MEDICAL-SURGICAL NURSING

Alterations of Renal and Urinary Tract Function Concept Maps

Potential Causes & Process of Renal Failure
Obstruction Renal Cancer Glomerulonephritis

UTI

Pylenephritis

Renal Failure

Acute
-Reverses - Abrupt ↓ renal functions

Chronic
Progressive/ Irreversible

End Stage Renal Disease

Impaired Renal Blood Flow

Complete Renal Failure GFR gradually ↓ Intra renal Acute tubular necrosis Acute glomerulonephritis Renal Vascular Obstruction Cortical Necrosis Allograft Rejection Transplant

Pre renal (Renal Ischemia) Shock ↓ CO Anaphylaxis

Post renal Kidney Stones
Neoplastic Disease

Nephrons destroyed

Remaining Nephrons ↑ Workload -Hypertrophy - ↓ability to concentrate urine

Dialysis

↑ Bladder = infection
Renal

Tumors

Bladder

Obstruction
Hydroureter Hydronephrosis
Lower Urinary Tract Obstructions Kidney Stones Neurogenic Bladder
Bladder Neck Dyssynergia Interruption of nerve supply

Wilms Tumor

↓Bladder = Acute or Chronic Renal Failure

Embryonal Tumor Nephroblastoma Sporadic and inherited origins Associated with other anomalies

Prostate Enlargement

Urethral Stricture

Severe Pelvic Organ Prolapse

Most common in pelvis of kidney Calcium or Phosphate 7580 % of the time

Gender Race Geographic Location Seasonal Factors Fluid Intake Diet Occupation

Upper Motor Neuron Lesion

Lower Motor Neuron Lesion

Loss of Voluntary control of voiding

Loss of voluntary and involuntary control of voiding

Congenitally abnormal ureter Reflux of urine from bladder to kidney Infection, renal scarring, pyelonephritis

Vesicoureteral Reflux

Caused By Bacteria, Fungal and Parasite

UTI
Pyleonephritis Virulence of Uropathogens Host Defense Mechanisms
Periurethral Mucus Secreting Gland
Bacteria Form Biofilm Body Immune System (Bladder Wall) Acute

Cystitis

Most Common Site for UTI

Bacterial Attaches to Uroepithelium

Sphincter Mechanisms Chronic

Causes: E. Coli, Klebsiella, Pseudomonas, Staph

Infection initiates inflammatory response

Tumors
Association: Tobacco Use, Obesity, Long-term Analgesic use

Common Causes: Kidney Stones Vesicoureteral Reflux Pregnancy Neurogenic Bladder Instrumentation Female Sexual Trauma

Bladder Tumors Renal Adenoma Renal Cell Carcinoma
Primary Associated with mutation of gene P53

Secondary

Benign Tumors Located near cortex of kidney

Most common renal neoplasm Proximal tubule epithelial cells

Increase Risk

Smokers (men)

Workers exposed to chemicals, rubber, & in textile industry

Result of invasion of cancer from bordering organs

Pyelonephritis

Acute
Common Cause: E Coli

Chronic
Recurrent Autoimmune Infections

Infection of renal pelvis and interstutium

Common Causes Kidney Stones Vesicoureteral Reflux Pregnancy Neurogenic Bladder Instrumentation Female Sexual Trauma

Inflammatory Process damages tubular cells

Inflammation and scarring of kidney Pelvis, calyces – dilated & blunted

Destruction of tubules Areas of atrophy/dilation/ diffuse scaring

Usually localized abscesses Healing occurs Deposition of Scar tissue Atrophy of affected tubules

Impairment of function Urine-concentration ability affected

Excretion of diluted urine

Affects primarily the pelvis, calyces, and medulla Rarely causes renal failure

Renal Failure

Glomerular Disorders
Glomerulonephritis
Acute Glomerulonephritis S/S Hematuria Red Blood Cell Casts Protenuria ↓ GFR Oliguria Edema HTN Abrupt onset 7-10 after infection Group A Strep S/S 10-21days after infections

IgA Nephropathy Berger Disease

Nephrotic Syndrome

Crescentic Glomerulonephritis (Rapidly Progressive)

Most Common Form Most individuals Children recover with minimal loss of renal function Disturbance in Glomerular Basement Memb (metabolic, biochemical, physiochemical) leads to increase permeability to protein

Chronic Glomerulonephritis

Several Glomerular Diseases

Idiopathic Proliferative glomerular diseases

Unknown cause 24-48 hrs after URI or GI infection

Focal or Diffuse Segmental fibrosis and deterioration

Antiglomerular Basement Membrane (Good-pasture Syndrome) Prognosis variable 20-50% progress to Renal Fail

Hypoalbuminema

Hyperlipidemia

Proteinuria

Lipiduria

Tubular dilation and atrophy Cause: Immune response Toxin/Drugs Vasc. Disorders Damage: Biochemical Mediators of Inflammation Complement activation Neutrophils/Monocytes Poor Prognosis

Example of Crescent Glomerulonephritis

Hypocalcemia

Antibody Formation Affects: Pulmonary Capillary Glomerular Basement Membs

Poor Prognosis

Treatment: Normal, Low-fat Diet; Salt Restriction Diuretics; Antigoagulants; Removal of toxins; Steroids; Albumin Replacements

Renal Failure

Structural Abnormality Hypospadias

Definition
Congenital condition in which the urethral meatus is located on the ventral side of the penis

Facts
Related to disruption in male hormones Accompanied by Chordee or penile torsion Corrective Surgery

Epispadias Exstrophy of Bladder

Exstrophy of the bladder- Urethral opening on the dorsal surface of penis.

Urethral opening small and situated behind the glans with fissure extending the length of penis Constant dribbling of urine Caused by intrauterine failure of the abdominal wall and the mesoderm of the anterior bladder to fuse Reconstructive surgery girls – teens Boys – 2-3 yrs of age Intrinsic malformation of smooth muscle or urothelial development produces obstruction in 90% of cases. Causes kinking and scarring Polyps rarely arise form the prostatic urethra – often cause sever obstruction and impair renal embrogenesis leading to UTI, Vesicoureteric reflux, and renal failure. Resection as soon as possible Associated with a functional or organic obstruction of the collecting system Obstruction may begin prior to birth

Extensive congenital anomaly in which the lower urinary tract is exposed directly to the surface of the body

Ureteropelvic Junction Obstruction Bladder Outlet Obstruction Hypoplastic(Dysplastic Kidneys Renal Agenesis Polycystic Kidneys

Blockage of the tapered point where the renal pelvis transitions into the ureter

A urethral valve is a thin membrane of tissue that occludes the urethral lumen and obstructs urinary outflow in males.

