3. Reflex incontinence
 involuntary loss of urine due to hyperreflexia in the
absence of normal sensations usually associated
with voiding
4. Overflow incontinence
 the involuntary loss of urine associated with
overdistention of the bladder. Such overdistention
results from the bladder’s inability to empty
normally, despite frequent urine loss.
Assessment and diagnostics findings
 detailed description of the problem and a history of
medication use. The patient’s voiding history, a diary of
fluid intake and output, and bedside tests
 Urinalysis and urine culture
 Timed voiding involves establishing a set voiding frequency
(such as every 2 hours if incontinent episodes tend to occur 2 or
more hours after voiding). The individual chooses to “void by the
clock” at the given interval while awake, rather than wait until a
voiding urge occurs.
 Prompted voiding is timed voiding that is carried out by staff or
family members when the individual has cognitive difficulties that
make it difficult to remember to void at set intervals. The
caregiver checks the patient to assess if he or she has remained
dry and, if so, assists the patient to use the bathroom while
providing positive reinforcement for remaining dry.
 Habit retraining is timed voiding at an interval that is more
frequent than the individual would usually choose. This technique
helps to restore the sensation of the need to void in individuals
who are experiencing diminished sensation of bladder filling due
to various medical conditions such as a mild cerebrovascular
accident (CVA).
 Bladder retraining, also known as “bladder drill,”
incorporates a timed voiding schedule and urinary urge
inhibition exercises to inhibit voiding, or leaking urine, in
an attempt to remain dry for a set time. When the first
timing interval is easily reached on a consistent basis
without urinary urgency or in continence, a new voiding
interval, usually 10 to 15 minute beyond the last, is
established. Again, the individual practices urge inhibition
exercises to delay voiding or avoid incontinence until the
next preset interval arrives. When an acceptable voiding
interval is reached, the patient continues that timed
voiding sequence throughout the day.
Pharmacologic management
 TCAs
 Anticholinergics—Sudafed, Detrol, Ditropan
 Estrogen in women
Therapy for incontinence
 Weight loss in obese
 Fluid management
 Transvaginal or transrectal electrical stimulation
 Inflatable cuff
 Vaginal cone retention exercises
 Urinary catheterization
 Scheduled toileting
 Pelvic muscle exercises
ADULT VOIDING DYSFUNCTION
 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
URINARY RETENTION
 inability to empty the bladder completely during attempts
to void
 Chronic urine retention often leads to overflow
incontinence (from the pressure of the retained urine in
the bladder).
 Residual urine is urine that remains in the bladder after
voiding. In a healthy adult younger than age 60, complete
bladder emptying should occur with each voiding.
 In adults older than age 60, 50 to 100 mL of residual urine
may remain after each void because of the decreased
contractility of the detrusor muscle.
 Urinary retention can occur postoperatively in any patient,
particularly if the surgery affected the perineal or anal
regions and resulted in reflex spasm of the sphincters.
General anesthesia reduces bladder muscle innervation
and suppresses the urge to void, impeding bladder
emptying
Complications
 Urine retention can lead to chronic infection. Infections
that are unresolved predispose the patient to calculi,
pyelonephritis, and sepsis. The kidney may also
 eventually deteriorate if large volumes of urine are
retained, causing backward pressure on the upper urinary
tract. In addition, urine leakage can lead to perineal skin
breakdown, especially if regular hygiene measures are
neglected.
Nursing Management
 Promoting normal urinary elimination
 Promoting urinary elimination
 Promoting home and community-based care
 A variety of diseases can affect the glomerular capillaries,
including acute and chronic glomerulonephritis, rapidly
progressive glomerulonephritis, and nephrotic syndrome.
 In all of these disorders, the glomerular capillaries are
primarily involved.
 Antigen–antibody complexes form in the blood and
become trapped in the glomerular capillaries (the filtering
portion of the kidney), inducing an inflammatory response.
IgG, the major immunoglobulin (antibody) found in the
blood, can be detected in the glomerular capillary walls.

