Download PANRE/PANCE GU Review Craig Ensign, MPAS, PA-C

PANRE/PANCE GU Review
Craig Ensign, MPAS, PA-C
BPH
Incidence:
• The most common benign tumor in men
• 50% of men over 75 years of age are symptomatic
Irritative Symptoms
• Urgency
• Frequency
• Nocturia
Obstructive Symptoms
• Slow stream
• Hesitancy
• Intermittency
• retention
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Proliferative growth generally in transition zone
Size does not correlate directly with symptoms
Progression of symptoms is not inevitable
7-10% may develop retention
50% marked improvement over time
Differential Diagnoses
• Stricture
• UTI
• Balder Stone
• Bladder tumor
• Prostate cancer
• Neurogenic bladder
• Overactive bladder
Medical Treatment
• PDE5 Inhibitors
-Cialis
• Alfa Blockers
•
-Tamsulosin
• 5 ARI
-Proscar
• Phyto Therapy
-Saw Palmetto
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Surgical Treatment
TURP
TURMT
Laser ablation
TUIP
Open prostatectomy
Electrovaporization
Erectile Dysfunction
ED: Definition & Incidence
The inability to achieve an erection sufficient
for satisfactory sexual function
Men who Meet Definition
100%
50%
40%
50%
60%
70%
0%
40 Years
50 Years
60 Years
70 Years
Work Up/Treatment
Signs &
Symptoms
Laboratory
Findings
Treatment
History
• Severity of problem
maintain vs attain
• Comorbidities
Lipids, HTN, DM, CKD
• Hx of trauma
• Medications (25%)
BP, BPH, ED, alcohol
ED: Work Up/Treatment
Signs &
Symptoms
Laboratory
Findings
Treatment
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CBC
Fasting lipid profile
Glucose
Testosterone
Prolactin
FSH & LH if abnormal
to distinguish pituitary
vs testicular cause
ED: Work Up/Treatment
Signs &
Symptoms
Laboratory
Findings
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Treatment
PDE5 Inhibitors
Sildenifil (Viagra)
Vardenafil (Levitra)
Tadalifil (Cialis)
Requires sexual
stimulation
Potentiate rather than
trigger response
ED: Work Up/Treatment
Signs &
Symptoms
Laboratory
Findings
Treatment
Other Options
• Injections
Caverject (alprostadil)
PPP (papaverine, prostaglandin, phentolomine)
• Vacuum devise
• Surgery
IPP
Vascular
Cryptorchidism
Cryptorchidism
• Failure of one or both testicles to migrate into scrotum
• 3% term babies, 30% of preterm babies
• 33% spontaneously descent in first four months
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Complications
Sub fertility
Testicular carcinoma
Contralateral risk 10%
Risk does not decrease
with orchiopexy
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Treatment
Orchiopexy
Surgical removal
Surgical treatment best
at 6 months of age
Fertility best preserved early
No treatment for retractile
testis
Hydrocele
• Painless fluid accumulation around testicle
• 10% children congenital, 80% resolve spontaneously
• 10% of men > 40, does not resolve spontaneously
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Risk Factors
Injury
Infection/STI
Radiation to pelvis
Congenital
Not cancer or pre cancer
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Diagnosis & Treatment
History—injury/onset
Physical exam:
R/O tumor, infection,
hernia, spermatocele
Transillumination
Surgery/observation
Scrotal Transillumination
Moderate Hydrocele
Varicocele
Varicocele
• Dilation of the pampiniform plexus,
“Bag of Worms”
• Varicose veins in the scrotum
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Incidence
Found in 15% healthy males
Found in 40% subfertal males
Rare in prepubescence boys
Surgically correctable infertility
Will not resolve spontaneously
Most occur on left side
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Problems
Ipsilateral atrophy
Poor sperm motility
Generally not
painful but can be
Infertility
Grading
• Sub-clinical
• Grade I: Palpable only
with valsalva
• Grade II: Palpable without valsalva
• Grade III: Visible upon
inspection
Treatment Options
• No treatment
• Surgical repair under general anesthesia
• Embolization performed by interventional
radiologist
Incontinence
Detrusor Overactivity (OAB)
• Symptoms of urgency, frequency and nocturia
with or without leakage
• Common in men and women
• Cause not well understood
• May be exacerbated by BPH, inflammation,
DM, stress and anxiety
Medical/Behavior Treatment
• Medications (Anticholinergics):
Oxybutynin (Ditropan, Gelnique)
Talterodine (Detrol LA)
Darifenacin (Enablex)
Trospium (Sanctura)
Fesoterodine (Toviaz)
Solifenacin (Vesicare)
• Eliminate exacerbating factors
• Bladder retraining
Urethral Incompetence (Stress)
• Pregnancies increase risk
• Result of weakened pelvic floor and poor
support of vesicourethral sphincter
• Leakage with chronic or sudden increase in
abdominal pressure—cough, sneeze, jumping,
running
• Rare in men, RRP is risk factor
Treatment
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Surgical: sling, AP repair
Injectable bulking agent: collagen
Pelvic floor exercises
Medications usually not effective
Urolithiasis
Remember Kramer’s Stone?
