genito-urinary disorders
TRANSCRIPT
Anatomic and Physiologic Overview
• The urinary system comprises the kidneys, ureters, bladder,
and urethra.
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Kidneys • The kidneys are a pair of brownish-red structures located
retroperitoneally
• The kidney consists of two distinct regions, the renal
parenchyma and the renal pelvis.
• The renal parenchyma is divided into the cortex and the
medulla.
• The cortex contains the glomeruli, proximal and distal tubules,
and cortical collecting ducts and their adjacent peritubular
capillaries.
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Kidneys
• The afferent arteriole branches to form the glomerulus, which
is the capillary bed responsible for glomerular filtration.
• Blood leaves the glomerulus through the efferent arteriole and
flows back to the inferior vena cava.
• Each kidney contains about 1 million nephrons, the functional
units of the kidney.
• Each kidney is capable of providing adequate renal function if
the opposite kidney is damaged or becomes nonfunctional.
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Glomerulus • The glomerulus is composed of three filtering layers: the
capillary endothelium, the basement membrane, and the
epithelium.
• The glomerular membrane normally allows filtration of fluid
and small molecules yet limits passage of larger molecules,
such as blood cells and albumin.
• Kidney function begins to decrease at a rate of approximately
1% each year beginning at approximately age 30.
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Urine Formation • Urine is formed in the nephrons through a complex three-step
process: glomerular filtration, tubular reabsorption, and
tubular secretion.
• The various substances normally filtered by the glomerulus,
reabsorbed by the tubules, and excreted in the urine include
sodium, chloride, bicarbonate, potassium, glucose, urea,
creatinine, and uric acid.
• Within the tubule, some of these substances are selectively
reabsorbed into the blood.
• Some substances, such as glucose, are completely reabsorbed in
the tubule and normally do not appear in the urine. 10/17/2013 9
Urine Formation
• Amino acids and glucose are usually filtered at the level of the
glomerulus and reabsorbed so that neither is excreted in the
urine.
• Glucose, however, appears in the urine (glycosuria) if the
amount of glucose in the blood and glomerular filtrate exceeds
the amount that the tubules are able to reabsorb.
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Urine Formation
• Normally, glucose is completely reabsorbed when the blood
glucose level is less than 200 mg/dL (11 mmol/L).
• In diabetes, when the blood glucose level exceeds the kidneys’
reabsorption capacity, glucose appears in the urine.
• Glycosuria is also common in pregnancy.
• Protein molecules are also generally not found in the urine;
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Urine Formation
• however, low-molecular-weight proteins (globulins and
albumin) may periodically be excreted in small amounts.
• Transient proteinuria in amounts less than 150 mg/dL is
considered normal and does not require further evaluation.
• Persistent proteinuria usually signifies damage to the
glomeruli.
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Glomerular filtration:
• The normal blood flow through the kidneys is about 1,200
mL/min.
• As blood flows into the glomerulus from an afferent arteriole,
filtration occurs.
• The filtered fluid, also known as filtrate or ultrafiltrate, then
enters the renal tubules.
• Under normal conditions, about 20% of the blood passing
through the glomeruli is filtered into the nephron, amounting to
about 180 L/day of filtrate. 10/17/2013 14
GFR
• The filtrate normally consists of water, electrolytes, and other
small molecules, because water and small molecules are
allowed to pass, whereas larger molecules stay in the
bloodstream.
• Efficient filtration depends on adequate blood flow maintaining
a consistent pressure through the glomerulus.
• Many factors can alter this blood flow and pressure
– hypotension, decreased oncotic pressure in the blood, and
increased pressure in the renal tubules from an obstruction.
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Tubular reabsorption and tubular secretion
• In tubular reabsorption, a substance moves from the filtrate
back into the peritubular capillaries.
• In tubular secretion, a substance moves from the peritubular
capillaries into tubular filtrate.
