Renal II Flashcards
Type II RTA
Defect in bicarbonate reabsorption
Faconi, PAGU
Isolated proximal RTA
Hereditary dysfunction of basolateral sodium bicarbonate cotransporter
What causes faconi
Inherited or acquired due to myeloma, chronic IN (Chinese herbal nephropathy), or drugs (ifosfamide, tenofovir)
Treat type II or faconi
Large doses of bicarbonate which may aggravate hypokalemia
Type IV
Hyporeninemic hypoaldosteronism or resistance
50-80% of women have at least one __ and 20-50% have recurrent episodes
UTI
Ribs factors for acute cystitis
Recent use of diaphragm with spermicide, frequent sexual intercourse, a history of UTI, DM, incontinence; also increase risk of pyelonephritis
Most common UTI bacteria
E. coli 75-90
Staph saprophyticus 1-15%
Klebsiella , proteus, enterococcus, citrobacter rest
Iwhat gram positives cause UTI
Staph aureus and enterococci
Candida UTI path different than other organisms
Hematogenous route
Candida in urine or noninstrumetned immunocompetent
Genital contamination or widespread visceral dissemination
Papillary necrosis
Can occur in pets with obstruction, dibatetes, sickle cell disease, or analgesic nephropathy
Emphysematous pyelonephritis
Severe
Associated with the production of gas in renal and perinephric tissues, and occurs almost exclusively in diabetics
Xanthogranulomatous pyelonephritis
Chronic urinary obstruction (often staghorn), together with chronic infection, leads to suppurative destruction of renal tissue
Prostatis
Infectious or not
More common not
Complicated UTI
Symptomatic disease in a man or woman with an anatomical predisposition to infection, with a foreign body into e urinary tract, or with factors predisposing to a delayed response therapy
Diagnose UTI uncomplicated
Clinical history 96% LIEKLYHOO if have dysuria and urinary frequency in absence of vaginal discharge
Confirm with dipstick positive for nitrite or leukocyte esterase in patients with a high pretext probability of disease
Detection of bacteria in a urine culture is gold standard
Want colon count 10^2 OR OVER
What three factors determine the initial rate of spread of any STI within a population
Rate of sexual exposure of susceptible to infectious ppl, efficiency of transmission per exposure, and duration of infectivity of those infected
What are 4C’s of sti
Contact tracing, ensuring compliance with treatment, counseling on risk education, including condom promotion and provision
What causes urethritis in men
Gonococcal or nongonococcal (chlamydia trachomatis)
Mycoplasma genitalium, ureaplasma, urealyticum, trichomonas vaginalic, HSV
What causes most non gonococcal urethritis in men
Chlamydia and mycoplasma genitalium
Symptoms or male urethritis
Urethral discharge, dysuria, without frequency of urination
Diagnose male urethritis
Pts present with mucopurulent urethral discharge can be expressed by milking the urethra
Grams stained smear of an anterior urethral specimen containing 5PMN/1000x field confirms the diagnosis
Centrifuged sediment of the days first 20-30 mL or voided urine can be examined instead
N gonorrhea can be identified if intracellular gram negative diplodocus are present in grams strained samples
Early oring, first voided uring should be used in multiplex acid amplification testes (NAATs ) for gonorrhea and chlamydia
Treat gonorrhea
Ceftriaxone
Azithromycin
Treat chlamydia
Azithromycin
Treat mycoplasma genitalium
Azithromycin
Treat recurrent symptoms of male urethritis
Both patient and partner treated if re exposure
Without re exposure, infection with T vaginalis (with culture or NAATs)
Shock
Ok
Possibly harmful systemic response to shock
Two or more of the following
- fever or hypothermia
- tachypnea
- tachycardia
- leukocytosis
Sepsis
Harmful systemic response with a proven or suspected microbial etiology
Septic shock
Sepsis with hypotension (90< or below pts normal bp for at least 1 h despite fluid resuscitation) or need for vasopresors to maintain systolic bp 290 mmHg or MAP 270 mmHg
Etiology shock
Blood cultures are positive in 20-40% of sepsis causes and in 40-70% of septic shock cases
For infected patients in ICUs, respiratory infections have been most common (64%) . Microbiological results have revealed that 62% of isolates are gram negative bacteria (pseudomonas spp and E. coli) , 47% are gram positive (staph aureus) and 19% are fungi (candida)
Epidemiology shock
Incidence of severe sepsis and septic shock in US increases with >750000 cases each year contributing to over 200000 deaths. Invasive bacterial infections are a prominent cause of death areound the world, especially among young kids
Sepsis related incidence and mortality rates increases with age and preexisting comorbidity, with 2/3 of cases occurring in pts with significant underlying disease
What has the increased incidence of sepsis been attributed to
The aging population, longer survival of patients with chronic disease, a relatively high frequency of sepsis among AIDS, and medical treatments that circumvent host defenses 9immunosuppresive agents, catheters)
Local and systemic host response to septic shock
