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
How many times have to do bp to say someone is htn
Blood pressure over 90th percentile at three different visits
Primary vs secondary
Systolic high
Systolic and diastolic high
White coat
Up, from stress of doctor
Measure bp outside of clinical settting is important
Ambulatory measure
Good
Diastolic
Sound disappear
If found never goes away use 4th
Ok
ECG good enough to say if there is left ventricular hypertrophy
Establishment of cronicity of high bp!!!!!!
Too small
High bp
Too big
Low bp
Hematuria
3-5 RBC per high power field (microscopic)
How many blood cells to turn urine red
A ton hundreds of thousands
Urine dipstick positive for blood
Myoglobin, hemoglobin (need to determine which? Rhabdo-myoglobin is devastating to the kidneys-happens a lot in army bases get rhabdoid and get liters of IV fluid to keep kidney working)
Does positive dipstick tell you if RBC in urine in tact
No
Need to do microscopy
-
Color urine babies
Uric acid crystals-red brick colorjust hydration will make it go away
Bilirubin
If want to confirm blood of urine is from blood
Look under microscope
Glomerular bleeding
RBC dysmorphic
Bleeding along urinary tract
More normal appearing
Blood in urine
Is there protein? Protein with blood is diagnostic for…
Post strep glomerulonephritis kids
Edema, urine dark, gross hematuria, elevated ASO, serum compliment low (used up in immune complex forming)
Lupus
Glomerulonephritis
Most common cause of glomerulonephritis in lupus
MPGN
Henoch schonlein purpura
Bruise then come in with lots of them
- usually after viral(cold)
- immune complex vasculitis, IgA
- gross hematuria
- ab pain
- intestinal vasculature
- really sick
Every kid with henoch
Blood in urine
If blood and protein-SIGNIFICANT-progress to end stage renal failure
We know blood there, but if protein then nephrologist involved
Rarely kids with asymptomatic isolated hematuria
Have prob
Usually goes away
But monitor for protein and and htn
UTI kids
Same signs and symptoms BUT cant tell you anything, if not potty trained harder
Fever and cant find source of infection
Always urine in kids espicially if non verbal
Best way to get urine sample from kids
Catheter or suprapubic tap-used in neonates(rarely newborns or young infants)
Bag urine-negative fine , but if positive cant send bag in for culture bc contaminants, so gotta do catheter or suprapubic tap
Urine nitrate testing on dipstick
Some bacteria change nitrates to nitrites
So positive nitrites indicative of bacteria present
Most common bacterial pathogen for kid UTI
E. coli
Treat
Cephalosporin is standard
If too sick use parenteral or IV or shot
When image kid urinary tract
After first UTI in boys
Get renal and bladder US
And VCUG
Girls-first UTI both renal US and renal UCVG if symptoms of chronic renal disease or HTN ….
weird pathogen
Second or third if no other symptoms of renal disease
AKI
Onset days increase in serum Cr
Volume of output decreases
What can alter serum Cr
Age
-less muscle mass
, sex, race, muscle mass, catabolic rate
AKI prognosis
50% mortality
Acute non chronic
Obtain the most recent serum cr
Pre renal
Affects kidney
How it originates
Dehydration, fluid shift into different place in body from heart or liver problems, NSAIDS,
Intrinsic
Renala glomerular, tubulointerstitial/interstitial
Vascular-vascultis/rheumatologist, malignant HTN, TTP HUS
Tubulointerstitial causes
Ischemia Sepsis/infection Exogenous nephrotoxicity -iodinated contrast -aminoglycosides, amphotericin B, cisplastin, PPI, NSAIDS
OTC PPI, NSAIDS
Make sure know herbal, vitamin
Endogenous nephrotoxicity
Hemolysis, rhabdomyolysis (myoglobin), myeloma, intratubular crystals
Flu, running
Rhabdomyolysis
Dipstick rhabdomyolysis
Positive blood, but its not blood-its myoglobin! Make sure get microscopic.
Myeloma
Tylenol 3 lots post phoned diagnose cancer
-
Post renal AKI
Bladder outlet obstruction
Bilateral pelvoureteral obstruction
History
all medications
Toxins-work/home
-lead,
PMH/PSH?ROS
Physical signs AKI
Dehydration, ascites, jaundice, fluid in lungs
What order
Serum na and cr
Urine na and cr
Why order serum and urine na and cr
FENa.