NEUROGENIC BLADDER
 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
Assessment and diagnostics findings
 fluid intake, urine output, and residual urine volume;
urinalysis; and assessment of sensory awareness of
bladder fullness and degree of motor control.
Comprehensive urodynamic studies
Clinical manifestations
 proteinuria, hematuria, decreased glomerular filtration
rate, and alterations in excretion of sodium (leading to
edema and hypertension)
ACUTE GLOMERULONEPHRITIS
Glomerulonephritis is an inflammation of the glomerular capillaries.
Acute glomerulonephritis is primarily a disease of children older than 2
years of age, but it can occur at nearly any age.
 is primarily a disease of children older than 2 years of
age, but it can occur at nearly any age.

BLADDER CANCER Sequence of Events in Acute Glomerulonephritis:

 Urothelial
 Tx with BCG
 Radiation
 Chemotherapy
 Ureterostomy
 Conduits—to intestine and stoma
 Sigmoidostomies-divert urine to large intestine so no
stoma
 Ileal reservoir—surgically created pouch

NURSING CARE OF CLIENTS WITH RENAL DISORDERS

NEPHROSCLEROSIS
 hardening, or sclerosis, of the arteries of the kidney due to
prolonged hypertension.
 This causes decreased blood flow to the kidney and
patchy necrosis of the renal parenchyma. Eventually,
fibrosis occurs and glomeruli are destroyed.
 Nephrosclerosis is a major cause of ESRD.

2 forms of nephrosclerosis
1. Malignant nephrosclerosis
 is often associated with malignant hypertension
(diastolic blood pressure higher than 130 mm Hg).
 It usually occurs in young adults, and men are
affected twice as often as women.
 The disease process progresses rapidly. Without
dialysis, more than half of patients die from uremia
in a few years.
2. Benign nephrosclerosis
 is usually found in older adults and is often
associated with atherosclerosis and hypertension.
Assessment and diagnostic findings
 Symptoms are rare early in the disease, even though the
urine usually contains protein and occasional casts.
 Renal insufficiency and associated signs and symptoms
occur late in the disease.
Medical management
 aggressive antihypertensive therapy. In hypertensive
nephrosclerosis, therapy containing an ACE inhibitor,
alone or in combination with other antihypertensive
medications, significantly reduces the incidence of renal
events. This effect is independent of blood pressure
control.
In most cases of acute glomerulonephritis, a group A betahemolytic
streptococcal infection of the throat precedes the onset of
glomerulonephritis by 2 to 3 weeks. It may also follow impetigo
(infection of the skin) and acute viral infections (upper respiratory tract
infections, mumps, varicella zoster virus, Epstein-Barr virus, hepatitis B,
and human immunodeficiency virus infection). In some patients,
antigens outside the body (eg, medications, foreign serum) initiate the
process, resulting in antigen-antibody complexes being deposited in the
glomeruli. In other patients, the kidney tissue itself serves as the inciting
antigen.
Infectious Causes:
 Staph, klebsiella, Cytomegalovirus (CMV), mono,
hepatitis B, mycoplasma, group A beta-hemolytic strep
Clinical Manifestations:
 Hematuria
 Edema
 Azotemia - accumulation of nitrogenous wastes
 Urine appearance may be cola colored
 Hypertension
 Hypoalbuminemia
 Hyperlipidemia
 Rising BUN and creatinine