Stone Types
Uric Acid 5%
Struvite & 0thers 5%
Calcium 90%
Work-up
• History
– Previous, family hx, onset, duration, N/V, fever
– 3:1 male to female ratio
– 50% recurrence rate in the next 5 years
• Physical Exam
– Movement, CVAT, other pain location
• Imaging
– Non contrast CT
Treatment
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Pain management, let stone pass
Alpha blockers—evidence does not support
Copious fluid intake
Alkalinization—for uric acid stones
Surgery
– ESWL, basket retrieval, PCNL, open resection
Phimosis & Paraphimosis
Phimosis
• Foreskin cannot retract over glans
• May be congenital or develop as result of
chronic infection and poor hygiene
• Balanitis may lead to phimosis—eveluate for
diabetes mellitus
• Phimosis in children almost always
physiological
Phimosis in a Child
Balanitis in Adult
Paraphimosis
• Retracted foreskin cannot be replaced over
the glans
• Almost always iatrogenic cause
• Can almost always be reduced at bedside
• Rarely is surgery indicated—circumcision
Forgot to Replace Foreskin
Testicular Torsion
Definition
Testicular torsion is
the twisting of a
testis on its
spermatic cord so
that the blood
supply is blocked
Epidemiology
• Most common between puberty and 25 years
of age
• Occurs due to malformation of the tunica
vaginalis
• Generally occurs during sleep
• Testicle will die within six to eight hours if not
resolved
Evaluation & Treatment
• Signs and Symptoms
– Acute onset of severe testicular pain and swelling
– May be accompanied by nausea and vomiting
– Generally not associated with trauma, usually
occurs during sleep
• Treatment
– Medical emergency—loss of testicle with delay
– Requires bilateral surgical repair
Infections/Inflammatory
Conditions
Common Organisms:
Applies to All GU Infections
• Gram Negative—most common
– Escherichia Coli
– Klebsiella
– Enterobacter
– Proteus
• Gram Positive—less common
– Enterococcus Faecalis
– Staphylococcus aureus
75-90%
6-12%
2-12%
4-6%
Pathogenesis:
Applies to All GU Infections
Four possible modes of infection:
1. Periurethral migration of bacteria
2. Hematogenous spread in immunecompromised patients
3. Direct contamination from fistulas
4. Theoretically, urine can be contaminated
through the lymphatic system
Cystitis
Epidemiology
Incidence (%)
Age
<1
Female
0.7
Male
2.7
1-5
6-15
4.5
4.5
0.5
0.5
16-35
36-65
>65
20
35
40
0.5
20
35
Risk Factors
Foreskin, anatomic GU
abnormality
Anatomic GU abnormality
Functional GU
abnormality
Intercourse, diaphragm
Surgery, BPH, catheters
Surgery, BPH, catheters
Symptoms
• Symptoms
– Dysuria
– Urgency/Frequency
– Suprapubic pain
– Hematuria
• Signs
– Suprapubic tenderness
– UA—nitrites, leukocytes, hemoglobin
Treatment Options
• Nitrofurantoin (Macrobid)
– 100 mg bid X 7 days (no change in resistance)
• Fluroquinolones
– Cipro 500 mg bid X 1-3
• TMP/SMX (Septra, Bactrim)
– DS bid X 1-3 days (increasing resistance)
Epididymitis
Orchitis
Clinical Presentation
• Bacterial infection, E. Coli or STI
• Scrotal enlargement and induration
• Voiding symptoms: dysuria, urgency,
frequency
• Fever, nausea and vomiting may be present
• Prehn’s sign—pain resolves when scrotum is
elevated above pubic bone
Treatment
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Bed rest
Scrotal elevation and ice
Antibiotic treatment similar to UTI
Treat for gonorrhea or chlamydia as indicated
Scrotal US if any concern for torsion
Prostatitis
Prostatitis: Types
• Acute/bacterial prostatitis
• Chronic prostatitis/non-bacterial prostatitis
• CPPS/CP—should be at top of differential
Acute/Bacterial
• Irritative voiding symptoms
• Perineal or suprapubic discomfort, often dull
and poorly localized
• Fever
• May have positive urine culture
• Pathogen similar to UTI
• Do not do prostate massage—sepsis risk
• DRE elicits chandelier response
Chandelier Response
Treatment
• 4-6 week course of antibiotics is indicated for
initial treatment—longer regiments are sometimes necessary
