Renal Flashcards
AKI
major side effect of other medical procedures, diverse spectrum of molecular, biochemical and structural processes that characterize the AKI syndrome
The RIFLE Classification of AKI
Risk for renal dysfunction –Injury to kidney –Failure of kidney function –Loss of kidney function –End stage renal disease
These classes represent degrees of injury
R = Risk for renal dysfunction I = Injury to the kidney F = Failure of kidney function
These classes represent outcome measures
L = Loss of kidney function, E = End stage renal disease (ESRD)
R = Risk for renal dysfunction
Increase in serum creatinine ≥ 1.5× baseline, Decrease in GFR ≥ 25%, UO < 0.5 mL/kg/h for 6 h
I = Injury to the kidney
Increase in serum creatinine ≥ 2.0× baseline, Decrease in GFR ≥ 50% < 0.5 mL/kg/h for 12 h
F = Failure of kidney function
Increase in serum creatinine ≥ 3.0× baseline OR serum creatinine ≥ 4.0mg/dL in the setting of an acute rise ≥ 0.5 mg/dL, Decrease in GFR ≥ 75%, < 0.3 mL/kg/h for 24 h or anuria for 12 h
L = Loss of kidney function
Persistent failure > 4 weeks
E = End stage renal disease (ESRD)
Persistent failure > 3 months
AKIN criteria
• To further refine the definition of AKI • Proposed a modified version of the RIFLE classification, known as the AKIN• An abrupt (within 48 h) reduction in kidney function as measured by an absolute increase in serum creatinine ≥ 0.3 mg/dL, • A percentage increase in serum creatinine ≥ 50%, • Or documented oliguria (
AKIN with RIFLE
AKIN replaces the three levels of severity R, I and F with stages 1, 2 and 3.
Besides Establishing the Early Diagnosis Biomarkers are needed to determine:
- Location of injury
- Duration of AKI
- AKI subtypes
- AKI etiologies
- Differentiate from other forms of acute kidney disease
- Risk stratification and prognostication
- Defining course of AKI
- Monitoring interventions
Biomarkers also used for
Also- desperately needed for use as surrogate endpoints in clinical trials evaluating potential therapeutics for AKI
validation
This linking of the surrogate endpoint to the clinical endpoint is referred to as validation and is an essential step in the biomarker discovery process
the most important AKI biomarkers remain
those that are clinically applicable and can lead to early diagnosis and treatment of AKI
prevalence of CKD in the general population
10-13% A complex disease that often affects multiple organ systems and often coexists with numerous associated conditions, such as cardiovascular disease, diabetes mellitus, lupus, & chronic inflammation
The ‘gold standard’ measurement for CKD
is the ‘true’ glomerular filtration rate (GFR) as tracked by 24-h urine isotope clearance, Method is quite expensive and not always practical in the clinical
setting
A commonly used clinical surrogate for nuclear GFR
serum creatinine clearance, the accuracy of serum creatinine is greatly affected by a number of patient dependent and -independent variables, Serum creatinine may fall to one-third of its normal level in advanced kidney disease, unrelated to its renal clearance, Serial 24-h creatinine measurements fail to determine risk progression in approximately 20% of CKD patients
CKD Definition
The presence of kidney damage or a glomerular filtration rate less than 60 mL/min/1.73 for 3 months or greater, regardless of cause However, significant increases in cardiovascular disease risk occur at
more subtle loss of kidney function (75) so it needs to be caught earlier
AKI definition
abrupt reduction in GFR –> Acumulation of nitrogenous wastes, disturbed f+e balance, and abnormal volume status. Can be polyuric, nonliguric, anuric - can do AKIN or RIFLE. Increase in sCr by 50% in 7 days, or increase by 0.3 in 2 days or oliguria
AKD
Classifies patients who may need intervention to restore kidney function or reverse kidney damage. GFR < 60 for < 3 months
Proteinuria
Shown to directly represent kidney damage and higher levels of proteinuria correlate well with a more rapid progression of kidney disease, The earliest known marker of kidney damage in glomerular diseases, diabetes and hypertension, and is the most common marker of kidney damage in the adult population Early diagnosis would entail routinely screening asymptomatic patients
However, proteinuria has limitations
May occur long after the renal injury has occurred
• Not always present in many types of renal disease
Stages of chronic kidney disease
stages 1-5.