When order UA with micro
Don’t get Cr and Na
Need BMP and urine specified Na and Cr
For pre post or intrinsic important o order
For AKI why use K and Cl
Anion gap
Hemoglobin and hematocrit CBC, platelet count
Need may be changes
Coagulation time
PT TPP
May lead to liver problem if have ascites
If have to do procedures or biopsy if put in dialysis catheter need to know
Ekg
See if k problem going on
Treat presok
Ok
Night before fulllness suprapubically size of golf ball no fever
Flocked fluids
Routing dipstick
Positive if 300 mg of albumin
Multiple types of protein though and multiple underlying causes
Negative dipstick
Doesn’t mean have no albumin
UA
Get dipstick
UA and micro
Dipstick and microscopic evaluation-casts, cells, bacteria
Next step
Quantify
ACR-albumin/Cr ration
Spot urine
Random urine sample
Best urine
First morning , bc false negative increases as patient takes in more fluid
24 hour urine
Protein, albumin, Cr clearance
Sample that need for electrophoresis-tell what type of protein , has to be on 24 hours urine
Issue with 24 hour urine
Lot of urine
Containers to store
Arthritis in hands
Store on ice
Other possible next steps
Based on differential
DDX derived from thorough history and PE
Blood test
Albumin eleven
Chemistry panel
Electrolytes, lipid(must specify), blood sugar
Blood count CBC
Hemoglobin hematocrit
If have protein in urine -kidney primary MCD or a secondary cause (anemic and chronic disease)
Platelets
What systemic disease effect the kidney
Lupus Rheumatologist disorders -ANA for possible lupus -CHF look at CMP -chest x ray see if fluid in pulmonary
Not having these symptoms yet still check
Syndrome
Constellation of problems
Nephrotic range proteinuria
Large amount of protein 3.5 g/3500 mg
Negative dipstick
Doesn’t mean have no albumin
UA
Get dipstick
UA and micro
Dipstick and microscopic evaluation-casts, cells, bacteria
Next step
Quantify
ACR-albumin/Cr ration
Spot urine
Random urine sample
Best urine
First morning , bc false negative increases as patient takes in more fluid
24 hour urine
Protein, albumin, Cr clearance
Sample that need for electrophoresis-tell what type of protein , has to be on 24 hours urine
Issue with 24 hour urine
Lot of urine
Containers to store
Arthritis in hands
Store on ice
Other possible next steps
Based on differential
DDX derived from thorough history and PE
Blood test
Albumin eleven
Chemistry panel
Electrolytes, lipid(must specify), blood sugar
Blood count CBC
Hemoglobin hematocrit
If have protein in urine -kidney primary MCD or a secondary cause (anemic and chronic disease)
Platelets
What systemic disease effect the kidney
Lupus Rheumatologist disorders -ANA for possible lupus -CHF look at CMP -chest x ray see if fluid in pulmonary
Not having these symptoms yet still check
Syndrome
Constellation of problems
Nephrotic range proteinuria
Large amount of protein 3.5 g
Nephrotic syndrome
Need proteinuria
Hyperlipidemia-fasting cholesterol/lipids
Hypoalbuminemia
Edema
63 yo male polyuria polydipsia (drinking a lot) and facial swelling for 3 months.
Anytime patient thirsty or urinating a lot
-tip off for diabetes (losing sugar and fluid-osmotic diuretic)
What is DM associated with
Nephrotic syndrome-may cause it
Hypoalbuminemia
Why low albumin in blood stream and spilling protein in urine cause swelling
Lose colloid osmotic so leak out interstitial then think low so raas
DM with edem
Most likely effecting kidney
Drug decrease proteinuria
ACE ARB
Type II DM
Annual ACR (albumen/Cr ratio)
lupus and rheumatoid arthritis and nephrotic syndrome
Ok
Infection nephrotic
Hep BC-cryoglobinuremia
HIV
Syphilis
Tuberculosis
HIV
Focal segmental glomerulosclerisus
Hematologic/oncologist cause of nephrotic
Amyloidosis
Multiple myeloma
Sickle cell
Liquid and solid tumors
Drugs cause nephrotic
NSAIDS
Lithium
IV heroin
72 year old male severe back pain for year. Works a small farm. No specific identifiable injury. He works in hostpital. Couple different physician give pain pill on separate occasion, not aware of other. Tylenol 3.
Hazards of opoids. Codeine is controlled. Any prescription should be done with caution.
They didn’t do PE, no chart, they just gave him pills.
Huge risk to patient and postponed care
What else might patient take with this constellation
NSAIDS twice the recommended
Effect
Proteinuria
-as did evaluation, did 24 hour urine to quantify and get protein electrophoresis bc his age group prone to multiple myeloma-he has indirectly transposed treatment to malignancy
AAFP article on hematuria in adult
Ok
22 yo male going to do triathlon needs physical before . Runs and does weight. He has 1+ blood
Hematuria in athletics
Heavy exercise induce hematuria in 80% of athletes and may have proteinuria
Why
Exercising heavily, get renal ischemia for short periods of time. Result in red cells in urine. More common in swimmers, track, and lacrosse.
Athletes have pains
Take NSAIDS
Also can cause hematuria
Take home message
Occult hematuria always get a microscopy and a culture and sensitivity
Then re check
Why need microscopy
See where cellls come from
NSAIDS
Inhibit COX in kidney ibueprofin bigger offender than acetaminophen
In drug classes have variation
Net effect of renal ischemia activates RAAS*** vasoconstriction
RAAS from NSAID
Up up vasoconstrict
26 yo female ab paina fter meal better if eat tums
UA-2+ blood
Menstruation give false positive up to 24 hours realize starting mesntral cycle and can persist for several days after
Need UA epigastric pain? No
Dipstick false positive
Up to 35% false positive
UA how collect
Mid stream mid catch, wash urethra this eliminates debris around urethra that would give false information
Myoglobin in urin
Give heme positive result false positive in dipstick
Ph>9 urine, certain types of proteus infection get
False positive
Vitamin C false positive
Can give false positive in cold a flu season can get this
What is hematuria
3 RBC per high powered field
19 yo male presents with blood in urine. Plays football was struck from right and has bruise since then urine darker than usual but has continued to play foot ball 1+ blood 2+ urobilinogen
Kidney protected can just observe these patients and re check in 48 to 72 hours.
Need US depending on history and physical
Falls and rapid deceleration injuries hurt kidney?
If they are hemodynamics stable do not need a US or CT to look at kidney
Ok
22 yo african American male need veal so can play college basketball . Exam normal. 6’7
2+ blood
Sickle cell trait
Sickle cell trait
Infants screened at birth
If not causing problem then, don’t worry
Can get renal papillary necrosis and get focal segmental glomerulonephropsis-RENAL MEDULLARY CARCINOMA
What cancer worry about with sickle cell trait
Renal medullary carcinoma
What do
Send for UA and culture and sensitivity
55 yo male comes for refill bp meds. Former smoker quick when given high BP 1+ blood . UA neg for blood and protein a year ago
Probably cancer related to smoking
Number one risk for bladder cancer
Smoking
Other question
How much NSAIDS
Other exposures
Gross hematuria painless
CANCER until proven otherwise
Irritation voiding symptoms with hematuria
Dysuria, urgency, frequency
Tips balance away from cancer-
What could have
Catheter, chronic UTI, pelvic irritation, schistosomiasis
Blood with urine
Also microscopy and culture and sensitivity and
Get BUN, Cr serum eval
Radiographically?