Hosts have numerous receptors that recognize highly conserved microbial molecules, triggering the release of cytokines and other host molecules that increase blood flow and neutrophil migration to the infected site, enhance local vascular permeability, and elicit pain
Many local and systemic control mechanisms for septic shock dismiss cellular responses to what
Microbial molecules,
-intravascular thrombosis (which prevents spread of infection and inflammation) and an increase in anti inflammatory cytokines (IL4 and 10(
Organ dysfunction and shock
Widespread vascular endothelial injury is believed to be the major mechanism for multiorgan dysfunction
Septic shock is characterized by compromised oxygen delivery to tissues followed by a vasodilary phase ( a decrease in peripheral vascular resistance despite increased levels of vasopressin catecholamines)
Clinical features septic shock
Hyperventilaition that produces respitoary alkalosis
Encephalopathy (disorientation, confusion)
Acrocyanosis and ischemic necrosis of peripheral tissues due to hypotension and DIC
Skin-hemorrhagic lesions, bullae, cellulitis, pustules. Skin lesions may suggest specific pathogens
GI-nausea, vomiting, diarrhea, ileus, cholestatic jaundice
What infection suggested petechiae and purpura
Neisseria meningitidis
What skin infection ssuggests pseudomonas aeruginosa
Acthyma and gangrene
Cardiopulmonary manifestations of septic shock
Ventilation-perfusion mismatch, increased alveolar capillary permeability, increased pulmonary water content, and decreased pulmonary compliance impede oxygen exchange and lead to ARDS (progressive diffuse pulmonary infiltrates and arterial hypoxemia) in 50% of patients
Hypotension: normal or increased cardiac output and decreased systemic vascular resistance distinguish septic shock from cardiogenic and hypovolemia shock
The ejection fracture is decreased, but ventricular dilation allows maintence of a normal stroke volume
Adrenal insuffiency of septic shock
May be difficult to diagnose in critically ill patients
Renal manifestations septic shock
Oliguria and polyuria, azotemia, proteinuria and renal failure due to tubular necrosis
Neurological manifestations of septic shock
Delirium in the acute phase, polyneuropathy with distal motor weakness in prolonged sepsis. Survivors may have long term cognitive impaiement
Immunosuppression with septic shock
Patients may ave reactivation of HSY, CMV, or VZv
CBC SEPTIC SHOCK
LEUKOCYTOSIS WITH A LEFT SHIFT, thrombocytopenia
Coagulation with septic shock
Prolonged thrombin time, decreased fibrinogen, presence of n diners suggestive of DIC. With DIC , platelet counts usually fall below 50000
Chemistries septic shock
Metabolic acidosis, elevated anion gap, elevated lactate levels
LFTs septic shock
Transaminitis, hyperbilirubinemia, azotemia
Hypobilirubinemia
Diagnose septic shock
Need isolation of microorganisms from blood or a local site of infection. Culture of infected cutaneous lesions may help establish the diagnosis
Treat septic shock and sepsis
Antibiotic
Removal of drainage of a focal source of infection
Hemodynamics, respiratory, and metabolic support
-saline, hydrocortisone(if hypotension not responding), erythrocytes transfusion
General support
Prognosis septic shock
20-35% of patients with severe sepsis and 40-60% of patients with septic shock die within 30 days , and further deaths occur within 6 months. Prognostic stratification systems can estimate the risk of dying of severe sepsis
Oliguria
Less than 400
Anuria
No Rhine
Setting of oliguria
Volume depletion and/or renal hypoperfusion, resulting in prerenal azotemia and acute renal failure
What can cause anuria
Complete bilateral urinary tract obstruction; a vascular catastrophe, renal vein thrombosis; renal cortical necrosis; severe acute tubular necrosis; nonsteroidal antiinflammatory drugs, ACE I, angiotensin receptor blockers , hypovolemia, cardiogenic or septic shock
Polyuria
Over 3 Lid
Setting of polyuria
Nocturnal and urinary frequency , hypernatremia and can occur as a response to solute load and vasopressin ADH
Diabetes insipidus
Central insufficient AVP
Nephrogenic-insensitivity
What is associated with nephrogenic diabetes insipidus
Tubulointerstitial diseases, lithium therapy, and resolving acute tubular necrosis or urinary tract obstruction can be associated with nephrogenic diabetes insipidus, which is more rarely caused by mutations in the V2 AVP receptor, the aquaporin 1 water channel in the descending thin limb of the loop of henle and the AVP regulated water channel in principal cells, aquaporin 2
Proteinuria causes
Excessive fluid intake-primary polydipsia, latrogenic (IV)
Therapeutic-diuretics
Osmotic diuresis-hyperglycemia
Azotemia
Mannitol
Nephrogenic diabetes insipidus cause
Lithium, UT obstruction, papillary necrosis, reflux nephropathy, interstitial nephritis, hypercalcemia, hereditary
Causes central diabetes insipidus
Tumor, postoperative, head trauma, basilar meningitis, neurosarcoidosis
Polyuria with <250 mosmol and low serum sodium
Primary polydipsia
=psychogenic, hypothalamic disease drugs(thioridazine, chlorpromazine, anticholinergic agents)