Stage 1
Kidney damage with normal or high GFR ≥ 90 mL, increased Cr x 1.5 or > 0.3mg/dL. UO <0.5ml/kg/h x 6 h
Stage 2
Kidney damage and mild decrease in GFR 60–89, increase Cr x 2, UO < 0,5ml/kg/h x 12 h
Stage 3
Moderate decrease in GFR 30–59, increased Cr x 3 or Cr > 4, U0 < 0.3 X 24 or anuria
Stage 4
Severe decrease in GFR 15-29
Stage 5
Kidney failure, <15 or dialysis
AKI is broadly defined
as a rapid deterioration in kidney function as manifested by a reduction in GFR Comprised of a variety of syndromes that are characterized by kidney
dysfunction that occurs over hours to days it can
occur in previously healthy individuals with completely normal kidneys The most commonly employed markers of AKI are serum creatinine and BUN, both of which rise in this setting
Azotemia
A buildup of nitrogenous wastes in blood
Uremia
A constellation of symptoms and signs of multipleorgan
dysfunction caused by retention of “uremic toxins” in the setting of renal failure
Oliguric
<400 mL/day
Oligoanuric
<100 mL/day
Polyuric
> 3L/day
Anuric
none
Does AKI need specific urine output
the presence of urine output does not exclude the possibility of AKI
Most common cause of AKI
Pre Renal
Does creatitine concentration reflect a true GFR?
Because changes in serum creatinine concentration do not precisely correlate with changes in GFR, it actually
is a poor reflection of true GFR because changes in Cr does not correlate with GFR — Why: Cr is cleared through GFR and tubular secretion, drugs can compete w tubular secretion, can be falsely elevated by lab techniques, muscle is the primary source of creatine which is coverted to Cr in the liver females w low muscle mass will have a decrease
Pre Renal AKI
A decrease in GFR that occurs as a consequence of reduced renal bloodflow
Intrinsic AKI
A decrease in GFR due to direct parenchymal injury in the kidney, subdivided by various compartments (vascular, glomerular, interstitial, tubular)
Post renal AKI
a decrease in GFR from obstruction to urine flow from the pelvis to the urethra
ARF
Acute renal failure, renal impairment is sustained.
RIFLE v AKIN
Rigle is based on serum Cr, AKIN is based on serum Cr, estimated GFR and UO
AKI functional criteria
Increase in SCr by 50% within 7 days OR increase in Cr by 0.3 within 2 days OR oliguria, no structural criteria
CKD functional criteria
GFR < 60 for > 3 months, structural criteria - kidney damage for > 3 months
AKD
AKI or GFR < 60 for < 3 months or a decrease in GFR by > 35% or an increase in SCr by > 50% for < 3 months. Structural critera - kidney damage for < 3 months
NKD
GFR > 60, Stable Cr, no damage
Lab tests to identify AKI
BUN, GFR/Cr most commonly used
A abrupt increase in Serum Cr usually reflects a decline in ____, signalling the development of AKI
GFR
BUN influenced by
level of underlying renal function, slow urine flow rates, GI bleeding, protein intake, catabolic states, protein malnutrition, cirrhosis
Prerenal causes of AKI
Volume depletion, n/v, diarrhea, overdiuresis, renal salt wasting, DI, sepsis, cardiomyopathy, cirrhosis (hepatorenal syndrome), RAS, ACE, ARB, NSAIDS,
Intrarenal causes of AKI
Glomerular diseases – glomerulonephritis. acute tubular necrosis, interstitial nephritis, infection
Post renal causes of AKI
Pelvic, ureteral obstructions, kidney stones, fungus balls omg what gross, blood clots, bladder obstruction, BPH, urethral obstruction
Blood tests that can diagnose prerenal specifically
FENa (<1%), FEUrea (<35%) , RFI (<1%) DDx use a urine microscopy
Intrinsic renal disease
Anatomic compartments that have been acutely injured – vasculature, glomerulus, tubules, insterstitium
Large vessel disease leading to AKI
from a thrombosis of RAS or thromboembolism from cardiac thrombus
UTI
bacterial infection of the urinary tract, urinary frequency and urgency from spontaneous bladder contraction due to irritation of the trigone