US
No radiation cheaper
Less sensitive for smalls tones, small bladder mass, good for hydronephrosis!!!
CTU
2 phase radiographically test sensitive for renal calculi bc done in two phases
Expensive , radiation,
CTU. Work
1st scan wo contrast second with
Cytoscopy
Direct visualization if sure its a lower GU how we go in to get renal stones
If stone can get with basket , can get biopsy, can cauterize active bleeding, it is invasive (risk UTI and different thought)
US or IVP negative
Can go straight to cystoscopy
RBC gone through glomerulus
Dysmorphic
Rbc from down
Looks fine
Chronic glomerulonephritis
Scarring
Cortical tubular atrophy
Interstitial inflammation
Interstitial fibrosis
Atherosclerosis
RAAS effect
Vasoconstriction
Increase
50 yo male quick smoking last week when brother died from heart attack. Works for postal service, no exercise. What are his risk factors
Male
Smoker (non smoker until haven’t touched for 6 months)
Diet
Obese
No exercise
2+ edema
Prolonged expiration-typical of obstructive disease
Bilateral carotid bruits
Sinus rhythm with left ventricular hypertrophy and no t wave abnormalities
What’s wrong with this guy
Atherosclerosis , HTN,
What get
24 hour urine and BUN, Cr, Na, 24 hour urine
Glomerulonephritis
Hematuria)microscopic vs gross)
Have some degre of proteinuria
Acute vs chronic glomerulonephritis
Detailed history
Renal US-chronic kidney smaller
All nephropathy
Give some hematuria
Red cell casts or sysmorphic
Glomerulonephritis
As few as 3-5
Sustained proteinuria
> 1-2 g/24 hours
Edema and or foamy urine
Benign proteinuria
Functional or transient
1-2 g/24
Fever exercise, orthostatic
Treat
Low fat diet and salt reduction
Exercise lose weight
MOA in HTN nephropathy
RAAS and hyperfiltration
HTN initiate RAAS and glomerulus comes under pressure with hyperfiltration from changes and fibrosis
Hypertensive nephrosclerosis who gets
African americans-young
All old people
POL1
In black people
Risk factors for hypertensive nephrosclerosis
Smoking, HTN< low birth weight, preexisting renal injury
Signs hypertensive nephrosclerosis
HTN, microhematuria and moderate proteinuria
How control progression
BP
Diabetic nephropathy
ECM damage changes the glomerular filtration surface makes more leaks.
Type I vs Type 2 diabetics
1-changes in parallel independent of albuminuria
2-develop albuminuria without changes to nephron
Both present with edema and worsening of HTN are late findings and related to LOSS OF NEPHRONS NOT CHANGE IN GLOMERULUS
Changes in flow
Ok
Initial phase obstruction of unilateral obstruction
Urine backflow-increases intraluminal hydrostatic pressure
A simultaneous increase in glomerular capillary pressure induced by afferent arteriolar vasodilation which maintains GFR
Activation of RAAS leads to the second phase
Second phase 6 hours
Decrease glomerular blood flow due to afferent arterioles vasoconstriction
Third phase unilateral
Decreased luminal hydrostatic pressure and renal blood glow below baseline
Persistence unilateral obstruction>24 hours can cause what
50% drop in GFR
US
Solid white fluid black
Inject dys to find obstruction
Dye see how dilated ureter is in unilateral obstruction
Bilateral 2 phases
Initial-urine backflow-increases intraluminal hydrostatic pressure
-simultaneous increase in glomerular capillary pressure induced by afferent arteriolar vasodilation which maintains GFR
RAAS is activated which leads to second phase
Second phase bilateral
Decrease glomerular blood flow due to afferent arterioles vasoconstriction maintains GFR
Why just two phases
ANP may maintain GFR and arteriolar function
Tubular dysfunction unilateral
Inability to reabsorbed sodium
Salt eating
Downregulation of receptor and anxyme activity
Have high salt regular urine from the one kidney
Tubular dysfunction bilateral obstruction
Presence of volume expansion
ANP blocks effects of renin->decreased angiotensin II therefore net result is diuresis and natiuresis
Urinary concentration
Inability to absorb Na int he ascending limb and dilute the filtrate int he distal convoluted tubule, the solutes are excreted
Defective urea recycling: transporter defect reduces concentrating effect and allows urea to be excreted
Potassium tubular dysfunction
Low flow luminal state and high urinary K
Small amounts of urine high K , but minimal have hyperK
Even though lot of K in urine is small opposed to what is supposed to be filtered
Acute and chronic outlet obstruction
Acute-stone, one ureter
Chronic-enlarged prostate as time goes on not emptying bladder backflow reasons
Acute bilateral ureteral obstruction
Increase RBF
Decrease GFR
Decrease medullary blood flow
Increased vasodilator prostaglandins, NO
Increase ureteral and tubule pressure
Increase reabsorption of Na, urea, water
Pain , azotemia, oliguria or anuria
Chronic bilateral ureteral obstruction
Decrease RBF
Decrease GFR
Increase vasoconstrictor prostagladin
Increase refine
Decreasemedullary osmolarity
Decrease concentrating ability
Structural damage; parenchymal atrophy
Decrease transport functions for Na, K, H
Azotemia HTP-AVP insensitive polyuria/nature’s is, hyper Khyper Cl
Ring picture of outlet obstruction