Polyuria urine osmolarity <250 and diabetes insipidus
Nephrogenic DI vasopressin
Polyuria urine osmolarity >300
Solute diuresis
Diagnose proteinuria
Dipstick estimates protein concentration
Detect albumin, not light chains (require testing with sulfosalicylic acid)
Urine albumin
24 hour protein collection
When may transient proteinuria be seen
After vigorous exercise, changes in body position, fever, or CHF
What is nephrotic range proteinuria
3 g/d
When can massive proteinuria be seen
MCD, primary focal segmental glomerulosclerosis, membranous nephropathy, diabetic nephropathy, collapsing glomerulopathy
How treat proteinuria
ACE inhibitor or angII blocker
This will decrease rate of progression to end stage renal disease in diabetic nephropathy
Hematuria causes
Lower urinary tract disease or intrinsic renal disease
Cyst rupture in polycystic kidney disease and postpharyngitic flares of IgA nephropathy
Microscopic hematuria accompanies by proteinuria, HTN, and an active urinary sediment is most likely related to an inflammatory glomerulonephritis, classically post streptococcal glomerulonephritis
Ok
Major causes of hematuria lower urinary tract
Bacterial cystitis Interstitial cystitis Urethritis Passes or passing kidney stone Transitional cell carcinoma of bladder or structures proximal to it Squamous cell carcinoma of bladder
Upper urinary tract causes of hematuria
Renal cell arcinoma
Age related renal cysts
Neoplasms
Acquired renal cystic disease
Congenital cystic disease, including autosomal dominant form
Glomerular diseases
Intestinal renal diseases)interstitial nephritis
Nephrolithiasis, pyelonephritis
Renal infarction, hypercalcuria, hyperuricosuria
Free hemoglobin and myoglobin on dipstick and negative urinary sediment with strong heme positive dipstick
Hemolysis or rhabdomyolysis, which can be differentiated by clinical history and laboratory testing
RBC cast specific for what
Glomerulonephritis
Acute renal failure/ AKI
Measurable increase in serum Cr concentration and happens in 5% of hospitalized patients and associated with increase in hostpital mortality and morbidity
Treat AKI
Nothing specific maintain renal perfusion and intravascular volume
Cofactors of AKI
Hypovolemia and drugs that interfere with renal perfusion and/or glomerular filtration (NSAIDS) ACE I ang blockers
Prerenal failure
Most common in hospital
May result from true volume depletion or arterial underfilling (reduced renal perfusion in the setting of adequate or excess blood volume
Reduced renal perfusion may be seen in CHF
Pre renal causes of AKI
Volume depletion-blood loss, diuretic use
Volume overload with reduced renal perfusion-CHF, hepatic cirrhosis, severe hypoporteinemia
Renovascular disease
Drugs-NSAIDS, ciclosporin,
Hypercalcemia “third spacing )pancreatitis, systemic nflammatory response, whepatorenal syndrome
Intrinsic causes of AKI
ATN
Ttubulointerstitial diseaseatheroembolic disease after vascular procedures
Glomerulonephritis
IgA nephropathy
Glomerular endoliopathies
Post renal AKI
Bladder neck obstruction, bladder calculi
Prostatic hypertrophy, urethral obstruction due to compression
-pelvic or ab malignancy
Nephrolithiasis
Papillary necrosis with obstruction
Causes of intrinsic failure in hspoiratl
Surgical services or ICU, ATN, rhabdomyolyssi, allergic penicillins, NSAIDS, radiographically contrast dies, thrombotic microangiopathies,
Post renal
Ambulatory more common than hospitalized more common men
AKI with prerenal azotemia due to volume depletion presentation
Orthostatic hypotension, tachycardia, low jugular venous reassure, anddry mucoud membranes
Prerenal azotemia and CHF
Jugular venous distention and S gallop, peripheral and pulmonary edema.
Signs pre renal
BUN Cr high, volume depletion and CHF cirrhosis
Uric acid may be up
Na <10-20 urine FEN <1%
Hyaline and few granular casts, without cells or cellular casts . Renal ultrasonography is usually normal
Intrinsic renal disease GN
HTN and edema
Fractional excretion of Na
Urine Na
Urine Cr to plasma ratio
Urine urea N to plasma uraea N
Urine specific gravity
Urine osmolality
Plasma BUN/Cr ration
Renal failure index
Urnary sediment
Prerenal vs intrinsic
<1, >1
<10, >20
> 40, >20
> 8, <3
> 1.018, <1.015
> 500, <300
> 20, <10-15
<1, >1
Hyaline casts, muddy brown granular casts
Dialysis
ESRD-depends on patients symptoms, comorbid conditions and laboratory parameters, unless a living donor is identified, transplantation is deferred by necessity, due to the scarcity of decreased donor organs . Dialysis options include hemodialysis and peritoneal dialysis. Roughly 85% of US patients are started on hemodialysis. Absolute indications for dialysis include severe volume overload refractory to diuretic agents, severe hyperkalemia and/or acidosis, severe encephalopathy not. Otherwise explained, and pericarditis or other serositis. Additional indications for dialysis include symptomatic uremia, nause, vomiting , pruritis, difficulty maintains attention and concentration. And protein every malnutrition failure to thrive without other overt cause.