Urinary tract is usually sterile – why
Urinary tract is normally sterile due to the fact that bacteria moving upwards are regularly washed out by urination
Types of normal flora in the urinary tract
lactobacillus and staphylococcus
Generally speaking –UTI is infections in any components linked to the urinary tract:
kidney, bladder, prostate, urethra
To make a diagnosis of UTI you must
know and start with the site –and then the nature of the infection
Normal Mechanisms that Maintain Sterility of Urine
adequate urine volume, free flow from kidneys through the urinary meatus, complete bladder emptying, normal acidity of the urine, peristalsis of ureters and competent junction, Increased intravesicularpressure preventing reflux, In males, antibacterial effect of zinc in prostatic fluid
Risk Factors of UTI - aging
Aging – increased risk of DM, urinary stasis and impaired immune response. In females:
Risk factor of UTI – females
short urethra, having sexual intercourse, use of contraceptives that alter normal bacteria flora of vagina and perineal tissues; with age increased incidence of cystocele, rectocele (incomplete emptying)
Risk factors of UTI – males
prostatic hypertrophy, bacterial prostatitis, anal intercourse
Risk factors for UTI - UTI
tumor or calculi, strictures. Another risk: bladder innervation
Lower UTI
Urethritis (often is sexually transmitted), prostatitis, cystitis (traditional UTI)
Upper tract infection
pyelonephritis, perinephric abscess
Bladder patho
smooth triangular region of the internal urinary bladderformed by the two ureteral orifices and the internal urethral orifice
Trigone
Sensitive to expansion and once stretched to a certain degree, the urinary bladder signals the brain of its need to empty
The signals become stronger as the bladder
The normal bladder is capable of clearing itself of organisms within X days of their introduction.
2 to 3
Defense mechanisms of UTIs
(1) the elimination of bacteria by voiding
(2) the antibacterial properties of urine and its constituents
(3) the intrinsic mucosal bladder defense mechanisms
(4) an acid vaginal environment (female)
(5) prostatic secretions (male)
Dysuria-
inflammation of the urethra
Symptoms of Urinary Tract Infection
Dysuria, increased frequency, hematuria, fever – now systemic, N/V (pyelo) and increased vagal activity, flank pain (pyelo) from stretching of the capsule, pain with defacation from irritation of the trigone or an inflammed prostate
Findings on Exam in UTI
Physical Exam:
CVA tenderness (pyelonephritis)
Urethral discharge (urethritis)
Tender prostate on DRE (prostatitis)
UA Labs
\+ leukocyte esterase \+ nitrites More likely gram-negative rods \+ WBCs \+ RBCs
most valuable laboratory diagnostic test for UTI
Urinalysis for evaluation of pyuria
This makes the diagnosis of UTI
presence of pyuria and bacteria
Pyuria is present in almost all men with
acute cystitis or pyelonephritis
The absence of X strongly suggests an alternative diagnosis or, in a patient with pyelonephritis, the presence of an obstructing lesion
Pyuria
The gold standard to diagnose a UTI
Urine culture
Positive Urine Culture
Bacterial colony >10^2CFU/mL (Symptomatic Patient)
•
Or, 10^5CFU/mL (Asymptomatic) + leukocytes
Colony count is most beneficial in the
asymptomatic patient, or pregnant patient
Most common pathogen for cystitis, prostatitis, pyelonephritis:
Escherichia coli-80%
Staphylococcus saprophyticus-15%The rest made up of Gram –negative rods
Most common pathogen for urethritis
Chlamydia trachomatis, Neisseria Gonorrhea
Lower Urinary Tract Infection -Cystitis
Most common symptomatic bladder infection
Uncomplicated (Simple) cystitis
In healthy woman, with no signs of
systemic disease
Complicated cystitis
In men, or woman with comorbid medical problems.