Patient with azotemia, hyper K and metabolic acidosis
343 Harrison table 19th edition
Ok
Causes of obstruction
Nephrolithiasis Strictures Malignancy BPH/prostate Neurogenic bladder Congenital Pregnancy
VUR
VU has one way valve that fails
Primary or secondary
More in male kids
Most common inherited anomaly of GU
Frequent UTI and pyelonephritis
Kid with upper and lower infections
Evaluated for reflex
Adults with voiding trouble may develop reflux that predisposes them to what
UTI and pyelonephritis
BPH
Slow stream increase urgency
Dribble
Nocturnal
Urine forced into the ureters cause hydronephrosis
Vague pain pattern-may include low back, perineum or suprapubic area
BPH can lead to hydronephrosis
Ok
Overflow incontinence
Ok
Post void residual
US on full and empty bladder
If >100ml indicate incomplete emptying
See overflow incontinence
100mL urine
Crest pool for bacteria and infections
Stress incontinence
Women child birth
Muscles of perineum lost ability to control urethra and emptying
Cough sneeze laugh too hard lose control
What do with stress incontinence
Kegal sit on toilet start and stop urine stream will take time to get msucle control to stop them can do kegal anywhere
Neurogenic bladder
Spinal cord trauma
Spinal myelomeningocele
Less common-spinal stenosis, herniated disc
Disruption of coordination of relaxation of sphincter during bladder contraction
As volume increases, resting pressure rises
> 40 cm H2) increases risk of
Hydronephrosis and subsequent decrease in GFR
Treat neurogenic bladder
Monitor as hydronephrosis may occur before irreversible injury
Renal Lithiasis cause
RTA, other hormone
Result renal lithiasis
Unilateral obstruction
Pain back pain radiates to groin and episodic
Insert dye into renal lithiasis
See where caught
Treat lithiasis
Try to pass drink a on of water and strain urine
Unable to pass-in through urethra with basket and pull through and stento to keep it open and drains hen remove stent
Pregnancy and obstruction
Proximity to uterus
May persist 6 weeks post partum
First trimester-hydronephrosis in 10-15 percent
Do stent if problem but usually monitor
Malignancy obstruction
Constitutional symptoms but may come in for fatigue, weight loss,
Kidney cancer
Transitional CA can obstruct ureter
But can be colon, ovarian, lymphoma
Postobstructive diuresis
Combo of fluid overload, urea accumulation and electrolyte imbalance
250ml/hr but can be as high as 750 ml/h
Why get it
Down regulation of Na transporters during obstruction
ANP released in response to cardiac preload during obstruction
Treat post obstructive
Fluid replacement in response to diuresis-75% of ruine volume and careful monitor or urine and serum osmolality as well as serum electrolytes
58 male dysuria 8 days pain radiates back and perineum. Chills, achiness, cant start stream . Doesn’t feel like bladder is empty when finish pee.
Now small amounts of urine and spontaneous incontinence
Spontaneous incontinence-overflow
BPH, prostatis, UTI,
Get UA with microscopy, US, CT,
Found he had enlarged bladder
Ureteral dilation
Hydronephrosis either unilateral or bilateral
Ok
Nephrotic range proteinuria
Large amount of protein 3.5 g
Nephrotic syndrome
Need proteinuria
Hyperlipidemia-fasting cholesterol/lipids
Hypoalbuminemia
Edema
63 yo male polyuria polydipsia (drinking a lot) and facial swelling for 3 months.
Anytime patient thirsty or urinating a lot
-tip off for diabetes (losing sugar and fluid-osmotic diuretic)
What is DM associated with
Nephrotic syndrome-may cause it
Hypoalbuminemia
Why low albumin in blood stream and spilling protein in urine cause swelling
Lose colloid osmotic so leak out interstitial then think low so raas
DM with edem
Most likely effecting kidney
Drug decrease proteinuria
ACE ARB
Type II DM
Annual ACR (albumen/Cr ratio)
lupus and rheumatoid arthritis and nephrotic syndrome
Ok
Infection nephrotic
Hep BC-cryoglobinuremia
HIV
Syphilis
Tuberculosis
HIV
Focal segmental glomerulosclerisus
Hematologic/oncologist cause of nephrotic
Amyloidosis
Multiple myeloma
Sickle cell
Liquid and solid tumors
Drugs cause nephrotic
NSAIDS
Lithium
IV heroin
72 year old male severe back pain for year. Works a small farm. No specific identifiable injury. He works in hostpital. Couple different physician give pain pill on separate occasion, not aware of other. Tylenol 3.
Hazards of opoids. Codeine is controlled. Any prescription should be done with caution.
They didn’t do PE, no chart, they just gave him pills.
Huge risk to patient and postponed care
What else might patient take with this constellation
NSAIDS twice the recommended
Effect
Proteinuria
-as did evaluation, did 24 hour urine to quantify and get protein electrophoresis bc his age group prone to multiple myeloma-he has indirectly transposed treatment to malignancy
AAFP article on hematuria in adult
Ok
22 yo male going to do triathlon needs physical before . Runs and does weight. He has 1+ blood
Hematuria in athletics
Heavy exercise induce hematuria in 80% of athletes and may have proteinuria
Why
Exercising heavily, get renal ischemia for short periods of time. Result in red cells in urine. More common in swimmers, track, and lacrosse.