Ureteric duct grows into the metanephric tissue, triggering the formation of the kidneys in utero. If this growth does not occur the kidney is absent or hypoplastic (small) Renal dysplasia results from abnormal differentiation of renal tissue Absence of one or both kidneys Potter syndrome (bilateral renal agenesis) Autosomal dominant inherited disorder PKD-1 and PKD-2 mutations account for the disease

Clearly hereditary Bilateral agenesis is usually fatal Unilateral – males more affected The gene products regulate epithelial growth and differentiation.

References
Corwin, E. J. (2000). Handbook of Pathophysiology (2nd ed.). Philadelphia, PA: Lippincott. Gray, M., Huether, S., & Forshee, B. (2006). Alterations of renal and urinary tract function. In K. L. McCance & S. Huether (Eds.), Pathophysiology: The Biologic Basis for Disease in Adults & Children (pp.13011336). St Louis, MO: ElSevier Mosby. Huether, S. (2006) Alteration of renal and urinary tract functions in children. In K.

MANAGEMENT OF PATIENTS WITH GUT DYSFUNCTION

MANAGEMENT OF PATIENTS WITH GUT DYSFUNCTION

REVIEW OF THE GENITOURINARY SYSTEM

THE URINARY SYSTEM
 The urinary system consists of the kidneys,

ureters, urinary bladder and urethra.  The urinary system eliminates wastes, controls blood volume regulates blood ion concentration and pH, and regulates blood cell production.

THE KIDNEYS
 Each kidney is behind the peritoneum, and

surrounded by a renal capsule and a renal fat pad.  The ureter expands to form the renal pelvis within the renal sinus, and the renal pelvis has flower-like extensions called renal calyces.  The kidney is divided into an outer cortex and an inner medulla. Each renal pyramid in the medulla has a base that extends into the cortex. The apex of each renal pyramid projects to a calyx.

The Kidneys and the Nephron

THE NEPHRON
 The functional unit of the kidney is the

nephron.  The parts of the nephron are the renal corpuscle, the proximal convoluted tubule, the loop of Henle, and the distal convoluted tubule.  The filtration membrane is formed by the glomerular capillaries, the basement membrane and the podocytes of Bowman’s capsule.

The Kidneys and the Nephron

Ureters, Urinary Bladder and Urethra
 Ureters carry urine from the renal pelvis to

the urinary bladder.  The urethra carries urine from the urinary bladder to the outside of the body.  The ureters and the urinary bladder are lined with transitional epithelium and have smooth muscle in their walls.  The internal and external urinary sphincter muscles regulate the flow of urine through the urethra.

Ureters, Urinary Bladder and Urethra

Urinary System Function
 Removal of toxic waste products
 Regulation of blood volume  Regulation of electrolyte balance  Regulation of acid-base balance  Regulation of fluids/electrolytes in tissue

fluid  Production of erythropoietin*

MANAGEMENT OF PATIENTS WITH GUT DYSFUNCTION

ASSESSMENT OF RENAL AND URINARY TRACT FUNCTION

HEALTH HISTORY
 Urinary symptoms:  Dysuria  Hesitancy or straining  Intermittency  Terminal Dysuria  Urgency  Strangury

HEALTH HISTORY
 Urinary volume and frequency:  Frequency  Polyuria  Nocturia  Oliguria (< 400 cc/day)  Anuria (<50 cc/day)

HEALTH HISTORY
 Urinary appearance / sediments:  Hematuria (gross and microscopic)  Pyuria (gross and microscopic)  Lithuria

HEALTH HISTORY
 Inquire about the following:

Presence or history of genital lesions Habits: use of tobacco, alcohol or recreational drugs Any prescription and over-the-counter medications (including those prescribed for renal or urinary problems)

HEALTH HISTORY
RISK FACTORS FOR SELECTED RENAL OR UROLOGIC DISORDERS RISK FACTOR Childhood disease: “strep throat,” impetigo, nephrotic syndrome POSSIBLE RENAL OR UROLOGIC DISORDER Chronic renal failure

Advanced age
Instrumentation of urinary tract, cystoscopy, catheterization

Incomplete emptying of the bladder leading to urinary tract infection
Urinary tract infection, incontinence

Immobilization
Occupational, recreational, or environmental exposure to chemicals (plastics, pitch, tar, rubber) Diabetes mellitus

Kidney stone formation
Acute renal failure

Chronic renal failure, neurogenic bladder

HEALTH HISTORY
RISK FACTORS FOR SELECTED RENAL OR UROLOGIC DISORDERS RISK FACTOR Hypertension POSSIBLE RENAL OR UROLOGIC DISORDER Renal insufficiency, chronic renal failure

Systemic lupus erythematosus
Gout, hyperparathyroidism, Crohn’s disease

Nephritis, chronic renal failure
Kidney stone formation

Sickle cell disease, Multiple myeloma
Benign prostatic hypertrophy

Chronic renal failure
Obstruction to urine flow, leading to frequency, oliguria, anuria, obstructive uropathy and chronic renal failure Cystitis, fibrosis, fistula Inadvertent trauma to the ureters or bladder Neurogenic bladder, UTI, incontinence

Radiation therapy to the pelvis Recent pelvic surgery Spinal cord injury

PHYSICAL EXAMINATION
 Head-to-toe assessment with special

   

emphasis on the abdomen, suprapubic region, genitalia and lower back, and lower extremities Direct palpation of the kidneys Rectal examination (men) Vulva, urethral meatus and vagina (women) Valsalva maneuver (men and women)

Age related changes
 Urinary bladder  Decreased bladder size & tone of detrusor muscle  Kidneys  Decreased ability to concentrate urine  GFR decreases  Nephrons decrease  Males  Enlarged prostate  Females  Pelvic floor muscle weakness  Prone to bladder infections, urinary incontinence, & urethral irritation

Warning Signs of Kidney Disease
     

Burning or difficulty during urination. Increase in the frequency of urination, especially at night. Passage of bloody appearing urine. Puffiness around the eyes, or swelling of the hands and feet, especially in children. Pain in the small of the back just below the ribs (not aggravated by movement). High blood pressure.