Uncomplicated simple cystitis symptoms
Urinary bacteria, dysuria, lower abdominal cramping, frequency, urgency. Typical for the healthy outpatient, non pregnant, no fever nausea, vomiting flank pain. (if fever look for renal parenchyma pyelonephritis. Diagnose with dipstick UA (no culture, no lab testing)
present in almost all patients with complicated UTI
Pyuria (absense suggests an alternative dx) White cell casts – pyuria from renal origin. Can have absent pyuria if infection does not communicate with the collecting system or the system is obstructed
Tx uncomplicated simple cystitis
Bactrim for THREE DAYS. One double strength tablet (160/800) twice daily.
Tx uncomplicated simple cystitis with a sulfa allergy
May use fluoroquinolone(ciprofoxacinor levofloxacin) in patient with sulfa allergy, areas with high rates of bactrim-resistance
optimal duration of antibiotic therapy in men
Few studies have evaluated the optimal duration of antibiotic therapy in men, although treatment has traditionally been given for 7 to 14 days.
Risk factors for simple cystitis
sex, may recommend post coital voiding or prophylactic abx use
recent TMP-SMX resistance is increasing and approached x%
20%
Complicated Cystitis
Females with comorbid medical conditions (DM. Immunosuppressed. Renal failure. Renal transplant. UTI in childhood)
All male patients
Indwelling foleycatheters
Urosepsis/hospitalization
Diagnosis of Complicated Cystitis
Urinalysis, Urine culture
Further labs, if appropriate.
Treatment of Complicated Cystitis
Fluoroquinolone (or other broad spectrum antibiotic) 7-14 daysof treatment (depending on severity)
May treat even longer (2-4 weeks) in males with UTI
Indwelling catheter complicated cystitis
Try to get rid of the foley. Only treat with symptomatic (fever, dysuria). WBC in UA, they are frquently colonized with great number of bacteria. Should change foley before obtaining culture.
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.
Pyelonephritis
Infection of the kidney, Associated with constitutional symptoms –fever, nausea, vomiting, headache
Dx pyelo
Urinalysis, urine culture, CBC, chemistry
Pyelonephritis Treatment:
2-weeksof Trimethroprim/sulfamethoxazoleor fluoroquinolone, Hospitalization and IV antibiotics if patient unable to take po.
Pyelonephritis Complications:
Perinephric/Renal abscess, Nephrolithiasis with UTI
Perinephric/Renal abscess:
Suspect in patient who is not improving on antibiotic therapy.
• 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
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 Prostatitis
- Typical clinical history (fevers, chills, dysuria, malaise, myalgias, pelvic/perinealpain, cloudy urine)
- The finding of an edematous and tender prostate on physical examination
- Will have an increased PSA
- Urinalysis, urine culture
Prostatitis tx
Trimethoprim/sulfamethoxazole, fluroquinoloneor other broad spectrum antibiotic
• 4-6 weeks of treatment to penetrate
Risk Factors Prostatitis:
Trauma, dehydration
Urethritis Chlamydia trachomatis
Frequently asymptomatic in females, but can present with dysuria, discharge or pelvic inflammatory disease. Send UA, urine culture (if pyuriaseen, but no bacteria, suspect Chlamydia)
Pelvic exam Urethritis
send discharge from cervical or urethral osfor Chlamydia PCR. recc for all females < 25 to be screened
Tx Urethritis Chlamydia trachomatis
Azithromycin –1 g pox 1 or
Doxycycline –100 mg poBID x 7 days
Neisseria gonorrhoeae Urethrtis
- May present with dysuria, discharge, PID
- Send UA, urine culture
- Pelvic exam –send discharge samples for gram stain, culture, PCR
Treatment Neisseria gonorrhoeae Urethrtis
•Ceftriaxone –125 mg IM x 1 •Cipro–500 mg pox 1 •Levofloxacin –250 mg pox 1 •Ofloxacin–400 mg pox 1 •Spectinomycin–2 g IM x 1 You should always also treat for chlamydia when treating for gonorrhea!