• Cipro 500 mg bid x 30-45 days
• Septra DS bid x 30-45 days
• CPPS/CP—identify exacerbating factors, pain
clinic
Pyelonephritis
Pyelonephritis
• Inflammation of the kidney and renal pelvis,
diagnosis is usually made clinically
• UTI symptoms with fever, chills, flank pain
• 20-30% of all sepsis originates with urinary
tract infection
Lab/Imaging
• CBC shows leukocytosis and a left shift
• Urine culture grows out offending pathogen—
always get culture
• Upper tract imaging shows evidence of
pyelonephritis and can rule in or out
obstructive complicating factors
Treatment
• Most can be treated outpatient
• Complications may require hospitalization:
stones, immune compromised patient, sepsis
• Urine and/or blood culture is essential
• Same antibiotic treatment as cystitis, may
treat initially IV, adjust based on culture
• Prognosis in healthy individuals is very good
with prompt diagnosis and treatment
Urethritis
Signs & Symptoms
• Urethritis usually STI
• In both men and women, dysuria, urgency and
frequency
• Discharge is often yellowish green with
gonorrhea
• Clear with chlamydia
• In women, discharge is less common
Treatment
• Empiric treatment is initiated based on
clinical presentation
• Ceftriaxone (Rocephin) 250 mg IM/Gonorrhea
• Azithromycin (Zithromax) 1 g single dose/
Chlamydia
• If STI is not likely, treatment similar to UTI is
appropriate
Bladder Cancer
Bladder Cancer
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Second most common cancer of the GU tract
Lower incidence in African Americans
75% confined to bladder
TCC 91%; Squamous 7%; Adenocarcinoma 2%
Risk factors smoking, chemical exposure, age >
35, chronic Foley use, history of GU surgery
Clinical Findings
S&S
• Hematuria—90%
present with micro
or gross hematuria
• LUTS—including
urgency, frequency,
dysuria, bladder
pain
Treatment
• TURBT, BCG,
cystectomy, radiation,
chemo
• Follow up—important
due to high rate or
recurrence
Prostate Carcinoma
Prostate Carcinoma
• Most common cancer in men
• 230,000 new cases per year
• Second leading cause of cancer death, but
mortality rates declining since 1990’s
• 95% adenocarcinoma
• 4% Transitional Cell Carcinoma
• 1% Neuroendocrine Carcinoma or Sarcoma
PSA
• Produced by benign and cancerous prostate
tissue
• Only a screening tool, used in connection with
DRE and TRUS/BX
• Not specific to cancer—increased with:
– BPH, retention
– Urethral instrumentation
– Infection
– Stars lining up just right
Signs & Symptoms
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Usually asymptomatic
DRE—nodule or induration, may be normal
Metastatic disease—bone pain
Cord compression
– Paresthesia, weakness, incontinence
• Definitive diagnosis with TRUS/BX
• PSA: > 4.0 Caucasian > 2.5 African American
Treatment
• Watchful waiting
• Radical prostatectomy
• Brachy therapy (radioactive seed
implantation)
• External beam radiation
Renal Cell Carcinoma
Etiology
• The cause of RCC is unknown
• Risk factors:
– Smoking: two times as likely to develop RCC
– Industrial exposure to asbestos, solvents and
cadmium (batteries)
– Hereditary factors: Von Hippel-Lindau disease
– Dialysis: especially in presence of cystic kidney
– Renal transplant
Clinical Findings/Treatment
• Triad of gross hematuria, flank pain and
palpable mass—only 7-10% at diagnosis
• Dyspnea, cough and/or bone pain implies
metastases
• Incidentally found on CT in >50% of patients
• Treatment: partial or total nephrectomy
Testicular Tumor
Types of Tumors
• Two general Divisions
• Non-germ Cell—5% of all testicular tumors
• Germ Cell—95% of all testicular tumors
– Seminoma (40%)
– Non-seminoma germ cell tumor (NSGCT)
Clinical Presentation
Symptoms
• Painless enlargement of testicle—pain is
present in 10% of patients
• Sensation of heaviness in testicle
• 10% of patients present with symptoms
related to mets: back pain, cough, dyspnea,
anorexia, bone pain, edema, gynecomastia