DIAGNOSTIC EVALUATION: Urinalysis and Urine Culture
 Urine color
 Urine clarity and odor  Urine pH and specific gravity

 Tests to detect protein, glucose and ketone

bodies  Microscopic examination of urine sediments after centrifuging to detect RBCs, WBCs, casts, crystals, and bacteria

DIAGNOSTIC EVALUATION: Renal Function Tests
 Used to evaluate the severity of kidney

disease and to assess the patient’s clinical progress.  Provide information on the effectiveness of the kidney in carrying out its excretory function.  Renal concentration tests, creatinine clearance, serum creatinine and blood urea nitrogen levels

DIAGNOSTIC EVALUATION: Renal Function Tests
TEST PURPOSE NORMAL VALUES

Renal Concentration Tests
Specific gravity Urine osmolality Evaluates the ability of kidneys to concentrate solutes in urine Concentrating ability is lost early in kidney disease; hence these test findings may disclose early defects in renal function Detects and evaluates progression of renal disease. Test measures volume of blood cleared in 1 minute which provides an approximation of the glomerular filtration rate. Sensitive indicator of renal disease used to follow progression of renal disease. 1.010 – 1.025 300 – 900 mOsm/kg/24hr; 50 – 1,200 mOsm/kg random sample

24-Hour Urine Test Creatinine clearance Age < 30 30-40 40-50 50-60 60-70 70-80 Male Female 88-146 81-134 82-140 75-128 75-133 69-122 68-126 64-116 61-120 58-110 55-113 52-105

DIAGNOSTIC EVALUATION: Renal Function Tests
TEST Serum Tests Creatinine level Measures effectiveness of renal function. Creatinine is end product of muscle energy metabolism. In normal function, level of creatinine, which is regulated and excreted by the kidneys, remains fairly constant in the body. Serves as index of renal function. Urea is nitrogenous end product of protein metabolism. Test values are affected by protein intake, tissue breakdown, and fluid volume changes. Evaluates hydration status. Elevated ratio seen in hypovolemia 0.6 – 1.2 mg/dL (50 – 110 μmol/L) PURPOSE NORMAL VALUES

BUN

7 – 18 mg/dL Patients over age 60: 8 – 20 mg/dL

BUN:Creat

About 10:1

IMAGING MODALITIES: X-ray Films
 An x-ray study of the abdomen or kidney,

ureters and bladder (KUB plain) may be performed to delineate the size, shape and position of they kidneys.  They reveal any abnormalities such as calculi, hydronephrosis, cysts, tumors, or kidney displacement by surrounding tissue abnormalities.

IMAGING MODALITIES: Ultrasonography
 Non-invasive procedure to detect

abnormalities such as fluid accumulation, masses, congenital malformations, changes in kidney size, or obstructions.  Lower abdomen or genitalia may need to be exposed.  Requires a full bladder, fluid intake should be encouraged before the procedure.

IMAGING MODALITIES: CT and MRI
 Non-invasive techniques that provide

excellent cross-sectional views of the kidney and urinary tract.  Used in evaluating GUT masses, lithiases, chronic renal infections, renal or urinary tract trauma, metastatic disease and soft tissue abnormalities.  Claustrophobia is often a problem especially with the MRI.

IMAGING MODALITIES: CT and MRI
 Patient preparation includes removal of

metallic objects such as jewelry and clothing with metallic clasps.  MRI is contraindicated in patients with pacemakers, surgical clips, or any metallic objects anywhere in the body.  Oral or intravenous radiocontrast agent may be used to enhance visualization

Computed Tomography

Magnetic Resonance Imaging

IMAGING MODALITIES: Intravenous Urography
 Includes excretory urography, IVP and

infusion drip pyelography.  An intravenous dye is administered and, via x-ray imaging, the dye is observed as it moves through the upper and lower urinary system.  Visualizes the collecting system of the kidneys and the length of the ureters, the appearance of the bladder lumen and the urethra.

IMAGING MODALITIES: Retrograde Pyelography
 Catheters are advanced through the urethra,

bladder, ureters and into the renal pelvis by means of cystoscopy, and a contrast agent is then injected.  X-ray films are taken to visualize the collecting system of the kidneys to assess kidney structure in patients who are allergic to intravenous contrast agents.

UROLOGIC ENDOSCOPE
 Can be performed in two ways: through a

cystoscope inserted into the urethra, or percutaneously through a small incision.  Used to directly visualize the urethra and bladder.  The nurse describes the examination to the patient and family to prepare them and to allay their fears.  If an upper cystoscopy is to be performed, the patient is usually kept on NPO for several hours beforehand.

UROLOGIC ENDOSCOPE
 Post-procedural management directed at

relieving any discomfort resulting from the examination  Moist heat to the lower abdomen and warm sitz baths are helpful in relieving pain and relaxing the muscles.  Monitor for urine retention  Monitor for signs and symptoms of UTI

KIDNEY BIOPSY
 Used in diagnosing and evaluating the extent

of kidney disease.  Indications:
Unexplained renal failure Persistent proteinuria or hematuria Transplant rejection Glomerulopathies
 Contraindications:

Bleeding tendencies Uncontrolled hypertension Solitary kidney

KIDNEY BIOPSY
 Patient is placed on NPO 6 to 8 hours before
  

the test and an IV line is established. Urine specimen is obtained and saved for comparison with the post-biopsy specimen. Usually performed under sonographic guidance. After the biopsy, pressure is applied to the site and the patient is placed flat on bed for 6 to 8 hours to minimize bleeding. Vital signs monitoring every 15 minutes for 4 hours or until stable, whichever comes first.

KIDNEY BIOPSY
 Collect all voided urine, one bottle per

voiding, for comparison.  Patient instruction: avoid strenuous activities, sports, heavy lifting for at least 2 weeks.