Athletes have pains
Take NSAIDS
Also can cause hematuria
Take home message
Occult hematuria always get a microscopy and a culture and sensitivity
Then re check
Why need microscopy
See where cellls come from
NSAIDS
Inhibit COX in kidney ibueprofin bigger offender than acetaminophen
In drug classes have variation
Net effect of renal ischemia activates RAAS*** vasoconstriction
RAAS from NSAID
Up up vasoconstrict
26 yo female ab paina fter meal better if eat tums
UA-2+ blood
Menstruation give false positive up to 24 hours realize starting mesntral cycle and can persist for several days after
Need UA epigastric pain? No
Dipstick false positive
Up to 35% false positive
UA how collect
Mid stream mid catch, wash urethra this eliminates debris around urethra that would give false information
Myoglobin in urin
Give heme positive result false positive in dipstick
Ph>9 urine, certain types of proteus infection get
False positive
Vitamin C false positive
Can give false positive in cold a flu season can get this
What is hematuria
3 RBC per high powered field
19 yo male presents with blood in urine. Plays football was struck from right and has bruise since then urine darker than usual but has continued to play foot ball 1+ blood 2+ urobilinogen
Kidney protected can just observe these patients and re check in 48 to 72 hours.
Need US depending on history and physical
Falls and rapid deceleration injuries hurt kidney?
If they are hemodynamics stable do not need a US or CT to look at kidney
Ok
22 yo african American male need veal so can play college basketball . Exam normal. 6’7
2+ blood
Sickle cell trait
Sickle cell trait
Infants screened at birth
If not causing problem then, don’t worry
Can get renal papillary necrosis and get focal segmental glomerulonephropsis-RENAL MEDULLARY CARCINOMA
What cancer worry about with sickle cell trait
Renal medullary carcinoma
What do
Send for UA and culture and sensitivity
55 yo male comes for refill bp meds. Former smoker quick when given high BP 1+ blood . UA neg for blood and protein a year ago
Probably cancer related to smoking
Number one risk for bladder cancer
Smoking
Other question
How much NSAIDS
Other exposures
Gross hematuria painless
CANCER until proven otherwise
Irritation voiding symptoms with hematuria
Dysuria, urgency, frequency
Tips balance away from cancer-
What could have
Catheter, chronic UTI, pelvic irritation, schistosomiasis
Blood with urine
Also microscopy and culture and sensitivity and
Get BUN, Cr serum eval
Radiographically?
US
No radiation cheaper
Less sensitive for smalls tones, small bladder mass, good for hydronephrosis!!!
CTU
2 phase radiographically test sensitive for renal calculi bc done in two phases
Expensive , radiation,
CTU. Work
1st scan wo contrast second with
Cytoscopy
Direct visualization if sure its a lower GU how we go in to get renal stones
If stone can get with basket , can get biopsy, can cauterize active bleeding, it is invasive (risk UTI and different thought)
US or IVP negative
Can go straight to cystoscopy
RBC gone through glomerulus
Dysmorphic
Rbc from down
Looks fine
Chronic glomerulonephritis
Scarring
Cortical tubular atrophy
Interstitial inflammation
Interstitial fibrosis
Atherosclerosis
RAAS effect
Vasoconstriction
Increase
50 yo male quick smoking last week when brother died from heart attack. Works for postal service, no exercise. What are his risk factors
Male
Smoker (non smoker until haven’t touched for 6 months)
Diet
Obese
No exercise
2+ edema
Prolonged expiration-typical of obstructive disease
Bilateral carotid bruits
Sinus rhythm with left ventricular hypertrophy and no t wave abnormalities
What’s wrong with this guy
Atherosclerosis , HTN,
What get
24 hour urine and BUN, Cr, Na, 24 hour urine
Glomerulonephritis
Hematuria)microscopic vs gross)
Have some degre of proteinuria
Acute vs chronic glomerulonephritis
Detailed history
Renal US-chronic kidney smaller
All nephropathy
Give some hematuria
Red cell casts or sysmorphic
Glomerulonephritis
As few as 3-5
Sustained proteinuria
> 1-2 g/24 hours
Edema and or foamy urine
Benign proteinuria
Functional or transient
1-2 g/24
Fever exercise, orthostatic
Treat
Low fat diet and salt reduction
Exercise lose weight
MOA in HTN nephropathy
RAAS and hyperfiltration
HTN initiate RAAS and glomerulus comes under pressure with hyperfiltration from changes and fibrosis
Hypertensive nephrosclerosis who gets
African americans-young
All old people
POL1
In black people
Risk factors for hypertensive nephrosclerosis
Smoking, HTN< low birth weight, preexisting renal injury
Signs hypertensive nephrosclerosis
HTN, microhematuria and moderate proteinuria
How control progression
BP
Diabetic nephropathy
ECM damage changes the glomerular filtration surface makes more leaks.