Clinical Presentation
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Signs
Testicular mass or enlargement
Tumors do not transilluminate
Lymphadenopathy: subclavicular or inguinal
Gynecomastia
Hemoptysis in advanced pulmonary disease
Tumor markers: HCG, AFP
Treatment
• Radical orchiectomy
• Pathology: tumor type and staging
– CXR, CT for staging
• Treatment based on tumor type and staging
– Further debulking surgery
– RPLND
– Chemotherapy
– Radiation
Renal Disease
Acid/Base Disorders
Sample ABG Question
A wheezing 14-year-old female with cystic
fibrosis complains of a productive cough and
shortness of breath. The following labs are
available:
pH:
pCO2:
HCO3:
7.30
50 mm Hg
24 mEq/L
The Question
What is the first step in treating this patient?
A.
B.
C.
D.
Decrease respirations to increase CO2
Alkalinize the blood to counter the acidosis
Treat the obstructed airway
Start broad spectrum antibiotics
Rule 1: pH Determines the Problem—
Acidemia vs Alkalemia
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Look at the pH
Normal arterial pH is between 7.35 and 7.45
pH > 7.45 = alkalemia
pH < 7.35 = acidemia
Rule 2: HCO3 and PaCO2 Determine
the cause of the problem
• Normal Values:
– HCO3
– PaCO2
22-26 mEq/L
35-45 mm Hg
• If HCO3 goes the direction of pH, metabolic
• If PaCO2 goes opposite to pH, respiratory
Blood Gas Scenarios
pH=7.21
PaCO2=40
HCO3=15.6
Rule 3: Mixed Conditions can Occur
• When PaCO2 and HCO3 shift in opposite
directions, they can both be responsible
• Examples:
– pH=7.21
– pH=7.51
PaCO2=51
PaCO2=31
HCO3=18
HCO3=29
Rule 4: Chronic Problems can be
Compensated
• Acute problems follow the rules
• Problems can compensate—PaCO2 and HCO3
are on the same side
• The offending problem is still identified by the
rules
– pH=7.35
PaCO2=51
HCO3=27
Rule 5: Respiratory Compensates
Faster than Metabolic
• PaCO2 is regulated by adjusting the
respiratory rate—adjusts within seconds to
minutes
• Renal adjustment (HCO3) may take hours to
days to adjust
Rule 6: Treat the respiratory or
metabolic problem
ABG questions on this test will cause me to drool,
Because I know the basics—I can follow these rules
When the pH is high there will be alkalosis,
But a lower pH indicates acidosis
Metabolic problems are easy for me,
Since bicarbonate follows pH, you see
But if respiration is the one to blame,
Carbon dioxide and pH are apposed, not the same
Don’t forget, on occasion, mixed problems reside,
When carbon dioxide and bicarbonate take opposite sides
Be aware acute problems will follow these rules,
But a compensated condition can leave me fooled
Remember respirations will compensate quickly,
But kidneys are slow and can leave one quite sickly
Now when that gas question appears on my test,
There is one more rule, I know all the rest
Labs only show me the pH position,
While treatment addresses the primary condition
Metabolic Acidosis
• Increased anion gap acidosis
– Lactic acidosis
– Diabetic, alcoholic ketoacidosis
• Normal anion gap acidosis
– Gastrointestinal HCO3 loss
– Renal tubular acidosis (RTA)
Metabolic Alkalosis
• Saline-responsive
– Contraction alkalosis
– Posthypercapnia alkalosis
• Saline-unresponsive
– Hyperaldosteronism
– Alkali administration with decreased GFR
Respiratory Acidosis
• Hypoventilation and subsequent hypercapnia
• Respiratory failure
• Chronic respiratory acidosis in patients with
underlying lung disease
• Renal compensation to excrete more acid and
generate more HCO3 takes days
Respiratory Alkalosis
• Hyperventilation reduces PaCO2 and increases
pH
• High altitude, hypotension
• Anxiety, infection, trauma, tumor, aspirin
• Interstitial lung disease, pneumonia, PE
Sample ABG Question
A wheezing 14-year-old girl with cystic fibrosis
complains of a productive cough and shortness
of breath. The following labs are available:
pH:
pCO2:
HCO3:
7.30
50 mm Hg
24 meq/liter
The Question
What is the first step in treating this patient?