• Of the 180 L of filtrate that the kidneys produce each day, 99%
is reabsorbed into the bloodstream, resulting in 1,000 to 1,500
mL of urine each day.
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Cont’d
• Although most reabsorption occurs in the proximal tubule,
reabsorption occurs along the entire tubule.
• Filtrate becomes concentrated under the influence of
antidiuretic hormone (ADH) and becomes urine
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GFR
• The normal adult GFR is about 100 to 120 mL/min .
• Creatinine clearance is an excellent measure of renal function;
as renal function declines, creatinine clearance decreases.
• The average person voids 1,200 to 1,500 mL of urine in 24
hours
• This amount varies depending on fluid intake,
sweating, environmental temperature, vomiting, or
diarrhea.
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Reading assignment
• What are the types of diagnostic tests used to identify
genito-urinary problems?
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Urinary tract infections
• Caused by pathogenic microorganisms in the urinary tract
• UTIs are generally classified as infections involving the upper
or lower urinary tract
• Lower UTIs include bacterial cystitis, bacterial prostatitis
and bacterial urethritis
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Urinary tract infections
• There can be acute or chronic nonbacterial causes of
inflammation in any of these areas that can be misdiagnosed as
bacterial infections.
• Upper UTIs are much less common and include acute or
chronic pyelonephritis, interstitial nephritis, and renal
abscesses.
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Findings on Exam in UTI
• Physical Exam:
– CVA tenderness (pyelonephritis)
– Urethral discharge (urethritis)
– Tender prostate on DRE (prostatitis)
• Labs: Urinalysis
– + leukocyte esterase
– + nitrites
• More likely gram-negative rods
– + WBCs
– + RBCs
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Culture in UTI
• Positive Urine Culture = >105 CFU/mL
• Most common pathogen for cystitis, prostatitis,
pyelonephritis:
– Escherichia coli
– Staphylococcus saprophyticus
– Proteus mirabilis
– Klebsiella
– Enterococcus
• Most common pathogen for urethritis
• Chlamydia trachomatis
• Neisseria Gonorrhea
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Lower Urinary Tract Infection - Cystitis
• Uncomplicated (Simple) cystitis
– In healthy woman, with no signs of systemic disease
• Complicated cystitis
– In men, or woman with comorbid medical problems.
• Recurrent cystitis
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Uncomplicated (simple) Cystitis • Definition
– Healthy adult woman (over age 12)
– Non-pregnant
– No fever, nausea, vomiting, flank pain
• Diagnosis
– Dipstick urinalysis (no culture or lab tests needed)
• Treatment
– Trimethroprim/Sulfamethoxazole for 3 days
– May use fluoroquinolone (ciprofoxacin or levofloxacin)
• Risk factors:
– Sexual intercourse
• May recommend post-coital voiding
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Complicated Cystitis
– Females with comorbid medical conditions
– All male patients
– Indwelling foley catheters
– Urosepsis/hospitalization
• Diagnosis
– Urinalysis, Urine culture
– Further labs, if appropriate.
• Treatment
– Fluoroquinolone (or other broad spectrum antibiotic)
– 7-14 days of treatment (depending on severity)
– May treat even longer (2-4 weeks) in males with UTI
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Recurrent Cystitis
• Want to make sure urine culture and sensitivity obtained.
• May consider urologic work-up to evaluate for anatomical
abnormality.
• Treat for 7-14 days.
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Pyelonephritis • Infection of the kidney
• Associated with constitutional symptoms – fever, nausea, vomiting, headache
• Diagnosis:
• Urinalysis, urine culture, CBC, Chemistry
• Treatment:
• 2-weeks of Trimethroprim/sulfamethoxazole or fluoroquinolone
• Complications:
– Perinephric/Renal abscess:
• Diagnosis: CT with contrast, renal ultrasound
• May need surgical drainage.