Type I vs Type 2 diabetics
1-changes in parallel independent of albuminuria
2-develop albuminuria without changes to nephron
Both present with edema and worsening of HTN are late findings and related to LOSS OF NEPHRONS NOT CHANGE IN GLOMERULUS
Changes in flow
Ok
Initial phase obstruction of unilateral obstruction
Urine backflow-increases intraluminal hydrostatic pressure
A simultaneous increase in glomerular capillary pressure induced by afferent arteriolar vasodilation which maintains GFR
Activation of RAAS leads to the second phase
Second phase 6 hours
Decrease glomerular blood flow due to afferent arterioles vasoconstriction
Third phase unilateral
Decreased luminal hydrostatic pressure and renal blood glow below baseline
Persistence unilateral obstruction>24 hours can cause what
50% drop in GFR
US
Solid white fluid black
Inject dys to find obstruction
Dye see how dilated ureter is in unilateral obstruction
Bilateral 2 phases
Initial-urine backflow-increases intraluminal hydrostatic pressure
-simultaneous increase in glomerular capillary pressure induced by afferent arteriolar vasodilation which maintains GFR
RAAS is activated which leads to second phase
Second phase bilateral
Decrease glomerular blood flow due to afferent arterioles vasoconstriction maintains GFR
Why just two phases
ANP may maintain GFR and arteriolar function
Tubular dysfunction unilateral
Inability to reabsorbed sodium
Salt eating
Downregulation of receptor and anxyme activity
Have high salt regular urine from the one kidney
Tubular dysfunction bilateral obstruction
Presence of volume expansion
ANP blocks effects of renin->decreased angiotensin II therefore net result is diuresis and natiuresis
Urinary concentration
Inability to absorb Na int he ascending limb and dilute the filtrate int he distal convoluted tubule, the solutes are excreted
Defective urea recycling: transporter defect reduces concentrating effect and allows urea to be excreted
Potassium tubular dysfunction
Low flow luminal state and high urinary K
Small amounts of urine high K , but minimal have hyperK
Even though lot of K in urine is small opposed to what is supposed to be filtered
Acute and chronic outlet obstruction
Acute-stone, one ureter
Chronic-enlarged prostate as time goes on not emptying bladder backflow reasons
Acute bilateral ureteral obstruction
Increase RBF
Decrease GFR
Decrease medullary blood flow
Increased vasodilator prostaglandins, NO
Increase ureteral and tubule pressure
Increase reabsorption of Na, urea, water
Pain , azotemia, oliguria or anuria
Chronic bilateral ureteral obstruction
Decrease RBF
Decrease GFR
Increase vasoconstrictor prostagladin
Increase refine
Decreasemedullary osmolarity
Decrease concentrating ability
Structural damage; parenchymal atrophy
Decrease transport functions for Na, K, H
Azotemia HTP-AVP insensitive polyuria/nature’s is, hyper Khyper Cl
Ring picture of outlet obstruction
Patient with azotemia, hyper K and metabolic acidosis
343 Harrison table 19th edition
Ok
Causes of obstruction
Nephrolithiasis Strictures Malignancy BPH/prostate Neurogenic bladder Congenital Pregnancy
VUR
VU has one way valve that fails
Primary or secondary
More in male kids
Most common inherited anomaly of GU
Frequent UTI and pyelonephritis
Kid with upper and lower infections
Evaluated for reflex
Adults with voiding trouble may develop reflux that predisposes them to what
UTI and pyelonephritis
BPH
Slow stream increase urgency
Dribble
Nocturnal
Urine forced into the ureters cause hydronephrosis
Vague pain pattern-may include low back, perineum or suprapubic area
BPH can lead to hydronephrosis
Ok
Overflow incontinence
Ok
Post void residual
US on full and empty bladder
If >100ml indicate incomplete emptying
See overflow incontinence
100mL urine
Crest pool for bacteria and infections
Stress incontinence
Women child birth
Muscles of perineum lost ability to control urethra and emptying
Cough sneeze laugh too hard lose control
What do with stress incontinence
Kegal sit on toilet start and stop urine stream will take time to get msucle control to stop them can do kegal anywhere
Neurogenic bladder
Spinal cord trauma
Spinal myelomeningocele
Less common-spinal stenosis, herniated disc
Disruption of coordination of relaxation of sphincter during bladder contraction
As volume increases, resting pressure rises
> 40 cm H2) increases risk of
Hydronephrosis and subsequent decrease in GFR
Treat neurogenic bladder
Monitor as hydronephrosis may occur before irreversible injury
Renal Lithiasis cause
RTA, other hormone
Result renal lithiasis
Unilateral obstruction
Pain back pain radiates to groin and episodic
Insert dye into renal lithiasis
See where caught
Treat lithiasis
Try to pass drink a on of water and strain urine
Unable to pass-in through urethra with basket and pull through and stento to keep it open and drains hen remove stent
Pregnancy and obstruction
Proximity to uterus
May persist 6 weeks post partum
First trimester-hydronephrosis in 10-15 percent
Do stent if problem but usually monitor
Malignancy obstruction
Constitutional symptoms but may come in for fatigue, weight loss,
Kidney cancer
Transitional CA can obstruct ureter
But can be colon, ovarian, lymphoma
Postobstructive diuresis
Combo of fluid overload, urea accumulation and electrolyte imbalance
250ml/hr but can be as high as 750 ml/h
Why get it
Down regulation of Na transporters during obstruction
ANP released in response to cardiac preload during obstruction
Treat post obstructive
Fluid replacement in response to diuresis-75% of ruine volume and careful monitor or urine and serum osmolality as well as serum electrolytes
58 male dysuria 8 days pain radiates back and perineum. Chills, achiness, cant start stream . Doesn’t feel like bladder is empty when finish pee.
Now small amounts of urine and spontaneous incontinence
Spontaneous incontinence-overflow
BPH, prostatis, UTI,
Get UA with microscopy, US, CT,
Found he had enlarged bladder
Ureteral dilation
Hydronephrosis either unilateral or bilateral
Ok
Acute renal failure/acute renal injury
Increase Cr seen in 6 percent of hospitalized
Treat AKI
Nothing proven maintain volume and stuff.