PRIMARY GLOMERULAR DISEASE

  abrupt onset preceded by a latent period between the
streptococcal infection and the first indications of renal
involvement averaging 10 days.
 Proteinuria
 headache, malaise, and flank pain
Complications:
 Hypertensive encephalopathy
 Heart failure
 Rapid decline in renal function can occur to ESRD (End
Stage Renal Disorder)
Pathophysiology
 In most cases of acute glomerulonephritis, a group A
betahemolytic streptococcal infection of the throat
precedes the onset of glomerulonephritis by 2 to 3 weeks.
 It may also follow impetigo (infection of the skin) and
acute viral infections (upper respiratory tract infections,
mumps, varicella zoster virus, Epstein-Barr virus, hepatitis
B, and human immunodeficiency virus infection).
 In some patients, antigens outside the body (eg,
medications, foreign serum) initiate the process, resulting
in antigen-antibody complexes being deposited in the
glomeruli.
 In other patients, the kidney tissue itself serves as the
inciting antigen.
Assessment and diagnostic findings
 the kidneys become large, swollen, and congested. All
renal tissues—glomeruli, tubules, and blood vessels—are
affected to varying degrees.
 Electron microscopy and immunofluorescent analysis help
identify the nature of the lesion; however, a kidney biopsy
may be needed for definitive diagnosis.
 Serial determinations of antistreptolysin O or anti-DNase
B titers are usually elevated in poststreptococcal
glomerulonephritis.
 Serum complement levels may be decreased but
generally return to normal within 2 to 8 weeks.
 More than half of patients with IgA nephropathy (the most
common type of primary glomerulonephritis) have an
elevated serum IgA and a normal complement level.
 Usually, more than 90% of children recover.
 The percentage of adults who recover is not well
established but is probably about 70%. Some patients
become severely uremic within weeks and require dialysis
for survival.
 Others, after a period of apparent recovery, insidiously
develop chronic glomerulonephritis.
Management:
 Treat s/s such as elevated BP
 Check GFR by 24h urine for creatinine clearance
 ANA (Anti-nuclear Antibody)
 Treat streptococcal infection with antibiotics, preferably
PCN (Percutaneous Nephrostomy)
 Corticosteroids
 Immunosuppressants
 Limit dietary protein, increase carbohydrates
 Restrict sodium
 May progress to chronic glomerulonephritis, will treat as in
CKD
Nursing management
 In a hospital setting, carbohydrates are given liberally to
provide energy and reduce the catabolism of protein.
 Intake and output are carefully measured and recorded.
 Fluids are given according to the patient’s fluid losses and
daily body weight.
 Insensible fluid loss through the respiratory and GI tracts
(500 to 1,000 mL) is considered when estimating fluid
loss.
 Diuresis begins about 1 week after the onset of symptoms
with a decrease in edema and blood pressure. Proteinuria
and microscopic hematuria may persist for many months,
and some patients may go on to develop chronic
glomerulonephritis.
 Other nursing interventions focus primarily on patient
education for safe and effective self-care at home.
CHRONIC GLOMERULONEPHRITIS
 due to repeated episodes of acute glomerulonephritis,
hypertensive nephrosclerosis, hyperlipidemia, chronic
tubulointerstitial injury, or hemodynamically mediated
glomerular sclerosis.
 The kidneys are reduced to as little as one-fifth their
normal size (consisting largely of fibrous tissue).
 The cortex shrinks to a layer 1 to 2 mm thick or less.
Bands of scar tissue distort the remaining cortex, making
the surface of the kidney rough and irregular.
 Numerous glomeruli and their tubules become scarred,
and the branches of the renal artery are thickened. The
result is severe glomerular damage that results in ESRD.
Clinical manifestations
 Some patients with severe disease have no symptoms at
all for many years.
 Their condition may be discovered when hypertension or
elevated BUN and serum creatinine levels are detected.
 The diagnosis may be suggested during a routine eye
examination when vascular changes or retinal
hemorrhages are found.
 The first indication of disease may be a sudden, severe
nosebleed, a stroke, or a seizure. Many patients report
that their feet are slightly swollen at night.
 Most patients also have general symptoms, such as loss
of weight and strength, increasing irritability, and an
increased need to urinate at night (nocturia). Headaches,
dizziness, and digestive disturbances are common.
 As chronic glomerulonephritis progresses, signs and
symptoms of renal insufficiency and chronic renal failure
may develop.
 The patient appears poorly nourished, with a yellow-gray
pigmentation of the skin and periorbital and peripheral
(dependent) edema. Blood pressure may be normal or
severely elevated. Retinal findings include hemorrhage,
exudate, narrowed tortuous arterioles, and papilledema.