– Nephrolithiasis with UTI
• Suspect in patient with severe flank pain
• Need urology consult for treatment of kidney stone
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Prostatitis • Symptoms:
– Pain in the perineum, lower abdomen, testicles, penis, and with ejaculation, bladder irritation, bladder outlet obstruction, and sometimes blood in the semen
• Diagnosis:
– Typical clinical history (fevers, chills, dysuria, malaise, myalgias, pelvic/perineal pain, cloudy urine)
– The finding of an edematous and tender prostate on physical examination
– Will have an increased PSA
– Urinalysis, urine culture
• Treatment:
– Trimethoprim/sulfamethoxazole, fluroquinolone
– 4-6 weeks of treatment
• Risk Factors:
– Trauma , Dehydration
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Urethritis • Chlamydia trachomatis
– Frequently asymptomatic in females, but can present with dysuria, discharge or pelvic inflammatory disease.
– Send UA, Urine culture (if pyuria seen, but no bacteria, suspect Chlamydia)
– Pelvic exam – send discharge from cervical or urethral or for chlamydia PCR
– Chlamydia screening is now recommended for all females ≤ 25 years
– Treatment:
• Azithromycin – 1 g po x 1
• Doxycycline – 100 mg po BID x 7 days
• Neisseria gonorrhoeae
– May present with dysuria, discharge, PID
– Send UA, urine culture
– Pelvic exam – send discharge samples for gram stain, culture
– Treatment:
• Ceftriaxone – 125 mg IM x 1
• Cipro – 500 mg po x 1
• Levofloxacin – 250 mg po x 1
• Ofloxacin – 400 mg po x 1
• Spectinomycin – 2 g IM x 1
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Nephrotic syndrome
Nephrotic syndrome (NS) results from increased permeability of
Glomeulrar basement membrane (GBM) to plasma protein.
It is clinical and laboratory syndrome characterized by massive
proteinuria, which lead to hypoproteinemia ( hypo-
albuminemia), hyperlipidemia and pitting edema.
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Nephrotic Criteria:-
*Massive proteinuria:
3+ or 4+,
*Hypo-proteinemia :
total plasma proteins < 5.5g/dl and serum albumin : < 2.5g/dl.
*Hyperlipidemia:
serum cholesterol : > 5.7mmol/L
*Edema: pitting edema in different degree
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Nephritic Criteria
• -Hematuria: RBC in urine (gross hematuria)
• -Hypertension:
• ≥130/90 mmHg in school-age children
• ≥120/80 mmHg in preschool-age children
• ≥110/70 mmHg in infant and toddler’s children
• -Azotemia（renal insufficiency）:
Increased level of serum BUN 、Cr
• -Hypo-complementemia:
Decreased level of serum c3 10/17/2013 37
Classification:
• Primary Idiopathic NS (INS): majority
The cause is still unclear up to now.
Recent 10 years ,increasing evidence has suggested that INS
may result from a primary disorder of T– cell function.
• Secondary NS:
NS resulted from systemic diseases, such as anaphylactoid purpura
, systemic lupus erythematosus, HBV infection.