A.
B.
C.
D.
Decrease respirations to increase CO2
Alkalinize the blood to counter the acidosis
Treat the obstructed airway
Start broad spectrum antibiotics
Fluid & Electrolyte Disorders
Fluid & Electrolyte Disorders
Work Up
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History
Physical Exam
Serum electrolyte concentration
Urine electrolyte concentration
Serum osmolality
Hyponatremia
• Defined as < 135 mEq/L
• Most common electrolyte abnormality
• Mismanagement can result in neurologic
catastrophe
• Iatrogenic complications may be more harmful
than hyponatremia itself
• Most cases of hyponatremia reflect water
imbalance
Hyponatremia
Serum Osmolality
Normal
280-295 mosm/kg
Low
<280 mosm/KG
High
>295 mosm/kg
Isotonic
Hyponatremia
1. Hyperproteinemia
2. Hyperlipidemia
Hypotonic
Hyponatremia
Hypertonic
Hyponatremia
1. Hyperglycemia
2. Mannitol, sorbitoll
3. Radiocontrast
agents
Hypotonic
Hyponatremia
Volume Status
Hypovolemic
Extrarenal Salt loss
1. Dehydration
2. Diarrhea
3. Vomiting
Renal Salt Loss
1. Diuretics
2. ACE inhibitors
3. Nephropathies
4. Mineralocorticoid deficiency
5. Cerebral sodium-wasting
syndrome
Hypotonic
Hyponatremia
Volume Status
Euvolemic
1. SIADH
2. Hypothyroidism
3. Psychogenic polydipsia
4. Beer potomania
5. Idiosyncratic drug reaction
6. Endurance exercise
7. Adrenocorticotropin deficiency
Hypervolemic
Edematous states
1. CHF
2. Liver disease
3. Nephrotic syndrome
4. Advanced kidney
disease
Hypernatremia
• Sodium concentration > 145 mEq/L
• Hypernatremia is almost always secondary to
free water loss—dehydration
• Rarely due to excess sodium intake
• Intact thirst mechanism and access to water
are primary defense against hypernatremia
Hypokalemia
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Causes
Insufficient dietary intake
Intracellular shifting
Extrarenal or renal loss
Diarrhea
Symptoms & Signs
Potassium < 3.5
Muscle weakness/cramps
Constipation
Hyporeflexia
Hypercapnia
Hypertension
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Treatment
Oral supplements
Dietary replacement
Intravenous
Based on cause and
tolerability
Hyperkalemia
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Causes
Advanced kidney disease
Acidemia
Urinary obstruction
ACE-I, ARB, Potassium sparing diuretics
Symptoms & Signs
Muscle weakness
Ileus
ECG changes—but only
50% demonstrate changes
V-fib, cardiac arrest
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Treatment
Identify/treat cause
Withhold potassium
Insulin, bicarbonate,
B-agonists, calcium
Hemodialysis in AKI
Calcium Concentration
• Normal total serum Ca 8.5-10.5 mg/dL
• Normal Ionized Ca 4.6-5.3 mg/dL
Hypocalcemia
• Mistaken for neurological disorders
• Check for low parathyroid hormone, vitamin D and
magnesium
• Ionized calcium main indicator of problem
Hypercalcemia
• Asymptomatic, mild—hyperparathyroidism
• Severe, symptomatic—due to malignancy
• Hypercalciuria usually precedes hypercalcemia
Phosphorus Concentration
Normal 2.4-4.1 mg/dL
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Hypophosphatemia
May cause tissue hypoxia and rhabdomyolysis
Renal loss diagnosed by phosphateuria
PTH causes renal loss of phosphate
Malnutrition and alcoholism common causes
Hyperphosphatemia
• Advanced CKD is most common cause
• In combination with hypercalcemia –high risk of
metastatic calcification
Magnesium Concentration
• Normal 1.8-3.0 mg/dL
• Altered magnesium concentration usually
associated with alteration of calcium
Hypomagnesemia
• Serum levels may remain normal even with depletion,
check magnesiumuria if wasting is suspected
• Causes neurologic symptoms and arrhythmias
• Impairs release of PTH
Hypermagnesemia
• Often associated with advanced CKD and chronic
intake of magnesium-containing drugs
Acid/Base Disorders
Acute Kidney Injury
(Acute Renal Failure)