Mucous membranes are pale because of anemia.
Cardiomegaly, a gallop rhythm, distended neck veins, and
other signs and symptoms of heart failure may be
present.
 Crackles can be heard in the lungs.
 Peripheral neuropathy with diminished deep tendon
reflexes and neurosensory changes occurs late in the
disease.
 The patient becomes confused and demonstrates a
limited attention span.
 An additional late finding includes evidence of pericarditis
with a pericardial friction rub and pulsus paradoxus
(difference in blood pressure during inspiration and
expiration of greater than 10 mm Hg).
Assessment and diagnostic findings
 Urinalysis reveals a fixed specific gravity of about 1.010,
variable proteinuria, and urinary casts (protein plugs
secreted by damaged kidney tubules).
As renal failure progresses and the GFR falls below 50 mL/min, the
following changes occur:
 Hyperkalemia due to decreased potassium excretion,
acidosis, catabolism, and excessive potassium intake
from food and medications
 Metabolic acidosis from decreased acid secretion by the
kidney and inability to regenerate bicarbonate
 Anemia secondary to decreased erythropoiesis
(production of RBCs)
 Hypoalbuminemia with edema secondary to protein loss
through the damaged glomerular membrane
 Increased serum phosphorus level due to decreased
renal excretion of phosphorus
 Decreased serum calcium level (calcium binds to
phosphorus to compensate for elevated serum
phosphorus levels)
 Hypermagnesemia from decreased excretion and
inadvertent ingestion of antacids containing magnesium
 Impaired nerve conduction due to electrolyte
abnormalities and uremia
Nursing management
 Changes in fluid and electrolyte status and in cardiac and
neurologic status are reported promptly to the physician.
 Anxiety levels are often extremely high for both the patient
and family.
NEPHROTIC SYDROME
 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
 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
Nephrotic Syndrome:
Sequence of Events in Nephrotic Syndrome:
Nephrotic syndrome can occur with almost any intrinsic renal disease or
systemic disease that affects the glomerulus. Although generally
considered a disorder of childhood, nephrotic syndrome does occur in
adults, including the elderly. Causes include chronic glomerulonephritis,
diabetes mellitus with intercapillary glomerulosclerosis, amyloidosis of
the kidney, systemic lupus erythematosus, multiple myeloma, and renal
vein thrombosis. Nephrotic syndrome is characterized by the loss of
plasma protein, particularly albumin, in the urine. Although the liver is
capable of increasing the production of albumin, it cannot keep up with
the daily loss of albumin through the kidneys. Thus, hypoalbuminemia
results
Complications:
 Massive proteinuria
 Hypoalbuminemia
 Edema
 Lipiduria
 Hyperlipidemia
 Increased coagulation
 Renal insufficiency
Treatment:
 Renal biopsy to determine specific cause
 Steroids
 Immunosuppressive agents
 Angiotensin-converting enzyme inhibitors (ACEIs) can
decrease proteinuria
 Cholesterol lowering agents
 Heparin to reduce coagulability
 Limit sodium intake
W.O.W. TIME: “Olrayt! Hindi nalalayo yung power point sa libro so your
book, class, is in detail. If you read your books, you will understand
everything ba. It’s like you also have to really set a time to read your
books.”
So basically guys, ginbabasa la niya it ppt and book with some w.o.w.
lmao so we just added some info from the book.
ACUTE RENAL FAILURE
 ARF manifests with oliguria, anuria, or normal urine
volume.
 Oliguria (less than 400 mL/day of urine) is the most
common clinical situation seen in ARF; anuria (less than
50 mL/day of urine) and normal urine output are not as
common.
 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
Causes of renal failure
1. Intrarenal actual parenchymal damage
 are the result of actual parenchymal damage to the
glomeruli or kidney tubules
 P r o l o n g e
burns), hemoglobinuria (transfusion reaction, hemolytic
anemia)
 Nephrotoxic agents like aminoglycosides, radiopaque
contrast, heavy metals, solvents, NSAIDs, ACEIs, acute
glomerulonephritis
2. Prerenal 60-70% of cases
 as a result of impaired blood flow that leads to
hypoperfusion of the kidney and a drop in the GFR
 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
3. Postrenal
 are usually the result of an obstruction somewhere distal
to the kidney. Pressure rises in the kidney tubules;
eventually, the GFR decreases
 Urinary tract obstruction by calculi, tumors, BPH, blood
clots
Phases of acute renal failure
1. Initiation occurs with the insult
2. Oliguria with urinary output less than 400ml/24h. rising
potassium, BUN, Cr. Not responsive to fluid challenges. In
this phase uremic symptoms first appear and life-
threatening conditions such as hyperkalemia develop.
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%.
Clinical manifestations