MANAGEMENT OF PATIENTS WITH GUT DYSFUNCTION

DYSFUNCTIONAL VOIDING PATTERNS

ADULT VOIDING DYSFUNCTION
 Both neurogenic and non-neurogenic

disorders  The micturition process involves several highly coordinated neurologic responses that mediate bladder function.  A functional urinary system allows for appropriate bladder filling and complete bladder emptying.  Usually involves the lower urinary system in adults, but may progress to involve the upper urinary system if not treated promptly.

URINARY INCONTINENCE
 Risk factors:

Pregnancy: vaginal delivery, episiotomy Menopause Genitourinary surgery Pelvic muscle weakness Incompetent urethra due to trauma Immobility High-impact exercise Diabetes mellitus Stroke

URINARY INCONTINENCE
 Risk factors:

Age-related changes in the urinary tract Morbid obesity Cognitive disturbances: dementia, Parkinson’s disease Medications: diuretics, sedatives, hypnotics, opioids Caregiver or toilet unavailable

URINARY INCONTINENCE: Clinical Types
 Stress incontinence
 Urge incontinence  Reflex incontinence

 Overflow incontinence

Classifications of Incontinence
   

Stress incontinence: leakage of urine from coughing, laughing, jogging, dancing, etc. Urge incontinence: occurs when a person is unable to suppress the sudden urge to urinate. Overflow incontinence: when the bladder becomes so full and distended that urine leaks out. Total incontinence: when no urine can be retained in the bladder, usually due to neurologic problem.

 Nocturnal

Enuresis: incontinence that occurs during sleep.

URINARY INCONTINENCE: Assessment and Diagnosis
 Detailed description of the problem and a

history of medication use  Voiding history and diary of fluid intake and output  Urodynamic tests (cystometrogram)  Urinalysis and urine culture

URINARY INCONTINENCE: Medical Management
 Depends on the underlying cause
 Behavioral therapy are always the first choice

to decrease or eliminate incontinence
Timed voiding Prompted voiding Habit retraining Bladder retraining or “bladder drill” Pelvic muscle exercises or Kegel exercises

URINARY INCONTINENCE: Medical Management
 Pharmacologic therapy

Anticholinergics (oxybutynin, dicyclomine) Tricyclic antidepressants (imipramine, doxepin) Pseudoephedrine (Sudafed) Estrogen

URINARY INCONTINENCE: Surgical Management
 Indicated in patients who have not achieved

continence using behavioral and pharmacologic therapy.  Options vary according to the underlying anatomic and physiologic problem

URINARY RETENTION
 Inability to empty the bladder completely

during attempts to void.  Chronic urine retention often leads to overflow incontinence.  Residual urine is urine that remains in the bladder after voiding (Normal: complete bladder emptying in healthy adults younger than 60; if > 60: 50 to 100 ml).

URINARY RETENTION
 Can occur postoperatively in any patient

particularly if the surgery affected the perineal or anal regions.  General anesthesia reduces bladder muscle innervation and suppresses the urge to void, impeding bladder emptying.

URINARY RETENTION: Pathophysiology
 Urinary retention may result from diabetes,

prostatic enlargement, urethral pathology, trauma, pregnancy, or neurologic disorders such as cerebrovascular accident, spinal cord injury, multiple sclerosis, or Parkinson’s disease.  May also be caused by medications

URINARY RETENTION: Complications
 Chronic infections
 Calculi  Pyelonephritis and sepsis

 Hydronephrosis and obstructive form of

uropathy and chronic renal failure  Urine leakage with perineal skin breakdown and irritation

Urinary Catheterization

CATHETERIZATION
 Relieve urinary retention
 Assist with postoperative drainage in urologic

and other surgeries  Provide means to monitor accurate urine output in critically ill patients  Promote urinary drainage in patients with neurogenic bladder dysfunction or urine retention  Prevent urinary leakage in patients with stage III to IV pressure ulcers

CATHETERIZATION: Indwelling Devices
 A closed drainage system is essential
 Has to be changed at least every two weeks

using aseptic techniques  Change drainage bags every three days using aseptic techniques

SUPRAPUBIC CATHETER
 Following some surgeries
 Long term situations  Suprapubic catheter – indwelling

catheter directly inserted through an incision into the lower abdomen directly into the bladder  Nursing: Keep area clean & dry

CATHETERIZATION: Nursing Management
 Assessing the patient and the system
 Minimizing trauma
 Use

an appropriate-sized catheter.  Lubricate the catheter adequately with a water-soluble lubricant during insertion.  Insert the catheter far enough into the bladder to prevent trauma to the urethral tissues when the retention balloon is inflated.  Secure catheter properly.

CATHETERIZATION: Nursing Management
 Retraining the bladder.
 Preventing complications.

MANAGEMENT OF PATIENTS WITH GUT DYSFUNCTION

URINARY DISORDERS

UTI
 Caused by pathogenic microorganisms in the

urinary tract and classified as either upper or lower urinary tract infections  Lower UTI:
  

Cystitis (inflammation of the urinary bladder) Prostatitis (inflammation of the prostate gland) Urethritis (inflammation of the urethra

 Upper UTI:  Acute and chronic pyelonephritis (inflammation of the renal pelvis)  Interstitial nephritis (inflammation of the kidney)

UTI
 One of the most common reasons patients

seek health care.  Most cases occur in women, with one of every five women in the US developing a UTI sometime during her life (higher incidence in developing countries).  Urinary tract is also the most common site of nosocomial infection.

UTI
 Risk factors:  Inability or failure to empty the bladder completely  Obstructed urinary flow  Decreased natural host defenses or immunosuppression  Instrumentation of the urinary tract  Inflammation or abrasion of the urethral mucosa  Contributing conditions:
   

Diabetes mellitus Pregnancy Neurologic disorders Gout

LOWER UTI
 Mechanisms which maintain the sterility of the

bladder:
    

Physical barrier of the urethra Urine flow Ureterovesical junction competence Various antibacterial enzymes and antibodies Antiadherent effects mediated by the mucosal cells of the bladder

LOWER UTI: Pathophysiology
 Bacteria gains access to the bladder, attach

to and colonize the epithelium of the urinary tract to avoid being washed out during voiding.  Pathogens evade host defense mechanisms.  Inflammation is initiated.  Most UTIs result from fecal organisms that ascend from the perineum to the urethra and the bladder and then adhere to the mucosal surfaces.