Prevalence of Acute Kidney Injury
• 5% of hospital admissions have AKI
• 30% of ICU admissions have AKI
• 25% of all inpatients will develop AKI
Acute Kidney
Injury
• Sudden decrease in kidney function
• Inability of kidneys to maintain acid-base,
fluid and electrolyte balance
• Build up of nitrogenous waste—Azotemia
• 20:1 (or greater) ratio of BUN to Creatinine
Prerenal
Azotemia
Postrenal
Azotemia
Intrinsic
Renal Disease
Prerenal
Azotemia
• Most common cause of AKI, 40-80%
• Caused by renal hypoperfusion
• Immediate resolution can prevent
intrinsic kidney injury
• If persists can lead to ischemia and
intrinsic kidney injury
Intravascular
Volume
Vascular
Resistance
Low Cardiac
Output
Post Renal
Azotemia
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•
•
•
Least common cause for AKI, 5-10%
Very reversible once found
Caused by urinary obstruction
BPH (most common cause), stricture,
cancerous mass, ureteral stones
Obstruction
Luminal
pressure
Kidney
damage
Poor
Perfusion
GFR
Intrinsic Renal
Disease
Acute Tubular
Necrosis
-Ischemic or toxic
Insult
-Accounts for 85%
Intrinsic AKI
Acute
Glomerulonephritis
Acute
Interstitial
Nephritis
-Immune complex -Interstitial inflamdeposition
matory response
-Rare, accounts for -Accounts for
5% Intrinsic AKI
10-15% of
Intrinsic AKI
Chronic Kidney Disease
(Chronic Renal Failure)
Chronic Renal Failure
Chronic Kidney Disease
20 million adults—1 out of 9
15% due to:
-Glomerulonephritis
-Poly Cystic
Kidney
-Urological
Causes
15% have
other or
unknown
causes
70% Late Stage Kidney Failure
Due to HTN and/or DM
General Considerations
• An inciting event starts the process
• Rarely reversible even after inciting event
removed
• Nephron destruction is the hallmark
• Compensatory hypertrophy of remaining
nephrons may keep serum creatinine normal
• ARBs and ACE inhibitors help reduce hyper
filtration injury—slow progression of CKD
Staging
GFR > 90
• Kidney damage with normal or > GFR
• Goals:
– Diagnose and treat cause (if found)
– Treat comorbidities (HTN & diabetes)
– Slow progression
Staging
GFR 60-89
• Kidney damage with mild < GFR
• Goals: estimate progression
Staging
GFR 30-59
• Moderate < GFR
• Goals: evaluate and treat complications
Staging
GFR 15-29
• Severe < GFR
• Goals: begin preparation for dialysis and/or
renal transplant
Staging
GFR < 15
• Kidney failure
• Goals:
– Dialysis when GFR < 10 mL/min for non diabetic
– Dialysis when GFR < 15 mL/min for diabetic
– Renal transplantation
Complications
GFR 60-89
Cardiovascular: CKD patients have > morbidity and
mortality than general population
– Hypertension: most common complication
– Coronary artery disease: address modifiable risk
factors
– Congestive heart failure
– Pericarditis
Complications
GFR 30-59
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•
•
•
•
Disorders of mineral metabolism
Bone disease and fracture risk
Also leads to increased vascular calcification
Anemia: due to < erythropoietin production
Coagulopathy: due to platelet dysfunction
Complications
GFR 15-29
• > phosphate, < calcium, < vitamin D and
secondary hyperparathyroidism
• > phosphate may be seen in stage 3 disease
• Most common bone lesion is osteitis fibrosa
cystica—subperiosteal lesions
Complications
GFR < 15
• Metabolic acidosis because loss of nephrons
does not allow for sufficient production of
bicarbonate
• Uremic syndrome: weakness, fatigue, pruritus,
SOB, neuropathies, < concentration, irritability
• Endocrine disorders: hypoglycemia in DM
Treatment
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•
•
•
•
Dietary Management/Renal Nutritionist
Protein restriction:
mixed reviews
Salt restriction:
2g/d Na
Potassium restriction:
< 50-60 mEq/d
Phosphorus restriction:
< 4.5 mg/dL Pre
dialysis, 3.5-5.5dL on dialysis
• Magnesium restriction: Magnesium containing
laxatives/antacids relatively contraindicated