Antibiotic choice and duration are determined by
classification of UTI.
Biggest bugs for UTI are
E. coli, S. saprophyticus, Proteus mirabilis, Enterococci and gram-negatives
Consider antibiotic resistance in
pyelonephritis
Among quinolones, don’t use
moxifloxacin.
Chlamydia screening is now recommended for all women 25 years and under since
infection is frequently asymptomatic, and risk for PID/infertility is high!
Urinary Incontinence Loss of bladder control due to
- Functional abnormalities of the bladder or urethra
- Bladder muscle contractions
- Weak pelvic floor and/or sphincter muscles
- Blockage in the urethral opening
About twice as common in
women (men complain about lower quality of life more)
Causes of incontinence
from localized tumor/cancer, diabetes, neurological disorders and physical changes associated with aging
Dual control of urination
Autonomic nervous system control and Central nervous system
Autonomic nervous system
- Nerve coming from the spinal cord and go directly to the bladder
- When bladder gets fuller, signals are sent to the brain
Central nervous system
Voluntary control to choose when to void
Voiding Physiology
- Normal voiding requires coordination between multiple structures and nerve pathways
- Key structures include the brain, brainstem, spinal cord, bladder, and urethral sphincter mechanism
The Brain and Social Continence
The brain(cerebral cortex) provides overall control and direction of bladder function. • The Detrusor area in the cerebral cortex controls bladder function by directing the micturition centers to initiate or delay voiding depending on the social situation. • This is called social continence
Any disruption in the cerebrocorticalfunction can cause or contribute to incontinence like which condition
CVA
The neural circuitry that controls this process is complex and highly distributed:
it involves pathways at many levels of the brain, the spinal cord and the peripheral nervous system is mediated by multiple neurotransmitters.
Diseases or injuries of the nervous system →can cause the
re-emergence of involuntary or reflex micturition,leading to urinary incontinence
pontine micturition center
The pontine micturition center in the brainstem provides for automatic coordinated voiding. Meaning the urethra opens before the bladder contracts
The pons
also holds the micturition ‘reflex’ centerwhich allows the bladder to empty when reaching a certain fullness regardless of social situation.
• Especially important for spinal cord patients.
The storage and periodic elimination of urine depends on
coordinated activity of smooth and striated muscles in the two functional units of the lower urinary tract: The reservoir (the urinary bladder) And the outlet
the outlet consists of
the bladder neck,
the urethra
the urethral sphincter
Spinal Cord Pathways - Parasympathetic
omes off at S2-S4 and cause the bladder to contract and the urethra to relax.
• Parasympathetic stimulation initiates voiding
Sympathetic pathways
come off at T-10 L2that cause bladder neck to tighten and also contribute to bladder relaxation.
• Sympathetic stimulation contributes to urine storage and promotes continence.