LOWER UTI: Pathophysiology
 Routes of infection:  Ascending infection (up the urethra)  Hematogenous (through the bloodstream)  Direct extension (fistulous tract from the intestines)

LOWER UTI: Clinical Manifestations
 Asymptomatic (50%)
 Frequent pain and burning on urination  Frequency, urgency, nocturia, incontinence

 Suprapubic or pelvic pain and tenderness
 Back pain and hematuria

LOWER UTI: Assessment and Diagnostic Findings
 UTI is diagnosed by bacteria in the urine:

colony count of 105 colony-forming units per mL of urine on a clean-catch midstream or catheterized specimen (major criterion).  UTI have subsequent sepsis have occurred with lower bacterial colony counts, however.  Cellular studies:
 

Microscopic hematuria (>4 RBCs/hpf) Pyuria (>4 WBCs/hpf)

LOWER UTI: Assessment and Diagnostic Findings
 Urine cultures remain the gold standard in

documenting a UTI and can identify the specific organisms present.  The following groups of patients should have urine cultures obtained when bacteriuria is present:

All men  All children  Women with a history of compromised immune function or renal problems  Diabetic patients

LOWER UTI: Assessment and Diagnostic Findings
 The following groups of patients should have

urine cultures obtained when bacteriuria is present (cont’d):

     

Patients who have undergone recent instrumentation (including catheterization) of the urinary tract Patients who were hospitalized recently Patients with prolonged or persistent symptoms Patients with 3 or more UTIs in the past year Pregnant women Postmenopausal women Sexually-active women or with new partners

LOWER UTI: Medical Management
 Management typically involves

pharmacologic therapy and patient education.  Acute pharmacologic therapy:

Uncomplicated in women: single-dose, shortcourse (3 to 4 days), or 7- to 10-day therapeutic courses Complicated UTI: cephalosporin or ampicillin/aminoglycoside combination for 7 to 10 days; TMP-SMZ; quinolones Emphasize completion of regimen even if symptoms subside

LOWER UTI: Medical Management
 Long-term pharmacologic therapy  Reinfection in women after completion of antimicrobial therapy: another short course of fulldose antimicrobial agent may be prescribed; if there is no recurrence, medication is taken every other night for 6 to 7 months.  Other options: a dose of antimicrobial agent after sexual intercourse, a dose at bedtime, or a dose every other night, or three time per week  Cranberry juice?

UPPER UTI: Acute Pyelonephritis
 Bacterial infection of the renal pelvis, tubules,

and interstitial tissue of one or both kidneys.  Frequently secondary to ureterovesical reflux; other causes include urinary tract obstruction, bladder tumors, strictures, BPH, urinary stones  Kidneys are often enlarged with interstitial infiltration of inflammatory cells.  Abscesses may be noted on the renal capsule.

ACUTE PYELONEPHRITIS: Assessment and Diagnosis
 An ultrasound or a CT scan may be

performed to locate any obstruction in the urinary tract.  IVP is rarely indicated during acute pyelonephritis (normal findings in 75% of patients)  Urine culture and sensitivity tests are performed to determine the causative organism so that appropriate antimicrobial agents can be prescribed.

ACUTE PYELONEPHRITIS: Medical Management
 Uncomplicated: treated as outpatients
 Other patients, including pregnant women,

may be hospitalized for at least 2 to 3 days of parenteral therapy. Once afebrile, oral agents may be substituted.  Pharmacologic therapy:

2-week course of TMP-SMZ, ciprofloxacin, gentamicin with or without ampicillin, or a thirdgeneration cephalosporin  Analgesics to relieve pain  Antipyretics to lyse the fever

CHRONIC PYELONEPHRITIS
 Usually results from repeated bouts of acute
  

pyelonephritis May cause end-stage renal disease Usually no symptoms of infection unless an acute exacerbation occurs Fatigue, headache, poor appetite, polyuria, excessive thirst, weight loss Tests to determine the extent of the disease: intravenous urogram, measurement of creatinine clearance, BUN and creatinine levels.

CHRONIC PYELONEPHRITIS
 Complications:  End-stage renal disease  Hypertension  Nephrolithiasis
 Medical management:  Nitrofurantoin or TMP-SMZ to suppress bacterial growth  Careful monitoring of renal function with proper adjustment of dosages depending on renal clearance

CHRONIC PYELONEPHRITIS
 Nursing management:  Monitoring of fluid intake and output  Unless contraindicated, liberal fluid intake up to 3 to 4 li/day  Monitor TPR every 4 hours and administer antipyretic drugs and antibiotics as prescribed  Patient education on the prevention of UTI: adequate fluid consumption, regular bladder emptying and proper perineal hygiene

UPPER URINARY TRACT INFECTIONS
ACUTE PN
Cause Onset Duration Course Poorly, untreated or complicated LUTI Fast, sudden Short, reversible Dramatic, “toxic”

CHRONIC PN
Recurrent APN Slow, imperceptible Chronic, irreversible Early: Insidious Late: “toxic”

Symptoms More severe than LUTI

Quiet at onset, with CRF symptoms later

UPPER URINARY TRACT INFECTIONS
ACUTE PN
Signs

CHRONIC PN

(+) Goldflam sign on Evidence of CRF in PE later stages

Labs
Treatment

Outcomes

KUB-UTZ: enlarged, inflamed kidney Aggressive antibx for > days Acute renal failure Sepsis, septic shock Recover or death

KUB-UTZ: small, scarred kidney Symptomatic, dialysis in CRF Chronic renal failure ESRD Death

PRIMARY GLOMERULAR DISEASES
 Includes acute and chronic

glomerulonephritis, rapidly progressive glomerulonephritis, and nephrotic syndrome.  The glomerular capillaries are primarily involved: antigen-antibody complexes form in the blood and become trapped in the glomerular capillaries, inducing an inflammatory response.  IgG can be detected in the glomerular capillary walls.