Prerenal failure
Most common in host. CHF, cirrhosis, nrenovascular disease
Intrinsic renal failure
ATN Rhabdo and ATN Radiocontrast dyese Emboli TPP/HUS Drugs HIV/SLE
Post Renal
Obstruction
Ambulatory not hospitalized
Stones, malignant, papillae-more proximal obstruction
Intrinsic renal finding
HTN, GN, edema
NA retention
Hemoptysis, pulmonary hemorrhage, vasculitis,
Rbc wbc cellular casts characteristic of GN
RBC CASTS
NSAIDs-proteinuria
Allergic nephritis-eosinophils with wrights or Hansel
WBC pyelonephritis
Post renal
Less ill
Delayed until azotemia is up
Fena>one Bland microscopic US is key Dilated Exeter calyces May also use furosemide renogram MAGthree
Treat AKI
Support
Pre renal vol loss-IV
CHF-vasodilator or inotropy
Intrinsic-GN SLE vasculitis corticosteroids and cytotoxic Plasma phones is-HUS Plasma exchange-TPP Pyelonephritis, endocarditis-antibiotics Allergic- Obstruction-urologist catch or stent
What I’d nonprerenal aki progresses
Dialysis
Indication dialysis
Volume overload refractory to diuretic agents, hyperkalemia, encephalopathy not explained, pericarditis, pleuritis, serositis, metabolic acidosis,
Provide in advance
Inability to requisite fluid for drugs
What kind of dialysis most patients given
Intermittent hemodialysis
Continuous renal replacement therapy
Only if IHD intolerant
SLED
SLOW EFFICIENCY DIALYSIS, HYBRID TECHNIQUES MAY BE SED INSTEAD OF CRRT
Chronic kidney disease
Irreversible impairment of kidney function
More esk or CKD
CKD
First step of ckd diagnosis
Establish chronicity
-history and prior labs and U(small kidney for chronic
What chronic diseases have large kidney though
Diabetic nephropathy, HIV, multiple myeloma or amyloidosis
Next step
Etiology
History, drugs disease,
PE masses , Bruit-renovascular
Electrophoresis, serum, light chains,
D< P, Ca, PTH for bone
What labs suggest nephrotic
Hypoalbuminemia, hyperchlosterolemia, edema
Uremic syndrome in CKD
Cr to estimate eGFR
Cr>five thirty
Symptoms uremia
Anorexia, weight loss, dyspnea, fatigue, pruritis, sleep, metallic taste, confusion, encephalopathy
Hypertension, jugular distension, pleural friction rub, muscle watering, asterisks, ecchmoyses , excessive bleeding
HyperK, P, acidosis, hyperU, anemia, hypoalbuminemia, hypoCa
Treat uremia
Dialysis or transplant or drug
How treat CKD
Treat the HTN to slow progression
-give diuretics bc of the volume overload that causes htn
EPO-for anemia, want 90 hemoglobin
Iron supp
Restrict P eat or calcium based salt
K>6
What potassium consider dialysis
Over 6 on repeat
What big signs start dialysis
Anorexia, hypoalbuminemia, hyper K, weight loss
How slow progression ckd
Control that htn ace arb , diuretics—-may also help control the high K
Median wait time for transplant
Three to six years
Absolute indications dialysis
HyperK, acidosis, encephalopathy no explained, pericarditis, serositis, uremia, failure to thrice,
What GFR get these symptoms
Ten
Does initiation of dialysis before uremic symptoms improve ESRD
No
Hemodialysis
Brescia imino fistula
Blood pumped in and bathed
Three times a week
Efficiency dialysis
Duration, blood flow rate, dialysate flow rate, surface area dialysis
Complication hemodialysis
Hypotension-diabetes who’s neuropathy prevents compensatory responses (tachy vasoconstriction)
Cns
Dialysis disequilibrium syndrome
Headache, confusion, from rapid solute removal early in the pts dialysis history, before adaptation to the procedure
How avoid disequilibrium syndrome
Incremental induction of chronic dialysic therapy in uremic patients short durationlower flow rate
Peritoneal dialysis
Don’t need circulation access.
Allows infusion of a dialysate solution into abdominal cavity across peritoneal membrane which is an artificial kidney
Difference between PD and heme dialysi solution
PD must be sterile and uses lactate rather than bicarbonate
Prob PD
Longer and less effective,
But what are advantages PD
Independence and flexibility, gentle hemodynamics profiles
Better preservation renal function
PD complication
Peritonitis -ab pain cloudy dialysate, peritoneal leukocyte count up with neutrophils
Protein loss HUGE
Organisms of peritonitis
Staph aureus and staph spp gram positice
Candida
Pseudomonas
Treatment of choice esrd
Transplant
How get best transplant results
Living related recipient
Less ischemia and waiting time usually done prior to symptoms and better graft survival
Graft matching
Improves survival
Why is imbalance of patients and donors going to increase
Obesity and diabetes
Expanded criteria donor and donors after cardiac death
Developed to increase dead donor kidney
ECD kidneys-who gets
People who expected fare less well on dialysis
Factors influence graft survival
Pretransplant blood transfusion avoid
-if encessary use leukocyte reduced irradiated blood
Contraindications renal transplant
Active GNm infection, malignancy, aids, hepatitis,
Patient should have what life expectancy to get kidney
Over five years
Rejection
Hyperacute-presensitization
Acute-week month
How detect rejection
Rise in Cr
HTN fever, reduced urine, tenderness
How confirm rejection
Percutaneous renal transplant biopsy
Treat rejection
Pulse of methylprednisone
Monoclonal antibody directed at human t lymphocytes
Immunosuppressive therapy transplant
Three dru regimen
Calcineurin inhibitors
Cyclosporine
Cyclosporine side effects