• Congenital NS: rare
*1st 3month of life ,only treatment renal transplantation
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Secondary NS • Drug,Toxic,Allegy: mercury, snake venom, vaccine,
pellicillamine, Heroin, gold, NSAID, captopril, probenecid,
volatile hydrocarbons
• Infection: APSGN, HBV, HIV, shunt nephropathy, reflux
nephropathy, leprosy, syphilis, Schistosomiasis, hydatid disease
• Autoimmune or collagen-vascular diseases: SLE,
Hashimoto’s thyroiditis,, HSP, Vasculitis
• Metabolic disease: Diabetes mellitus
• Neoplasma: carcinoma ( renal cell, lung, neuroblastoma,
breast, and etc)
• Genetic Disease: Alport syn, Sickle cell disease, Amyloidosis,
Congenital nephropathy
• Others: Chronic transplant rejection, congenital nephrosclerosis
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Idiopathic NS (INS):
• Minimal Change Nephropathy (MCN): <80%
The glomeruli appear normal basically Under Light microscopy, and Under Immunofluorescence
*under Electron microscopy – fusion of the foot processes of the podocytes
• (2) Non—MCN： ＜20%
*Mesangial proliferative glomerulonephritis
(MsPGN): about 10%
*Focal segmental glomerulosclerosis (FSGS): 5%
*Membranous Nephropathy (MN) : 2%
*Membrane proliferative glomerulonephritis
• (MPGN) : 1%
– *Others： rare,Cresent glomerulonephritis
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Pathogenesis of Proteinuria
• Increase glomerular permeability for proteins due to loss of
negative charged glycoprotein
Degree of protineuria:-
• Mild less than 0.5g/m2/day
• Moderate 0.5 – 2g/m2/day
• Sever more than 2g/m2/day
Type of proteinuria:-
• A-Selective proteinuria: where proteins of low molecular weight
such as albumin, are excreted more readily than protein of HMW
• B-Non selective :
• LMW+HMW are lost in urine
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Pathogenesis of hypoalbuminemia
*Due to hyperproteinuria----- Loss of plasma protein in urine
mainly the albumin.
*Increased catabolism of protein during acute phase.
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Pathogenesis of hyperlipidemia
*Response to Hypoalbuminemia → reflex to liver --→ synthesis of
generalize protein ( including lipoprotein ) and lipid in the
liver ,the lipoprotein high molecular weight no loss in urine →
hyperlipidemia
*Diminished catabolism of lipoprotein
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Pathogenesis of edema
• *Reduction plasma colloid osmotic pressure↓ secondary to
hypoalbuminemia Edema and hypovolemia
• *Intravascular volume↓ antidiuretic hormone (ADH ) and
aldosterone(ALD) water and sodium retention Edema
• *Intravascular volume↓ glomerular filtration rate
(GFR)↓ water and sodium retention Edema
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How many pathological types causes nephrotic syndrome?
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Clinical Manifestation 1.Main manifestations:
Edema (varying degrees) is the common symptom
Local edema: edema in face , around eyes( Periorbital
swelling) , in lower extremities.
Generalized edema (anasarca), edema in penis and scrotum.
2-Non-specific symptoms:
Fatigue and lethargy
loss of appetite, nausea and vomiting ,abdominal pain ,
diarrhea
body weight increase, urine output decrease
pleural effusion (respiratory distress)
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Investigations
1-Urine analysis:-
A-Proteinuria : 3-4 + SELECTIVE.
b-24 urine collection for protein
>40mg/m2/hr for children
c- volume: oliguria (during stage of edema formation)
d-Microscopically:-
microscopic hematuria 20%, large number of hyaline cast
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Investigations .. . ..
2-Blood: • A-serum protein: decrease >5.5gm/dL , Albumin levels are low (＜
2.5gm/dL). • B-Serum cholesterol and triglycerides:
Cholesterol ＞5.7mmol/L (220mg/dl).
• C-- ESR↑＞100mm/hr during activity phase
3. Renal function
• .
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Kidney Biopsy:-
• Considered in:
• 1-Secondary N.S
• 2-Frequent relapsing N.S
• 3-Steroid resistant N.S
• 4- Hematuria
• 5-Hypertension
• 6- Low GFR
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Differential Diagnosis of NS:
D.D of generalized edema:-
1-Protein –losing enteropathy
2-Hepatic Failure.
3-HF
4-Protein energy malnutrition
5-Acute and chronic GN
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Complications of NS
1-Infections:
Nephrotic pt are liable to infection because :
A-loss of immunoglobins in urine.
B-the edema fluid act as a culture medium.
C-use immunosuppressive agents.