Treatment
• Dialysis:
– Initiate at GFR 10 (Serum Cr 8) non DM
– Initiate at GFR 15 (Serum Cr 6) DM
• Types of Dialysis:
– Hemodialysis
– Peritoneal dialysis
• Kidney transplant
Glomerulonephritis
Glomerulonephritis
Glomerulonephritis
(Nephritic Syndrome)
• Relatively uncommon cause of acute kidney
injury, accounts for about 5% of intrinsic renal
failure
• Disorder of glomeruli
• Severity is based on the number of glomeruli
involved
Signs & Symptoms
•
•
•
•
Asymptomatic in 50% of acute cases
Edema: primarily eyes and scrotum
Hypertension with impaired renal function
Headache, visual disturbance, nausea and
vomiting
• Anorexia, abdominal pain, joint pain
• Malaise is common in older patients
Causes
• Peri or post infection—especially throat or
skin infection
• IgA nephropathy (Berger’s disease)
• Lupus nephritis
• Cryoglobulinemic glomerulonephritis—usually
associated with hepatitis C
• Membranoproliferative glomerulonephritis
Diagnosis
• Hematuria: red blood cell casts are specific to
glomerulonephritis
• Low to moderate proteinuria
• Anemia and elevated WBC
• Biopsy can help determine cause, amount of
scarring and potential for reversibility
• Physical exam as described
Treatment/Prognosis
• No specific treatment is available in most
cases
• Protein and sodium restriction
• Diuretics, steroids, cyclophosphamide
selectively
• Leads to chronic renal failure in about 0.1% of
children and 25% of adults
Nephrotic Syndrome
Nephrotic Syndrome
Nephrotic Syndrome
• Disorder of the glomeruli with excessive
proteinuria
• 1/3 have systemic renal disease: diabetes,
amyloidosis or systemic lupus erythematosus
• Remainder have idiopathic nephrotic
syndrome
• Most common in pediatric patients
Signs & Symptoms
• Early symptoms: anorexia and malaise
• Puffy eyelids and tissue swelling from excess
sodium and water retention
• Abdominal pain
• Muscle atrophy
• Frothy urine
Diagnosis
•
•
•
•
Based on history, PE and lab findings
Mistaken for heart failure in adults
24 hour urine shows proteinuria
Low serum albumin due to increased urinary
excretion
• Protein and fat casts noted in microscopic UA
• Urine: low sodium and high potassium
Treatment
• ACE Inhibitors or ARBs alone or in
combination for prevention and treatment
• Diet: normal protein and potassium; low
saturated fat, cholesterol and sodium
• High blood pressure is treated with diuretics
• Anticoagulants
• Infections—serious complication
• Steroids
Prognosis
• In infection, allergy or nephrotoxic drug use,
prognosis is based on effective treatment of
underlying cause
• In systemic lupus erythematosus or diabetes
mellitus, drug treatment often stabilizes or
decreases the amount of protein in the urine
• Renal failure develops without treatment
Polycystic Kidney Disease
Polycystic Kidney Disease: Etiology
• PKD is autosomal dominant or recessive
• Autosomal recessive PKD is rare; 1/10,000 and
causes renal failure during childhood
• Clinical manifestations are rare before
adulthood
• All patients ≥ 80 yr have some manifestations
Signs & Symptoms
• One half of patients remain asymptomatic and
are never diagnosed
• Low-grade flank, abdominal and lower back
pain due to cystic enlargement and infection
• Acute pain is due to hemorrhage into cysts or
passage of a calculus
Treatment
• Strict BP control
• Prompt treatment of UTIs
• Percutaneous aspiration or surgical removal of
cysts
• Hemodialysis, peritoneal dialysis, or kidney
transplantation (cysts do not recur in grafts)
Prognosis
• By age 80, 50 to 75% require dialysis or
transplantation
• Rapid progression risk factors: early diagnosis,
male, sickle cell trait, rapidly increasing kidney
size, gross hematuria, hypertension
• Patients usually die of heart disease
(sometimes valvular), disseminated infection,
or ruptured cerebral aneurysm
Thank You