Key features
 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
 Nonoliguric form also exists.
 Phases are similar.
Laboratory profile
 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
Management
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 dialysi
 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
 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
Nutritional therapy
 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
Role of nurse
 Monitor fluid and electrolyte balance
 Reduce metabolic demands
 Promote pulmonary function
 Prevent infection
 Provide skin care
 Provide support
CHRONIC RENAL FAILURE (END-STAGE RENAL DISEASE)
 Progressive, irreversibe deterioration in renal function
 Causation: #1 diabetes mellitus, hypertension,
glomerulonephritis, pyelonephritis, polycystic kidney
disease, vascular disorders, infections medications; or
toxic agents
 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
Kidney changes
 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
Stages of renal failure
 GFR greater than or equal to 90mL/min/1.73 m2. Kidney
damage w/normal or increased GFR
 GFR = 60-89, mild decrease in GFR
 GFR = 30-59, moderate decrease in GFR
 GFR = 15-29. severe decrease in GFR
 GFR < 15. Kidney failure
Clinical manifestations
 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
 Hematologic—anemia, thrombocytopenia
 Musculoskeletal—muscle cramps, renal osteodystrophy,
bone pain, bone fractures
 Metabolic changes—urea and creatinine, sodium,
potassium, acid-base, calcium and phosphorus
Medical management
 Calcium and phosphorus binders—Calcium carbonate,
calcium acetate
 Antihypertensives
 Antiseizure—valium or dilantin
 Erythropoietin
 Iron supplements
 Diet—CHO and fat, vitamins, restrict protein
DIALYSIS THERAPIES
Indications:
 Uremia
 Persistent hyperkalemia
 Uncompensated metabolic acidosis
 Fluid volume excess
 Uremic encephalopathy
 Remove toxic substances
DIALYSIS
 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
Complications of dialysis
 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
DIALYSIS DISEQUILIBRIUM SYNDROME
 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
Forms of dialysis
 Hemodialysis
 In ICUs where patient is too unstable to have
hemodialysis, can have CRRT
 Peritoneal dialysis
KIDNEY TRANSPLANTATION
 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
 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)
Preoperative management
 Preoperative management goals include bringing the
patient’s metabolic state to a level as close to normal as
possible, making sure that the patient is free of infection,
and preparing the patient for surgery and the
postoperative course.
Postoperative management
 The goal of care is to maintain homeostasis until the
transplanted kidney is functioning well. The patient whose
kidney functions immediately has a more favorable
prognosis than the patient whose kidney does not.
Postoperative nursing management
 Assessing the patient for transplant rejection
 Preventing infection
 Monitoring urinary function
 Addressing psychological concerns
 Monitoring and managing potential complications
 Promoting home and community-based care
DIABETIC NEPHROPATHY
 Occurs in types 1 and 2
 Severity of diabetic renal disease is related to extent,
duration and effects of atherosclerosis, htn and
neuropathy.
 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
Stages of progression of type i diabetic renal disease
 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.
 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 5, GFR decreases at an average rate of
10ml/min./year
UROLITHIASIS
 Presence of calculi in urinary tract
 Cause pain as they pass
 Nephrolithiasis is formation of stones in the kidney
Formation of stones
Involves three conditions:
 Slow urine flow resulting in supersaturation of the urine
with the particular element
 Damage to the lining of the urinary tract
 Decreased inhibitor substances in the urine that would
otherwise prevent supersaturation and crystal aggregation
Etiology of urolithiasis
 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 may be
causative
Diagnosis
 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
Treatment
 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
 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