PRIMARY GLOMERULAR DISEASES

PRIMARY GLOMERULAR DISEASES
 Major clinical manifestations of glomerular

injury:
     

Proteinuria Hematuria Decreased glomerular filtration rate Alterations in excretion of sodium Edema Hypertension

ACUTE GLOMERULONEPHRITIS
 Glomerulonephritis is an inflammation of the

glomerular capillaries.  AGN is a disease of children older than 2 years of age but can occur at any age group.

AGN: Pathophysiology
 In most cases, a group A β-hemolytic

streptococcal infection of the throat precedes the onset of glomerulonephritis (Poststreptococcal GN) by 2 to 3 weeks.  May also follow impetigo and acute viral infections (Post-infectious GN)  In some patients, antigens outside the body (medications, foreign serum) initiate the process, resulting in antigen-antibody complexes being deposited in the glomeruli.

AGN: Pathophysiology
ANTIGEN (GROUP A BETA-HEMOLYTIC STREPTOCOCCI) ANTIGEN-ANTIBODY PRODUCT

DEPOSITION OF ANTIGEN-ANTIBODY COMPLEX IN GLOMERULUS

INCREASED PRODUCTION OF EPITHELIAL CELLS LINING THE GLOMERULUS

LEUKOCYTES INFILTRATE THE GLOMERULUS

AGN: Pathophysiology
LEUKOCYTES INFILTRATE THE GLOMERULUS THICKENING OF THE GLOMERULAR FILTRATION MEMBRANE

SCARRING AND LOSS OF GLOMERULAR FILTRATION MEMBRANE

DECREASED GLOMERULAR FILTRATION RATE

RENAL FAILURE

AGN: Clinical Manifestations
 Hematuria (primary presenting feature)
 Proteinuria (primarily albumin)  Azotemia (elevated BUN and serum  


 

creatinine levels) Oliguria/anuria Anemia Edema and hypertension (75% of patients) Headache, malaise, flank pain CVA tenderness

AGN: Clinical Manifestations
 Circulatory overload with dyspnea, engorged

neck veins  Cardiomegaly and pulmonary edema  Confusion, somnolence and seizures (uremic encephalopathy)

AGN: Assessment and Diagnostic Findings
 Ultrasonography of the kidneys: large,

swollen and congested kidneys  Electron microscopy and immunofluorescent analysis if kidney biopsy samples: demonstration of immunoglobulins and typical glomerular changes  Serologic tests: increased serum complement levels (within 2 to 8 weeks)  Urinalysis showing RBC casts and other sediments

AGN: Complications
 Hypertensive encephalopathy
 Heart failure  Pulmonary edema

 Uremia

AGN: Medical Management
 Treating symptoms
 Preserve kidney function  Treat complications

 Pharmacologic therapy:  Penicillin (if with residual streptococcal infection)  Corticosteroids and immunosuppresants  Loop diuretics and antihypertensive medications
 Dietary protein restriction when renal

insufficiency develops  Sodium restriction

CHRONIC GLOMERULONEPHRITIS
 May be due to repeated episodes of acute

glomerulonephritis, hypertensive nephrosclerosis, hyperlipidemia, chronic tubulointerstitial injury, or hemodynamicallymediated glomerular injury and sclerosis.  Kidneys are reduced to as little as one-fifth their normal size consisting largely of scar or fibrous tissue.  The renal cortex decreases in thickness.  Glomeruli become scarred and branches of the renal artery become thickened.

CGN: Clinical Manifestations
 Hypertension
 Azotemia  Edema

 Uremia
 Nutritional derangements  Skin appears yellowish gray

 Anemia
 Cardiomegaly and pulmonary edema  Peripheral neuropathy

CGN: Assessment and Diagnostic Findings
 Urinalysis reveals fixed specific gravity of

      

about 1.010, variable proteinuria, and urinary casts Hyperkalemia Metabolic acidosis Anemia Hypoalbuminemia Hyperphosphatemia Hypocalcemia Impaired nerve conduction

CGN: Assessment and Diagnostic Findings
 Cardiac enlargement and pulmonary edema

on radiography  ECG: left ventricular enlargement, evidence of electrolyte abnormalities

CGN: Medical Management
 Symptoms guide the course of management
 Diet modification  Control of hypertension:  ACE-inhibitors and Angiotensin II receptor blockers  Calcium-channel blockers  Beta-adrenergic blockers  Central-acting drugs  Diuretics

CGN: Medical Management
 Hemodialysis
 Kidney transplantation

NEPHROTIC SYNDROME
 Apparent in any condition that seriously

damages the glomerular capillary membrane and results in increased permeability  Primary glomerular disease characterized by:
   

Marked increase in protein in the urine (proteinuria) Decrease in albumin in the blood (hypoalbuminemia) Edema High serum cholesterol and low-density lipoproteins

NEPHROTIC SYNDROME: Pathophysiology
 Can occur with almost any intrinsic renal

disease or systemic disease that affects the glomerulus  Generally considered a disease of childhood but it does occur in adults, including the elderly.  Causes:

  

Chronic glomerulonephritis Diabetes mellitus Amyloidosis and systemic lupus erythematosus Multiple myeloma

NEPHROTIC SYNDROME: Pathophysiology
DAMAGED GLOMERULAR CAPILLARY MEMBRANE LOSS OF PLASMA PROTEIN (ALBUMIN) STIMULATES SYNTHESIS OF LIPOPROTEINS HYPOALBUMINEMIA

HYPERLIPIDEMIA

DECREASED ONCOTIC PRESSURE

GENERALIZED EDEMA (FLUID MOVES FROM VASCULAR SPACE TO EXTRACELLULAR SPACE

ACTIVATION OF RENIN-ANGIOTENSIN SYSTEM

SODIUM RETENTION

EDEMA

NEPHROTIC SYNDROME: Clinical Manifestations
 Edema (major manifestation)
 Malaise, headache, irritability and fatigue  Hypertension usually not a manifestation

NEPHROTIC SYNDROME: Assessment and Diagnosis
 Proteinuria exceeding 3 to 3.5 g/day is

sufficient for the diagnosis of nephrotic syndrome.  Pyuria and granular and epithelial casts on urinalysis  Needle biopsy of the kidney may be performed for histologic diagnosis of the etiology  Serum markers (anti-C1q antibodies is the most reliable for assessing disease activity in lupus nephritis)