Complications of hemodialysis
Hypotension Accelerated vascular disease Rapid loss of residual renal function Access thrombosis Access or Cather sepsis
Dialysis related amyloidosis
Protein energy malnutrition
Hemorrhage
Anaphylactic reaction
Thrombocytopeniab
Hemodialysis
Direct access to the circulation, either via a native arteriovenous fistula; an arteriovenous graft, usually make of polytetra fluoriethylele; a large bore IV catherter , or a subcutaneous device
Solution in dialysis
Isotonic, free of urea and other nitrogenous compounds and generally low in K a
Dialysate (K) is varied from 1 to 4 , depending on predialysis K and clinical setting
Ca is typically and Na can be modified , depending on clinical
Usually 3 times a week for 3-4 hours
Peritoneal dialysis
Peritoneal catheter allows infusion of a dialysate solution into the abdominal cavity; this allows transfer of solutes across the peritoneal membrane, which serves as the artificial kidney, this solution is similar to that used for hemodialysis, except that is must be sterile
LO
Differentiate between uncomplicated UTI and complicated
Develop a differential diagnosis for dysuria based on pre disposing factors, clinical presentation, history and physical
Distinguish cystitis from pyelonephritis and their predisposing factors
Compare and contrast pyelonephritis with sepsis
35 male with dysuria for three days, urine is cloudy and yellow
There is drainage noted from end of penis
Multiple female partners with occasional condom use
Ok
Frequency
Every hour or two
Urgency
Abrupt strong and overwhelming
How frond ABU
Urine sample is obtained for another reason and shows bacteria on microscopic evaluation , like health screening or diabetes follow up
What is an uncomplicated UTI
Non pregnant female
No anatomical abnormalities
No instrumentation or urinary tract
Predisposing factors for female UTI
Use of spermicide with diaphragm
Frequent sex
What percent of women have recurrent UIT
20-30%
Recurrent of UTI in post menopausal females predisposing factors
Pre menopausal UTI
Anatomic factors affecting bladder emptying
- cystocele
- urinary incontinence
- residual urine
- tissue effect of estrogen depletion
Predisposing factors for male UTI
Prostatic hypertrophy
Non circumcised
Diabetic
Diabetic women are _x more likely to get UIT
2-3
Differential diagnosis for UTI
Cystitis
Cervicitis
- chlamydia
- neisseria
Vaginitis
- candida
- trichomonas
Urethritis-herpetic
Interstitial cystitis
Non infectious vaginal or vulvar irritation
Complicated UTI
Pregnant female-can lead to premature labor or low birth weight babies
More likely to develop sepsis
Untreated asymptomatic bacteriuria is more likely to cause what in pregnant women
Symptomatic pyelonephritis
Causes of complicated UTI in men and women
Anatomic variant (polycystic kidney
Foreign body in the urinary tract
-stones, urinary catheters, nephrostomy tubes/ureteral stents
Extrinsic compression of ureter/bladder
- tumors
- profound constipation
- other anomalies
Immune suppression conditions
- diabetes
- drugs induced
- HIV/AIDS
Prostatis
Can be chronic in prostatic hypertrophy
Prolonged antibiotic course necessary for 4-6 weeks
Most common precursors of pyelonephritis
Same as UTI
-since most commonly ascending from lower tract
Bacteremia develops in 20-30% of cases
Can be hematogenous but rare
- candida
- salmonella
- staph aureus
Three major subtypes/complications of pyelonephritis
Papillary necrosis
Emphysematous pyelonephritis
Xanthogranulomatous pyelonephritis
When does papillary necrosis occur
Obstruction
Diabetes
Sickle cell
Analgesic nephropathy
Emphysematous pyelonephritis
Production of gas in nephrin and perinephric area
Occurs almost exclusively in diabetic patients
Xanthogranulomatous pyelonephritis
Chronic obstruction
Chronic infections
Causes suppurative destruction of renal tissue
Can lead to abscess formation
Bacteremia
Blood cultures are positive
Sepsis/septicemia
Suspected or documented infection and an acute increase in organ failure
Dysregulated host response to infection
Septic shock
Progressive organ dysfunction leading to marked increase in mortality
- suspect of sepsis
- serum lactate greater than 2mmol/L (18 mg/dL)
When does acute ischemia occur
Defect in effective circulating volume
- decreased oxygen delivery
- impaired removal of cellular waste
- kidney receives 20-25% of CO
Couple whammy: direct tubular damage by endotoxins and inflammatory cytokines
Sepsis
Multiorgan involvement in infection removed from the source
Hypofunction of uninflected organs
Septic shock; hypotension that cannot be reversed with infusion of fluids
Shock: hypoperfusion regardless
Tachycardia
Hypotension
Tachypnea
Hypothermia/fever
Low oxygen-> celllular injury->inflammatory mediators-> worsening microvascular circulation
What history when shock
Trauma, recent surgery, signs of illness/infection
Three flow charts
Signs of inf
Septic shock signs
Infection sign: fever or hypothermia
Tachycardia: cardiac response to hypoperfusion and fever
Tachypnea: compensatory respiratory response
Hypotension!: sign of critical illness, responsive to fluid resuscitation
-how can you identify the source of infection
Circulating cytokines
Endothelial injury: decreased tone, increased permeability
Edema
Decreased oxygenation of tissues
Build up of lactic acid
Initiating treatment for sepsis/septic shock
Volume resuscitation (IV fluids)
Cultures: blood, urine, CSF,
Initiate antibiotics for most likely cause; generally broad spectrum
Pressers: norepinephrine, vasopressin, in addition for severe cases
Correct acid/base imbalance-fluids oxygenation(ventilator support)
Monitor electrolytes
Which is most important for treating sepsis/septic shock
Getting cultures or getting x ray lab results?
BUN :Cr sepsis and ischemia
Increase
-pre renal azotemia
FENa sepsis and ischemia
> 1%
Urine sepsis and ischemia
Decreased concentration
Proteinuria (minor)
Hematuria
Muddy brown casts on microscopy-sloughing of renal tubular epithelial. Cells
Prevent recurrent UTI: do it when they are interfering with patients lifestyle
Antibiotic therapy-continuous, post coital, patient initiated
Non medication preventative strategies for women
Empty bladder as soon as reasonable after intercourse
Wipe front to back
Shower not baths
Lactobacillus probiotics
Cranberry supplements
Vitamin c
Increase fluid intake!