Caveat: remember that the bladder has only two modes of operation:
storage and elimination
Trigone
Sensitive to expansion and once stretched to a certain degree, the urinary bladder signals the brainof its need to empty
The signals become stronger as the bladder continues to fill
Patients with urge or frequency
bladder pressure not greater than urethral pressure
Patients with urge incontinence
bladder pressure IS greater than urethral pressure
Urinary incontinence is Not a natural part of aging
It can happen at any age
Caused by many physical conditions
Many causes of incontinence are temporary and can be managed with simple treatment
Some causes of temporary incontinence are:
- Urinary tract infection
- Vaginal infection or irritation
- Constipation
- Effects of Rx
Stress Incontinence
urethral hypermobility & intrinsic sphinctericdeficiency People with stress incontinence lose urine when they exercise or move in a certain way. sneeze, cough, or laugh, up from a chair or out of bed, walking, going to the bathroom often to avoid accidents
Urge incontinence
immediately before involuntary leakagePeople with urge incontinence lose urine as soon as they feel a strong need to go to the bathroom.(AKA Overactive bladder)
Mixed stress/urge
combined stress & urge
Overflow (retention)
continuous leakage/ dribbling/un-empty bladder
If you have urge incontinence you may leak urine:
- When you can’t get to the bathroom quickly enough
- When you drink even a small amount of liquid, or when you hear or touch running water
- You may go to the bathroom very often; for example, every two hours during the day and night
- You may even wet the bed
Causes/Risk Factors of Urge
Aging is a risk factor simply due to: • reduced bladder capacity • delayed recognition of bladder filling • → reduced “response” time. • Bladder irritants, • neurological lesions, • Stones • cancer • obstructed flow • Idiopathic
Overflow Incontinence Causes
• Do not feel the urge to urinate.
• Incomplete bladder emptying
• Small amounts of urine are leaked on a nearly continuous basis
• Weak bladder muscles:
• caused by nerve damage from diabetes or other diseases
• a blocked urethra can be responsible for overflow incontinence.
Impaired contractibility of the detrusor muscle
Overflow Most frequently appears in older men because
BPH hinders the flow of urine; urinary stones or tumors also may block the urethra. Women is rare but can be caused by fibroids or ovarian tumors, Spinal cord injuries or nervous system disorders are additional causes
s/s Overflow incontience
- Feeling as though the bladder is never completely empty
- Feeling the urge to urinate, but not being able to
- Passing a dribbling stream of urine, even after spending a long time at the toilet
- Nocturia
- Although some people with overflow incontinence never have the feeling of a full bladder, they may leak urine day and night.
Functional Incontinence
Diagnosis: Intact urinary storage & emptying –but unable to toilet themselves
• Usually one of elimination.
•Patient voids large amounts at regular intervals.• Incontinence in patient with normal voiding patterns and normal bladder function: • Usually related to cognitive status • Motivation • And/or mobility issues Cortex doesn’t process the signals from the bladder.
• An automatic voiding when bladder is full. No social continence.
Tx Functional
prompted or timed voiding. Containment products and skin care. • Pelvic Muscle Rehabilitation • Behavioral therapy • Pharmacological Therapies • Pessary • Surgical Therapies
Assessment and Evaluation-ONE Idea
D-Delirium I-Infection A-Atrophic urethritis/vaginitis P-Pharmaceuticals P-Psychological Status E-Endocrine changes R-Restricted mobility S-Stool Impaction
Kegel Exercises
Pull in the pelvic muscles and hold for a count of 3. Then relax for a count of 3.
• Work up to 3 sets of 10 repeats.
• Start doing your pelvic muscle exercises lying down. This is the easiest position to do them because the muscles do not need to work against gravity.
• When your muscles get stronger, do your exercises sitting or standing. Working against gravity is like adding more weight.
Kegels - time frame
• It takes just 2-5 minutes a day. You may not feel your bladder control improve for 3 to 6 weeks. Still, most people do notice an improvement after a few weeks
Pelvic floor exercise benefits
- Helps strengthen the muscles of the pelvic floor –improves bladder stability
- Helps suppress the feeling of urgency
Bladder Training
- Bladder training has many variations but generally consists of three primary components:
- Education
- Scheduled voiding
- Positive reinforcement
Pharmacological
Work on parasympathetic nervous system-depends on type of incontinence.
Includes:
1.Alpha blockers
2.Antimuscarinics
3.Serotonin norepinephrine reuptake inhibitors
Diagnostic Evaluations
- Urodynamics-to determine voiding dysfunction etiology and bladder/urethra function
- Focused Physical examination and history
- Dexterity testing
- Pelvic muscle strength testing
- Prostate exam
- Cystoscopy to visualize bladder wall and identify lesions.