NEPHROTIC SYNDROME: Complications
 Infection (deficient immune response)
 Thromboembolism  Pulmonary emboli

 Acute renal failure
 Accelerated atherosclerosis

NEPHROTIC SYNDROME: Medical Management
 Objective is to preserve renal function
 Diuretic agents for severe edema  ACE-inhibitors in combination

 Cyclophosphamide and azathioprine
 Corticosteroids  Low-sodium, liberal-potassium diet  Protein intake should be about 0.8 g/kg/day

with emphasis on high biologic value proteins (dairy products, eggs, meats)  Diet should be low in saturated fats

RENAL FAILURE
 Transient or permanent inability of the

kidneys to perform their normal function of urine formation (filtration, secretion and reabsorption.  Two types:
renal failure – reversible, transient  Chronic renal failure – irreversible, permanent
 Acute

ACUTE RENAL FAILURE
 Stages:

phase – azotemia  Diuretic phase – increased urine output  Recovery phase – full recovery of renal function
 Oliguric/anuric

 Types:
 Pre-renal

ARF  Intrinsic renal ARF  Post-renal ARF

CHRONIC RENAL FAILURE
 Stages:
 Stage

I: 80-125 ml/min (normal renal function)  Stage II: 50-80 ml/min (diminished renal reserve; chronic renal impairment)  Stage III: 20-50 ml/min (chronic renal impairment)  Stage IV: 5-20 ml/min (chronic renal insufficiency  Stage V: < 5 ml/min (ESRD)

MANIFESTATIONS
 Azotemia / Uremia
 Uremic

frost  Uremic fetor  Uremic encephalopathy  Uremic cardiomyopathy / pericarditis  Uremic gastropathy

MANIFESTATIONS
 Edema
 Multiple electrolyte imbalance
 Hypernatremia  Hyperkalemia  Hypermagnesemia  Hyperphosphatemia  Hypocalcemia

MANIFESTATIONS
 Metabolic acidosis
 Anemia  Hypertension

MANAGEMENT
 Aggressive Management
 Supportive Management

Acute vs. Chronic Renal Failure
 Acute (Reversible!)  Sudden/complete loss kidney function  Cause: failure of renal circulation, tubular, or glomeruli dysfunction

Pre-renal: hypo-perfusion of kidney (shock, hemorrhage,etc.)  Intra-renal: damaged renal tissue (infection, transfusion rx’s, burns, drugs, etc.)  Post-renal: an obstruction somewhere distal to kidneys: renal flow (ex. calculi, stricture, tumor etc.)

Chronic: ESRD (Irreversible)  Progressive  uremia devps = affects all body systems  ↓ funct. Glomeruli = ↓GFR, *urine creatinine clearance↓, but serum *creatinine  & *BUN  , Na+ H20 retention = edema, CHF, crackles, *K+ , *metabolic acidosis

  S/S :

Acute vs. Chronic renal failure Acute  Chronic (ESRD)
may include: *anuria (less 50cc/day)  *oliguria (*less than 400cc/day or *30mL/hour)  * or a normal urine output!, however, the serum BUN and Creatinine will be elevated for all above!  appear critically ill, lethargic, n/v/d
 Anemia (dec. *erythropoetin)  Po4 & Ca+ imbalance  S/S:

 

 

+ JVD, peri-orbital edema, dependent/pitting edema, crackles, SOB Ammonia odor breath, anorexia, n/v Skin=”uremic frost”, gray-bronze skin, dry flakey, itchy skin, muscle cramps ? Bone fx Neuro = weakness, fatigue, confusion, seizures (anuria = less than 50cc/day) or *(oliguria=less 400cc/day)

Acute vs. Chronic renal failure  Chronic or ESRD  Acute
 skin & mucous membranes

 Management:

dry from dehydration, breath odor (uremic fetor), h/a, muscle twitch, ↓ specific gravity urine, BUN/creatinine, *↓ 24hour urine creatinine clearance, * K+* worry about cardiac dysrhythmias, tissue edema, uremic frost, metabolic acidosis, anemia, PO4/Ca+/and F&E imbalance.** negative nitrogen balance

Dietary: renal diet, low Protein, Na+, K+, fluid restriction, higher fats & CHO=calories, I&O  Antacids: correct Po4/Ca+ imbalance, aluminum or ca+ carbonate: give meals
Anti-hypertensives,  Erythropoietin (Epogen) = ↓ anemia,  to ↓ K+ levels = resin *Kayexelate = po or/enema = exchg Na+/K+ bowel = loose stool or *require dialysis to lower K+

Acute vs. Chronic renal failure
 Acute  4-phases of acute:  Initiation phase = starts w/insult and ends with oliguria  Oliguric Phase = period where uremic s/s begin, ↓ urinary output < 400mL/day,  Bun, Cr, K+, (FV Excess), hypernatremia ( Na+)  Diuretic Phase = signals U.O. , lab values better, dehydrated, uremia gone, GFR better! (FV deficit)  Recovery Phase = improved renal function last (3-12 mos)
 Chronic (ESRD)  Management is Dialysis

either Hemodialysis, or Peritoneal dialysis  Or possibly a kidney transplantation= must find a donor match/ must worry about graft- transplantation rejection!