Treat febrile UTI sepsis
Stabilize, resuscitate, treat with culture specific antibiotics for 2 weeks
Treat febrile UTI pyelonephritis
Treat with culture specific antibiotics 2 weeks
Treat non febrile UTI
Culture specific antibiotics 1 week
LO
Distinguish types of proteinuria and nephrotic syndrome
Develop a differential diagnosis for proteinuria based on pre disposing factors, clinical presentation, history and physical
Evaluate nephrotic range proteinuria
Recommend screening for proteinuria in patients with DM based on guidelines
Determine diagnostic approach for proteinuria
Discuss treatment strategies for diabetic nephropathy to prevent deterioration of renal function
Routine dipstick
Teststrip threshold is to turn positive for over 300 mg of albumen
Multiple types of proteins possible and multiple underlying causes
Quantify protein
Albumen Cr ratio
Can be done on random urine sample
Preferably first morning void
OR 24 hour urine collection-protein, albumen, Cr clearance
-also provides sample to do electrophoresis to determine which types of protein
Next step
Based on differential
DDx derived from thorough history and PE
Nephrotic range proteinuria vs nephrotic syndrome
Nephrotic syndrome-nephrotic range proteinuria, hyperlipidemia, hypoalbuminemia, edema
Screening recommendations
T2DM
-established diagnosisL annual ACR (albumen/Cr ratio)
Slow progression of proteinuria
Drug classes-ace inhibitors, arbs
Other possible causes of nephrotic syndrome
SLE, rheumatoid arthritis
Infection
0hepBC, HIV, syphilis, TB
Hematologists/oncologist
-amyloidosis, multiple myeloma, sickle cell, liquid and solid tumors
Drugs-NSAIDS, lithium, IV heroin
Routine dipstick
Teststrip threshold is to turn positive for over 300 mg of albumin
Multiple types of proteins possible and multiple underlying causes
Case 2
Ok
Exercise induced hematuria
50-80% of athletes
May also be accompanied by proteinuria
What does heavy exercise cause
Proteinuria
Decreased RBF leads to nephron ischemia, increased permeability , and subsequent passage of RBC
Who gets exercise issues
Swimmers, track, lacrosse
___ are common among athletes and another cause of microscopic hematuris
NSAIDS
Evaluate heavy exercise
Rule out infection
Treat heavy exercise
48-72 hours and recheck
NSAIDS how do they damage kidney
Inhibiting cyclooxygenase within the kidney
- cyclooxygenase is the rate limiting enzyme for prostaglandins
- PGE2 and PGI2 protect kidney by modulating renal vasoconstriction
Ibuprofen decreases GFR compared to placebo or acetaminophen
Indomethacin and celecoxib decreases free water clearance
Menstruation
Sloughingsee blood
History will help
Rule out infection
False positive dipstick
35%
UA false positives
Clean catch, mid strea,
-this eliminates urethral irritation and contamination from perineum
What else can give false positive
Myoglobinuria, hemoglobinuria
High alkaline (pH>9)
Ascorbic acid
How deal with false positives
Confirm with microscopy
Less than 3 RBBC/Hpv is negative for hematuria
Trauma of kidney common?
No due to location
What can traumatize the kidney
Blunt force, rapid deceleration
Who gets exercise issues
Swimmers, track, lacrosse
___ are common among athletes and another cause of microscopic hematuris
NSAIDS
Evaluate heavy exercise
Rule out infection
Treat heavy exercise
48-72 hours and recheck
NSAIDS how do they damage kidney
Inhibiting cyclooxygenase within the kidney
- cyclooxygenase is the rate limiting enzyme for prostaglandins
- PGE2 and PGI2 protect kidney by modulating renal vasoconstriction
Ibuprofen decreases GFR compared to placebo or acetaminophen
Indomethacin and celecoxib decreases free water clearance
Menstruation
Sloughingsee blood
History will help
Rule out infection
False positive dipstick
35%
UA false positives
Clean catch, mid strea,
-this eliminates urethral irritation and contamination from perineum
What else can give false positive
Myoglobinuria, hemoglobinuria
High alkaline (pH>9)
Ascorbic acid
How deal with false positives
Confirm with microscopy
Less than 3 RBBC/Hpv is negative for hematuria
Trauma of kidney common?
No due to location
What can traumatize the kidney
Blunt force, rapid deceleration
How does renal trauma present
Hematuria
(But lack doesn’t exclude)
Evidence of rib fracture
Guided on suspicion
Radiographically evaluation kidney trauma
Not if hemodynamically stable
Sickle cell screening
At birth
History is often lost, forgotten
Single hemoglobin S mutation
What does sickle cell cause
Impaired urinary concentration
Can develop renal papillary necrosis
Hyperfiltration elads to albuminuria, interstitial fibrosis, decreased number of nephrons
RENAL MEDULLARY CARCINOMA
Males at risk for transitional cell and bladder cancer
Males >35 Current or past smoker Analgesic Exposure to chemicals or dyes Exposure to carcinogenic agents or chemo
Other history of cancer
Gross hematuria Urologic disorder or disease Irritation voiding symptoms -what does this mean? Pelvic irradiation Chronic urinary tract infection chronic indwelling
Diagnosis of BHP should not preclude further evaluation of underlying cause
Huh
How evaluate malignancy
Know risk
Rule out infection with culture and sensitivity
Confirm with microscopy
Serum BUN Cr
Radiographically
US VC CTU
US
No radiation
Low cost
May miss other causes of hematuria: small stones, small bladder mass and urothelial transitional cell carcinoma
Very good for tumors >3cm, cysts, and hydronephrosis
CTU
CT or kidney, ureters, and bladder
With or without contrast
Sensitive for renal calculi!