D- malnutrition
The common infection : URI, peritonitis, cellulitis and UTI
Organisms: encapsulated (Pneumococci, H.influenzae), Gram
negative (e.g E.coli)
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Complication….. 2-Hypercoagulability (Thrombosis)
• Hypercoagulability of the blood leading to venous or arterial
thrombosis:
• Hypercoagulability in Nephrotic syndrome caused by:
– 1-Higher concentration of I,II, V,VII,VIII,X and
fibrinogen
– 2- Lower level of anticoagulant substance:
antithrombin III
– 3-decrease fibrinolysis.
– 4-Higher blood viscosity
– 5- Increased platelet aggregation
– 6- Overaggressive diuresis
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Complication…..
3-ARF: pre-renal and renal
4- cardiovascular disease :-Hyperlipidemia, may be a risk
factor for cardiovascular disease.
5-Hypovolemic shock
6-Others: growth retardation, malnutrition, . …
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Management of NS: • General (non-specific )
• *Corticosteroid therapy
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General therapy
• Hospitalization:- for initial work-up and evaluation of treatment.
• Activity: usually no restriction , except massive edema,
sever hypertension and infection.
• Diet
Hypertension and edema: Low salt diet (<2gNa/ day) only
during period of edema or salt-free diet.
Severe edema: Restricting fluid intake
• Avoiding infection: very important.
• Diuresis: Hydrochlorothiazide (HCT) ：2mg/kg.d
• Antisterone ： 2～4mg/kg.d
• Dextran ： 10～15ml/kg , after 30～60m,
• followed by Furosemide (Lasix) at 2mg/kg .
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Corticosteroid—prednisone therapy • Prednisone tablets at a dose of 60 mg/day (maximum daily dose,
80 mg divided into 2-3 doses) for at least 4 consecutive weeks.
• After complete absence of proteinuria, prednisone dose should be
tapered to 40 mg/day given every other day as a single morning
dose.
• The alternate-day dose is then slowly tapered and discontinued
over the next 2-3 months.
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Treatment of relapse in NS:
• Many children with nephrotic syndrome will experience at least 1
relapse (3-4+proteinuria plus edema).
• daily divided-dose prednisone at the doses noted earlier (where he
has the relapse) until the child enters remission (urine trace or
negative for protein for 3 consecutive days).
• The pred-nisone dose is then changed to alternate-day dosing and
tapered over 1-2 mo.
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According to response to prednisone therapy:
*Remission: no edema, urine is protein free for 5 consecutive
days.
* Relapse: edema, or first morning urine sample contains > 2 +
protein for 7 consecutive days.
*Frequent relapsing: > 2 relapses within 6 months (> 4/year).
*Steroid resistant: failure to achieve remission with prednisolone
given daily for 28 days.
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Side Effects With Long Term Use of Steroids
“Steroid toxicity”
• hyperglycemia
• myopathy
• peptic ulcer
• poor healing of wound.
• Hirsutism
• Thromboembolism
-Stunted growth
Cataracts
- Pseudotumor cerebri
-Psycosis
-Osteoporosis
- Cushingoid features
-Adrenal gland suppression
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Alternative agent
• When can be used:
• Steroid-dependent patients, frequent relapsers, and steroid-
resistant patients.