Acute vs. chronic renal failure
 Acute

 Chronic or ESRD
 I&O, fluid restriction ex. 700-

Management:

Strict I&O   K+ = Kayexelate po/enema first; if not better – must use dialysis  Check wt. daily,↓dietary protein, K+ (40-60mEq/day), & Na+ (2 gm./day) diet, ↓K+ foods; soda, bananas, citrus  Correction of *acidosis & elev PO4 levels = sodium bicarb, and phosphate binding agents like antacids (Phos-lo, Amphogel, calcium
carbonate, aluminum based antacids) thus,  Ca+

1000cc/24 hr, so break-it-up / shift  1-2 gm. of low Na+diet, low K+ diet, avoid salt substitutes for they contain K+ ! BAD for you  Low protein diet, however eat proteins of high biological value such as dairy products,

eggs, meat, fish in small portions only  RBC, Hbg/Hct: Give Epogen or Procrit SQ to increase (*erythropoetin)

Bedrest to ↓ BMR & ↓ catabolism, thus, ↓ K+ & nitrogen waste prod (BUN/Cr)

UROLITHIASIS
 Refers to stones (calculi) in the urinary tract.
 Formed when urinary concentrations of

calcium oxalate, calcium phosphate and uric acid increase (supersaturation) and dependent on the amounts of the substance, ionic strength, and pH of the urine

UROLITHIASIS: Pathophysiology
 Supersaturation of calcium oxalate, calcium

phosphate, uric acid  Deficiency of substances that normally prevent crystallization in the urine (citrate, magnesium, nephrocalcin, uropontin)  Stones often occur in dehydrated patients  They may deposit in many areas of the urinary tract, including the renal pelvis, ureters, ureterovesical junction and urinary bladder.

UROLITHIASIS: Pathophysiology
 Factors that favor the formation of stones:  Infection  Urinary stasis  Immobility  Hypercalcemia  Hyperuricemia
 75% of renal stones are calcium based, 5 to

10% are made up of uric acid, and 10 to 15% are cystine or struvite stones which are closely associated with infections.

UROLITHIASIS: Clinical Manifestations
 Depend on the location of the stone and the
    

presence of attendant urinary tract infection Intense, deep ache in the costovertebral and flank regions Acute pain + tenderness + nausea + vomiting (renal colic) Hematuria Oligoanuria Fever and chills

UROLITHIASIS: Assessment and Diagnosis
 Diagnosis is confirmed by x-ray films of the

kidneys, ureters and bladder (KUB) especially if the stone is calcium-based  Serum chemistries for uric acid, BUN creatinine and calcium  Chemical analysis of voided stones

UROLITHIASIS: Medical Management
 Basic goals: eradicate the stone, determine

   

the stone type, prevent nephron destruction, prevent recurrent stone formation Immediate goal: relieve the pain Nutritional therapy to prevent renal stones Liberal fluid intake, at least 8 8-oz glasses of water daily to keep the urine dilute Keep urine output of at least 2 li/day

UROLITHIASIS: Medical Management
 Dietary recommendations:  Restricting protein to 60 g/day to decrease urinary excretion of calcium and uric acid.  A sodium restriction of 3-4 g/day. Table salt and high-sodium foods should be reduced because sodium competes with calcium for reabsorption in the kidneys.  Low-calcium diets are not generally recommended, except for true absorptive hypercalciuria.  Oxalate-containing foods (spinach, strawberries, rhubarb, tea, peanuts, wheat bran) may be restricted.

UROLITHIASIS: Surgical Management
 Done if stone is not passed spontaneously or


if complications occur. Ureteroscopy Extracorporeal shockwave lithotripsy (ESWL) Laser lithotripsy (new technology, not yet widely performed) Percutaneous removal

Lithotripsy

HYDRONEPHROSIS/ NEPHROSTOMY
 Hydronephrosis- condition resulting from untreated
   

obstruction in the urinary tract Usually treatable Obstruction of urine can be from tumor, enlarged prostate, kidney stones Stent placement- to hold open Nephrostomy tube may be inserted directly into kidney pelvis to drain UA

TUMORS OF RENAL SYSTEM
 Cancer of bladder – most common

cancer of urinary tract  Twice as common in men  Common age between 50-70 yo
 Correlation

between cigarette smoking/bladder cancer

Chemicals pass between via bloodstream to kidneys

BLADDER CANCER
 S/S
 Painless hematuria  Bladder irritability  Urinary retention (clots)  Pelvic pain

 Pain in lower back
 Painful urination

CANCER OF KIDNEY
 Rare, but serious
 Most patients between 50-70 yo  Risk factors:  Smoking  Obesity  HTN  Years of hemodialysis  Radiation exposure  Asbestos  Industrial pollution

3 CLASSIC SYMPTOMS OF KIDNEY CANCER
 Hematuria
 Flank pain – dull  Mass in area

 Other symptoms:  Weight loss  Fever  Anemia  Fatigue  Swelling in legs

URINARY DIVERSION SURGERIES
 Continent urinary diversion surgeries

pouch – reservoir created from segment of ileum  Ileal conduit  Indiana pouch
 Kock

RENAL DISORDERS
 Diabetic nephropathy  Nephrotic syndrome  Nephrosclerosis

Diabetic Nephropathy
 Most common renal failure
 Long term effects of diabetes  Damage to small vessels in kidneys

 Risk factors include: hypertension,

genetic predisposition, smoking, chronic hyperglycemia  Progression to urine decrease, toxic waste build up leading to kidney failure

Nephrotic Syndrome
 Protein in urine >3.5g/per day
 May result from other disease processes  Large amts. of protein lost in UA  Serum albumin/total serum protein are decreased  Fluids low/leaks into tissues, causing edema  Low sodium diet/low protein diet/diuretics may be

used/*daily wts/I & O

Nephrosclerosis
 Thickening and hardening of the renal

blood vessels  Changes in kidney- result in decreased blood supply to the kidney-can eventually destroy kidney  High pressure within kidney cause damage  Treatment is to reduce HTN

KIDNEY TRANSPLANTATION
 Kidney transplantation has become the

treatment of choice for most patients with ESRD.  Involves transplanting a kidney from a living donor or human cadaver to a patient.  Transplants from well-matched living donors who are related to the patient are slightly more successful than those from cadaver donors.  Success rate increases if transplantation is done before dialysis becomes necessary.

KIDNEY TRANSPLANTATION
 PREOPERATIVE MANAGEMENT:  Donor screening  Patient and donor laboratory tests  Psychological evaluation and counselling  Continuation of renal replacement therapy while awaiting transplantation
 INTRAOPERATIVE MANAGEMENT:  Maintaining stable hemodynamic status for both donor and patient  Monitoring for potential intraoperative complications

KIDNEY TRANSPLANTATION
 POSTOPERATIVE MANAGEMENT  Immediate postoperative monitoring for complications  Monitoring for success of transplantation  Immunosuppressive therapy  Preventing infection  Addressing psychological concerns  Promoting home and community-based care

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