Able to detect small renal parenchymal masses, aneurysm, and renal and perirenal abscesses
Higher radiation
Exposure to contrast agents
Higher cost
More info
Cytoscope
Evaluate bladder by direct visualization
Better assessment of bladder wall for microstructiral changes
Can identify urethral stricture disease, BHP and bladder masses
Invasive, requires sedation, risk for UTI
Recommendations for cytoscopy
Vary
Primary care: after negative US or IVP
AUA: all patients >35 with asymptomatic microhematuria
Or all patients with risk factors for urologic malignancies regardless of age
Chronic glomerulonephritis
Glomerular scarring
Corticular tubular atrophy
Interstitial inflammation
Interstitial fibrosis
Atherosclerosis
Vascular/ hemodynamics effect of RAAS
Vasoconstriction of affferent and efferent and systemic arterioles
Increases glomerular pressures
Causes direct glomerular damage
Inflammatory effects of RAAS
Activated inflammatory system
Leads to interstitial and tubular fibrosisi
Glomerulonephritis
Hematuria
-microscopic vs gross
Proteinuria
-albumineria vs protein
Acute vs chronic
How tell acute vs chronic glomerulonephritis
HISTORY
Genetic disorders, systemic disease
Family history of lupus, sickles cell, autoimmune, diabetes, coronary artery
Recent infectionsL staph, malaria, schistomiasis
Infection HIC hep BC
ROS-itching, nausea, headache, anorexia, dyspnea, vomiting, diarrhea, hiccup, restlessness and depression
UA and chemistry
US-for size
Size of kidney in chronic disease
Smaller
Hematuria glomerulonephritis
Asymptomatic can be 3-5 RBC
RBC casts or dystrophic
Gross hematuria in sickle or IgA nephropathy
Always get UA with microscopy to verify findings
Culture and sensitivity to rule out infection
Microscopic hematuria needs to be differentiated from anatomic lesions-BPH, tumors, stones
Pyruvate in inflammatory glomerulonephritis and should be differentiations from UTI
Acanthocytes
Contracted, dense irregular
Dystrophic
Mickey Mouse
RBC have lost typical disc shape indicating what
Moved through nephron not just the Collecting system
Proteinuria sustained
1-2 g/24 h
Symptoms of edema and foamy urine
Benign proteinuria
Functional or transient
<1-2 g/24 hours
Fever, exercise, obesity, sleep apnea, emotional stress and CHF
Orthostatic proteinuria-only occurs with standing
24 hours albumin in normal, microalbuminuria and proteinuria
8-10
30-300
> 300
Albumin/creatinine ratio
Normal, microalbuminuria, proteinuria
<30
30-300
>300
Dipstick microalbuminuria proteinuria
+1
+3
24 hour protein normal proteinuria
<150
>150
Send for UA with microscopic evaluation
+15 dystrophic RBC
Return to office
Review BP log
Initiate antihypertensice-low fat sodium diet
Diabetic protocol
What is the mechanism of damage in hypertensive nephropathy
Ok
Hypertensive nephrosclerosis
Five times more common in black
APOL1 increased risk in black
Other risk of hypertensive nephrosclerosis
Smoking, male, hyerclorestelemia, HTN, low birth weight and preexisting renal injury
Signs hypertensive nephrosclerosis
HTN, microhematuria and moderate proteinura
Why blood pressure control with hypertensive nephrosclerosis
Delays progression to end stage renal
Diabetic nephropathy
Damage related to extracellular matrix accumulating in both GBM and tubular BM
Imbalance between synthesis and degradation of the ECM causes expansion of mesangial
The glomerular filtration surface is decreased by the reduced glomerular luminal space with leads to the reduction in GFR
Type 1 glomerular, tubular, interstitial and vascular lesions tend to progress more or less in parallel and independent of albuminuria
Type 2 variable in progression and can develop albuminuria with little change to the nephron
Both present how
Clinically stable. Edema and worsening HTN are late findings
What can traumatize the kidney
Blunt force, rapid deceleration
How does renal trauma present
Hematuria
(But lack doesn’t exclude)
Evidence of rib fracture
Guided on suspicion
Radiographically evaluation kidney trauma
Not if hemodynamically stable
Sickle cell screening
At birth
History is often lost, forgotten
Single hemoglobin S mutation
What does sickle cell cause
Impaired urinary concentration
Can develop renal papillary necrosis
Hyperfiltration elads to albuminuria, interstitial fibrosis, decreased number of nephrons
RENAL MEDULLARY CARCINOMA
Males at risk for transitional cell and bladder cancer
Males >35 Current or past smoker Analgesic Exposure to chemicals or dyes Exposure to carcinogenic agents or chemo
Other history of cancer
Gross hematuria Urologic disorder or disease Irritation voiding symptoms -what does this mean? Pelvic irradiation Chronic urinary tract infection chronic indwelling
Diagnosis of BHP should not preclude further evaluation of underlying cause
Huh
How evaluate malignancy
Know risk
Rule out infection with culture and sensitivity
Confirm with microscopy
Serum BUN Cr
Radiographically
US VC CTU
US
No radiation
Low cost
May miss other causes of hematuria: small stones, small bladder mass and urothelial transitional cell carcinoma
Very good for tumors >3cm, cysts, and hydronephrosis
CTU
CT or kidney, ureters, and bladder
With or without contrast
Sensitive for renal calculi!