– Cyclophosphamide Pulse steroids
– Cyclosporin A
– Tacrolimus
– Microphenolate
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Renal Failure
Acute and Chronic
Acute Renal Failure
• Sudden interruption of kidney function resulting from
obstruction, reduced circulation, or disease of the renal tissue
• Results in retention of toxins, fluids, and end products of
metabolism
• Usually reversible with medical treatment
• May progress to end stage renal disease, uremic syndrome, and
death without treatment
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Acute Renal Failure
• Persons at Risks
– Major surgery
– Major trauma
– Receiving nephrotoxic medications
– Elderly
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Acute Renal Failure
• Causes
– Prerenal • Hypovolemia, shock, blood loss, embolism, pooling of fluid d/t
ascites or burns, cardiovascular disorders, sepsis
– Intrarenal • Nephrotoxic agents, infections, ischemia and blockages, polycystic
kidney disease
– Postrenal • Stones, blood clots, BPH, urethral edema from invasive procedures
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Acute Renal Failure • Stages
– Onset – 1-3 days with ^ BUN and creatinine and possible
decreased UOP
– Oliguric – UOP < 400/d, ^BUN, Phos, K, may last up to 14 d
– Diuretic – UOP ^ to as much as 4000 mL/d but no waste
products, at end of this stage may begin to see improvement
– Recovery – things go back to normal or may remain
insufficient and become chronic
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Acute Renal Failure
• Subjective symptoms
– Nausea
– Loss of appetite
– Headache
– Lethargy
– Tingling in extremities
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Acute Renal Failure
• Objective symptoms
– Oliguric phase –
• vomiting
• disorientation,
• edema,
• ^K+
• decrease Na
• ^ BUN and creatinine
• Acidosis
• uremic breath (fishy odor)
• CHF and pulmonary
edema
• hypertension
• sudden drop in UOP
• convulsions, coma
• changes in bowels
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Acute Renal Failure
• Objective symptoms
– Diuretic phase
• Increased UOP
• Gradual decline in BUN and creatinine
• Hypokalemia
• Hyponaturmia
• Tachycardia
• Improved LOC
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Acute Renal Failure
• Diagnostic tests
– H&P
– BUN, creatinine, sodium, potassium. pH, bicarb. Hgb and Hct
– Urine studies
– US of kidneys
– ABD and renal CT/MRI
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Acute Renal Failure
• Medical treatment
– Fluid and dietary restrictions ( e.g. k+)
– Maintain E-lytes
– D/C or change cause
– May need dialysis to jump start renal function
– May need to stimulate production of urine with IV fluids,
Dopomine, diuretics, etc.
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Acute Renal Failure
• Medical treatment
– Hemodialysis
– Peritoneal dialysis
– Continous renal replacement therapy (CRRT)
• Can be done continuously
• Does not require dialysate
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Acute Renal Failure
• Nursing interventions
– Monitor I/O, including all body fluids
– Monitor lab results
– Watch hyperkalemia symptoms: malaise, anorexia, parenthesia, or muscle weakness, EKG changes
– watch for hyperglycemia or hypoglycemia if receiving TPN or insulin infusions
– Maintain nutrition
– Safety measures
– Mouth care
– Daily weights
– Assess for signs of heart
failure
– Skin integrity problems
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Chronic Renal Failure
• Results form gradual, progressive loss of renal function
• Occasionally results from rapid progression of acute renal
failure
• Symptoms occur when 75% of function is lost but considered
chronic if 90-95% loss of function
• Dialysis is necessary D/T accumulation or uremic toxins,
which produce changes in major organs
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Chronic Renal Failure • Subjective symptoms are relatively same as acute
• Objective symptoms
– Renal
• Hyponaturmia
• Dry mouth
• Poor skin turgor
• Confusion, salt overload, accumulation of K with muscle weakness
• Fluid overload and metabolic acidosis
• Proteinuria, glycosuria
• Urine = RBC’s, WBC’s, and casts
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Chronic Renal Failure
• Objective symptoms
– Cardiovascular
• Hypertension
• Arrythmias
• Pericardial effusion
• CHF
• Peripheral edema
– Neurological
• Burning, pain, and
itching, parestnesia
• Motor nerve
dysfunction
• Muscle cramping
• Shortened memory
span
• Apathy
• Drowsy, confused,
seizures, coma, EEG
changes
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Chronic Renal Failure
• Objective symptoms
– GI
• Stomatitis
• Ulcers
• Pancreatitis
• Uremic fetor
• Vomiting
• consitpation
– Respiratory
• ^ chance of infection
• Pulmonary edema
• Pleural friction rub
and effusion
• Dyspnea
• Kussmaul’s
respirations from
acidosis
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Chronic Renal Failure
• Objective symptoms
– Endocrine
• Stunted growth in
children
• Amenorrhea
• Male impotence
• ^ aldosterone
secretion
• Impaired glucose
levels R/T impaired
CHO metabolism
• Thyroid and
parathyroid
abnormalities
– Hemopoietic
• Anemia
• Decrease in RBC
survival time
• Blood loss from
dialysis and GI bleed
• Platelet deficits
• Bleeding and clotting
disorders – purpura
and hemorrhage from
body orifices ,
ecchymoses
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Chronic Renal Failure
• Objective symptoms
– Skeletal
• Muscle and bone pain
• Bone
demineralization
• Pathological fractures
• Blood vessel
calcifications in
myocardium, joints,
eyes, and brain
– Skin
• Yellow-bronze skin
with pallor
• Puritus
• Purpura
• Uremic frost
• Thin, brittle nails
• Dry, brittle hair, and
may have color
changes and alopecia
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Chronic Renal Failure
• Lab findings
– BUN – indicator of GFR and is affected by the breakdown
of protein. Normal is 10-20mg/dL. When reaches 70 =
dialysis
– Serum creatinine – waste product of skeletal muscle
breakdown and is a better indicator of kidney function.
Normal is 0.5-1.5 mg/dL. When reaches 10 x normal, it is
time for dialysis
– Creatinine clearance is best determent of kidney function.
– Must be a 12-24 hour urine collection. Normal is > 100 ml/min 10/17/2013 80
Chronic Renal Failure
• K+ -
– The kidneys are means which K+ is excreted.
– Normal is 3.5-5.0 ,mEq/L. maintains muscle contraction
and is essential for cardiac function.
– Both elevated and decreased can cause problems with
cardiac rhythm
– Hyperkalemia is treated with IV glucose and Na Bicarb
which pushes K+ back into the cell
– Kayexalate is also used 10/17/2013 81
Chronic Renal Failure
• Ca
– With disease in the kidney, the enzyme for utilization of Vit
D is absent
– Ca absorption depends upon Vit D
– Body moves Ca out of the bone to compensate and with
that Ca comes phosphate bound to it.
– Normal Ca level is 4.5-5.5 mEq/L
– Hypocalcemia = tetany
• Treat with calcium with Vit D and phosphate
• Avoid antacids with magnesium
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Chronic Renal Failure
• Other abnormal findings
– Metabolic acidosis
– Fluid imbalance
– Insulin resistance
– Anemia
– Immunoligical problems
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Chronic Renal Failure
Medical treatment
• IV glucose and insulin
• Na bicarb, Ca, Vit D, phosphate binders
• Fluid restriction, diuretics
• Iron supplements, blood, erythropoietin
• High carbs, low protein
• Dialysis - After all other methods have failed
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Chronic Renal Failure
• Hemodialysis
– Vascular access
• Temporary – subclavian or femoral
• Permanent – shunt, in arm
– Care post insertion
– Can be done rapidly
– Takes about 1 to 4 hours
– Done 3 x a week
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Chronic Renal Failure
• Peritoneal dialysis
– Semipermeable membrane
– Catheter inserted through abdominal wall into peritoneal cavity
– Cost less
– Fewer restrictions
– Can be done at home
– Risk of peritonitis
– 3 phases – inflow, dwell and outflow
• Automated peritoneal
dialysis
– Done at home at night
– Maybe 6-7 times /week
• CAPD
– Continous ambulatory
peritoneal dialysis
– Done as outpatient
– Usually 4 X/d
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Chronic Renal Failure
• Nursing care
– Frequent monitoring
– Hydration and output
– Cardiovascular function
– Respiratory status
– E-lytes
– Nutrition
– Mental status
– Emotional well being
– Ensure proper
medication regimen
– Skin care
– Bleeding problems
– Care of the shunt
– Education to client and
family
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Chronic Renal Failure
• Nursing diagnosis
– Excess fluid volume
– Imbalanced nutrition
– Ineffective coping
– Risk for infection
– Risk for injury
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Chronic Renal Failure
• Transplant
– Must find donor
– Waiting period long
– Good survival rate – 1 year 95-97%
– Must take immunosuppressant’s for life
– Rejection
• Watch for fever, elevated B/P, and pain over site of new
kidney
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Chronic Renal Failure
• Post op care
– ICU
– I/O
– B/P
– Weight changes
– Electrolytes
– May have fluid volume deficit
– High risk for infection
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Renal Calculi (Kidney Stones)
• Made of crystals of calcium phosphate and uric acid
• Gradually they get larger until they block ureters
• First sym severe pain
• Other sym nausea and vomiting, frequency, chills, fever, hematuria
• Diagnosis by symptoms, ultrasound, or x-ray
• Rx –increase fluids to flush out stone, medications, and if needed LITHOTRIPSY