Able to detect small renal parenchymal masses, aneurysm, and renal and perirenal abscesses
Higher radiation
Exposure to contrast agents
Higher cost
More info
Cytoscope
Evaluate bladder by direct visualization
Better assessment of bladder wall for microstructiral changes
Can identify urethral stricture disease, BHP and bladder masses
Invasive, requires sedation, risk for UTI
Recommendations for cytoscopy
Vary
Primary care: after negative US or IVP
AUA: all patients >35 with asymptomatic microhematuria
Or all patients with risk factors for urologic malignancies regardless of age
Chronic glomerulonephritis
Glomerular scarring
Corticular tubular atrophy
Interstitial inflammation
Interstitial fibrosis
Atherosclerosis
Both present how
Clinically stable. Edema and worsening HTN are late findings
Type 1 glomerular, tubular, interstitial and vascular lesions tend to progress more or less in parallel and independent of albuminuria
Type 2 variable in progression and can develop albuminuria with little change to the nephron
Diabetic nephropathy
Damage related to extracellular matrix accumulating in both GBM and tubular BM
Imbalance between synthesis and degradation of the ECM causes expansion of mesangial
The glomerular filtration surface is decreased by the reduced glomerular luminal space with leads to the reduction in GFR
Why blood pressure control with hypertensive nephrosclerosis
Delays progression to end stage renal
Signs hypertensive nephrosclerosis
HTN, microhematuria and moderate proteinura
Other risk of hypertensive nephrosclerosis
Smoking, male, hyerclorestelemia, HTN, low birth weight and preexisting renal injury
Hypertensive nephrosclerosis
Five times more common in black
APOL1 increased risk in black
What is the mechanism of damage in hypertensive nephropathy
Ok
Return to office
Review BP log
Initiate antihypertensice-low fat sodium diet
Diabetic protocol
Send for UA with microscopic evaluation
+15 dystrophic RBC
24 hour protein normal proteinuria
<150
>150
Dipstick microalbuminuria proteinuria
+1
+3
Albumin/creatinine ratio
Normal, microalbuminuria, proteinuria
<30
30-300
>300
24 hours albumin in normal, microalbuminuria and proteinuria
8-10
30-300
> 300
Benign proteinuria
Functional or transient
<1-2 g/24 hours
Fever, exercise, obesity, sleep apnea, emotional stress and CHF
Orthostatic proteinuria-only occurs with standing
Proteinuria sustained
1-2 g/24 h
Symptoms of edema and foamy urine
RBC have lost typical disc shape indicating what
Moved through nephron not just the Collecting system
Dystrophic
Mickey Mouse
Acanthocytes
Contracted, dense irregular
Hematuria glomerulonephritis
Asymptomatic can be 3-5 RBC
RBC casts or dystrophic
Gross hematuria in sickle or IgA nephropathy
Always get UA with microscopy to verify findings
Culture and sensitivity to rule out infection
Microscopic hematuria needs to be differentiated from anatomic lesions-BPH, tumors, stones
Pyruvate in inflammatory glomerulonephritis and should be differentiations from UTI
Size of kidney in chronic disease
Smaller
How tell acute vs chronic glomerulonephritis
HISTORY
Genetic disorders, systemic disease
Family history of lupus, sickles cell, autoimmune, diabetes, coronary artery
Recent infectionsL staph, malaria, schistomiasis
Infection HIC hep BC
ROS-itching, nausea, headache, anorexia, dyspnea, vomiting, diarrhea, hiccup, restlessness and depression
UA and chemistry
US-for size
Glomerulonephritis
Hematuria
-microscopic vs gross
Proteinuria
-albumineria vs protein
Acute vs chronic
Inflammatory effects of RAAS
Activated inflammatory system
Leads to interstitial and tubular fibrosisi
Vascular/ hemodynamics effect of RAAS
Vasoconstriction of affferent and efferent and systemic arterioles
Increases glomerular pressures
Causes direct glomerular damage
Issue with kidney
Effects every part in the body
Hyperfiltration
Kidneys beat themselves up when not functioning
Usually starts with AKI-damage to nephrons-problem linked to how quickly you turn around and co morbididies
What happens with hyperfiltration
Sclerosis, damage to nephron, lose function,
RAAS
Originally protective
Then damaging
How RAAS hurt
Build up in kidney with chronic kidney disease
Most common disease to cause kidney damage
Diabetes then HTN
Acute injury renal injury/failure related to what
Rise in Cr
Normal GFR
90, 100
Stage 2 AKI
GFR 60-89
Stage 3
30-59
Stage 5
Less than 15 for GFR
Stage 2
HTN that starts to get harder to control,
Stage 3
Increase Parathyroid hormone (doesn’t get filtered out) Bone effects (calcium, P, Mg)
Stage 4
Acidosis
Changes in K
Stage 5
Uremic syndrome
Na
Decrease Na excretion in dysfunctional kidney, making more water hang around, goes into third spaces (non vascular non cellular)->dependent edema easrly(becomes systemic later on)
Why will Na labs be in normal range
Bc extra water
Use diuretics
K
Doesn’t change a lot till late stages unless high intake or start pharmacologically getting rid of it (loop diuretics)
RAAS system
How one increase K
Foods-sweet potato
Acidosis
Once start losing functional nephrons (LOSS OF NEPHRONS IS PROBLEM) bc related to ammonia production
Initially hyperchloremia acidosis NAGMA at gfr 40
Then HAGMA bc of retained organic anions—— GFR 15 20 HAGMA
Late stages kidney disease
Catabolic state
Get sicker and sicker
*acidosis of kidney-inadequate ammonium production
Signs of uremia
Fatigue, anorexia, vomiting, hiccup, metallic taste
Hwy?changes in hormone an electrolytes
Chronic inflammation-
Really sick-effect bone, blood skin -effects everything
Late stage 3 changes uremia
Decreased P excretion, PTH and growth of parathyroid, D3 down, all effecting bone!