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Renal Calculi
• Called nephrolithiasis or urolithiasis
• Most commonly develop in the renal pelvis but can be anywhere
in the urinary tract
• Vary in size –from very large to tiny
• Can be 1 stone or many stones
• May stay in kidney or travel into the ureter
• Can damage the urinary tract
• May cause hydronephrosis
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Renal Calculi • Predisposing factors
– Dehydration
– Prolonged immobilization
– Infection
– Obstruction
– Anything which causes the urine to be alkaline
– Metabolic factors
• Excessive intake of calcium, calcium based antacids or Vit D
• Hyperthyroidism
• Elevated uric acid
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Renal Calculi
• Subjective symptoms
– Sever pain in the flank area, suprapubic area, pelvis or
external genitalia
– If in ureter, may have spasms called “renal colic”
– Urgency, frequency of urination
– N/V
– Chills
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Renal Calculi
• Objective symptoms
– Increased temperature
– Pallor
– Hematuria
– Abdominal distention
– Pyuria
– Anuria
– May have UTI on urinalysis
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Renal Calculi- Manifestations
• Kidney/Pelvis
– May be asymptomatic
– Dull, aching flank pain
• Ureter
– Acute severe flank pain, may radiate
– Nausea/vomiting
– Pallor
– Hematuria
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Renal Calculi- Manifestations
• Bladder
– May be asymptomatic
– Dull suprapubic pain
– Hematuria
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Renal Calculi
• Diagnostic procedures
– Urinalysis
– 24 hour urine
– Renal CT
– Kidney ultrasound
– Cystoscopy with retrograde pyleogram
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Renal Calculi • Treatment
– Most are passed without intervention
– May need cysto with basket retrieval
– Lithotripsy : Extracorporeal shock wave lithotripsy (ESWL)
is the non-invasive treatment of kidney stones (urinary
calculosis) and biliary calculi (stones in the gallbladder or in the
liver) using an acoustic pulse.
– Lasertripsy :
– Lithotomy: is a surgical method for removal of calculi, stones
formed inside certain hollow organs, such as the bladder and
kidneys (urinary calculus) and gallbladder (gallstones), that
cannot exit naturally through the urethra, ureter or biliary duct
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Renal Calculi
• Nursing interventions
– Primary is to treat pain – usually with opioids
– Ambulate
– Force fluids, may have IV
• Watch for fluid overload
– Strain urine – send stone to lab if passed
– Accurate I/O
– Medicate N/V
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Renal Calculi
• Surgical removal
– Routine pre and post op care
– May return with catheter, drains, nephrostomy tube and
ureteral stent – must maintain patency and may need to
irrigate as ordered
– Measure drainage from all tubes – need at least 30 cc/hr
– Watch site for bleeding
– May need frequent dressing changes due to fluid leakage,
or may have collection bag
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Renal Calculi
• Discharge and prevention
– Continue to force fluids post discharge
– May need special diet
• Stones are analyzed for calcium or other minerals
• May need to watch products with calcium
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Lithostripsy
• Surgical procedure to remove kidney stones
• Shock waves hit dense stones and break them up
• Done on outpatient basis
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