Hyper parathyroid-muscle weakness and fatigue, malaise, low energy
High turn over-fibrosis cystica-bone cysts, soft bones more likely to break (not recycling)
Without bone turnover
Lots of mineralization defects
Symptoms chronic kidney
HyperP?
HypoCa
HypoVD
Secondary hyperparathyroidism
Loss of nephron mass
Triggers cascade
Some decreased renal biosynthesis-vitamin D
Decreased VD-hypoCa (gut function)
Hyper P changes in excretion
Hyper P
Capture Ca so get P Ca complex and deposit in soft tissue
PTH keeps goes up
Parathyroid
Cardiac muscle fibrosis
Changes in flow bc CO
P up Ca down treat
Exogenous VD
Do people die of renal failure
No atherosclerosis changes in heart kill them
All related to inflammatory state
Patient with chronic renal disease
Cholesterol levels, have a better lifestyle , lose weight
Symptoms uremia
Fatigue, decreased appetite, malaise
CAREFULLY MANAGE
Anemia AKI
Associated with changes in EPO or bone marrow fibrosis
Dysfunctional platelets and decreased immune function
Normochronmic normocitic anemia how long do the red cells live
Not as long
Neocytolysis
Changing and destroying red cells
Anemia leads to what symptoms
Fatigue, decreased exercise tolerance, decrease cognition, heart hypertrophy(but parathyroid making it fibrose)
Can we replace EPO
Yup increase red cell count
Neuromuscular changes AKI when
Drop to 30-44
Effects neuromuscular
Cramping hicccups
Neuropathy lower extremities first more sensory then becomes motor
GI effects AKI
Uremic fetter-urine breath
Gastricis PUD Don’t want to eat Vomit Constipation
Catabolic state-
Treat AKI
Protein restriction Na restict——-but become calorie depleted
Insulin AKI
Increased plasma cells-largely excreted by kidney so if around longer prob
AKI testosterone and estrogen
Young woman-decreased estrogen and problems bearing children, irregular menstrual cycles, on top of bone disease
Kid CKI
Growth retardation failure to thrive
Skin changes
Hyperpigmentation
Pigments not filtering out
Will look spray on tanned-skin gets itchy as P up
Why chronic itching
P up
Treat AKI
Monitor BP
ACE and ARB(we have dysfunctional RAAS)
Monitor volume, volume can be measured in a lot of ways
-daily weight check
Na restrict-canned food
Avoid nephrotoxicity drug-anti inflammatory-IBUEPROFIN AND ALEVE EFFECT KIDNEY BC DONT FEEL WELL AND MORE TAKE MORE DAMAGE DO
Gentamycin
Contrast agents-CT skan? Catch lab? Iodine based bad
When a person gets to stage 4
Send to nephrologist GFR less than 30
Nephrolegist on board
Build relationship between attention and nephrologist bc if continue to more forward and need transplant and dialysis-
Dialysis types
Emergent-if no urine, can be short term-port in neck, can be used temporality maybe week or 2 at most
Peritoneal-uses abdominal cavity and lining as membrane-insert hyperosmolar solution with large amount of glucose or sugar creating osmotic gradient to pull solvents across and some albumin comes -leave till become steady state then flush it out
Complications peritoneal dialysis
Hernia
Avenue for infection
Can do at bedtime at night get flow then excreted in morning
Can do hourly
Not as reliable and failure rates are high-omentum can sclerosing and cause obstruction of GI
Solution is sugar so diabetic need to adjust insulin
Sclerosing encapsulating peritonitis
Peritoneal dialysis
External hemodialysis
Fistula in forearm join an artery and vein they will vibrate bc of change in pressure-palpable thrill
Blood out run though so solute move across membrane taking 4-6 hours then back in
Transplant list
Can’t have active malignancy, infection, CV and pulmonary evaluation
If any other underlying disease move further and further down on list
As kidney fail the ___
Shrink
How do transplant
Put kidney low in abdomen connect o iliac artery and create a ureter.
GFR 30
Send to nephrology
GFR15 or less
Dialysis transplant
Pediatric renal topics
Ok
Kids with HTN
End organ damage
Kidney
Normal BP in kid
Less than 90th percentile
When start check bp in kid
3
Unless risk factor-premature, known renal disease