Hyper K, HTN< tremor, hirstiusm, gingival hypertrophy, gout,
Tacrolimus
Hyperglycemia
Hair loss
Prednisone
Steroid-
Complication renal transplant
Neoplasia, infection bc of immunosuppression
Polyomavirus DNA virus BK
EPV
Non Hodgkin and squamous cell skin carcinoma
Month one
CMV
Use ganciclovir
After one month
Fungal pneumocystisi carinii
Nephritic syndrome
Salt and water retention from reduced GFR may get circulatory congestion
RBC casts
Proteinuria with nephrtis
Less than three
Acute post strep GN
Positive pharyngeal skin culture
ASO titres
Hypocomplementemia
GN on biopsy
Treat acute post strep GN
Correct fluid and electrolyte balance
Self limited
Postinfections GN
Bacterial or viral and parasitic
Endocarditis, sepsis, hep, pneumococcal pneumonia
Feature more mild that post strep
Post staph
IgA deposits IF
Treat post infections GN
Control infeciton but steroids often given to avoid dialysis
RPGN
GFR less than fifty percent
Complex like SLE
Pauli immune ANA
Anti GB
SLE lupus
Deposit circulating immune complex
Arthralgias-butterfly skin rash, serositis, alopecia, CNS
Nephrotic diffuse GN
Active sediment, proteinuria, progressive renal insuffiency
ANA, hhypocompl, anti ds-DNA
Treat SLE lupus
Glucocorticoids and cytotoxic agents
Cyclophosphamide
First bank sperm and egg before
Pauli immune GN
Renal limited or systemic
PANCE, MPO, cANCA
MPO and PRthree antigens
Treat Pauli
Methylprednisone and cyclophosphamide
Plasmapheresis
Pneumocystitis carnii prophylaxis
Diagnosis henoch
Biopsy
Urine spot for nephrotic
Yup easier
Complications NS
D defiency
MCD not respond steroids
Focal sclerosis
Membranous GN
Sub epithelial IgG
SLE, hep B, tumors, captopril, penicillamine
Treat membranous
Ace arb, prophylactic DVT
Focal glomerulosclerosis
Primary acute
Secondary chronic
MPGN
Ok
Diabetic nephropathy
Ace arb
Glucose control
Loop diuretics is get HyperK that cant be controlled
Asymptomatic
Thin basement and IgA nephropathy
Distinguish tubulointerstitial
Less HTN, hematuria and proteinuria
acute interstitial nephritis drugs
Increase Cr, eosinophilic rash arthralgias
Rapid if previously sensitized
Rifampin
Tubular dysfunction lab
Hyper K metabolic acidosis
How see eosinophilic
Hansel or wright stisan
Systemic cause AIN
Leptospirosis, strep
IgG4 plasma cells
Tubulointerstiial nephritis and uveitis syndrome
Weight loss, increase erythrocytes sedimentation ate
Self limited give prednisone
Chronic interstitial nephrtis
Analgesic nephropathy
Asprin phenacetin
Transitional cells arcinoma
Manifestations chronic IN
Papillary necrosis, calculi, sterile pyruvate, azotemia
Chinese herbal meds
Severe chronic tubulointerstitial fibrosis
Balkan endemic nephropathy
South east Europe
Lithium
Chronic tubulointerstitial nephritis
Give valproic acid instead
Metabolic cause of chronic IN
Hyper Ca with nephrocalcinosis, oxalosis, hypoK, hyperplastic Uric Emma
Chronic IN with what systemic disease
Sjorgen
Myeloma
Monoclonal immunoglobulin or light chain and AL amyloidosis
Filtered light chains aggregate and cause tubular obstruction, tubular damage, and inflammation
Hypercalcemia volume depletion
Diagnose cast nephropathy
Light chain in urine or serum
By electrophoresis
Dipstick negative
Light chain nephropathy
Positive AL amyloididid bc of proteinuria
Diagnose ADPCK
Between thirty and fifty nine at least two cysts in each kidney
ADPCK
HTN, normal GFR
RAAS
Give ace arb
What is common in ADPK
UTI cyst infections
RTA
Ok
When get renal calculi
Urine supersaturated with insoluble components form low urine volume, excessive or insufficient secretion of selected compounds.
Most stones
Ca based
Ca oxalate stone
Hypercalcuria, hyperoxaluria
High Na diet, loop diuretic, RTA 1, primary hyperPTH, VD excess, milk alkaloids
Hyperoxaluria
Malabsorption IBD, pancreatitis
Uric acid stone
Chemo low pH
Cystine stones
Acidic pH defect in intestinal tranpost
Obstruction insert bladder catheter and get diuresis
Obstruction below bladder neck
Insert catheter and no diuresis do US
Hydronephrosis obstruction above bladder neck
No hydronephrosis —low clinical suspicion—no work up, but high suspicion identify and relieve
Hydronephrosis
Identify site and relieve and identify cause
US
Hydronephrosis
CT IV
Site of obstruction
Tc99 MAG3
Renal scan to assess excretion before and after loop diuretic can assess function and difference between two kidneys
Distinguish tubulointerstitial
Less HTN, hematuria and proteinuria
acute interstitial nephritis drugs
Increase Cr, eosinophilic rash arthralgias
Rapid if previously sensitized
Rifampin
Tubular dysfunction lab
Hyper K metabolic acidosis
How see eosinophilic
Hansel or wright stisan
Systemic cause AIN
Leptospirosis, strep
IgG4 plasma cells
Tubulointerstiial nephritis and uveitis syndrome
Weight loss, increase erythrocytes sedimentation ate
Self limited give prednisone
Chronic interstitial nephrtis
Analgesic nephropathy
Asprin phenacetin
Transitional cells arcinoma
Manifestations chronic IN
Papillary necrosis, calculi, sterile pyruvate, azotemia
Chinese herbal meds
Severe chronic tubulointerstitial fibrosis
Balkan endemic nephropathy
South east Europe
Lithium
Chronic tubulointerstitial nephritis
Give valproic acid instead
Metabolic cause of chronic IN
Hyper Ca with nephrocalcinosis, oxalosis, hypoK, hyperplastic Uric Emma
Chronic IN with what systemic disease
Sjorgen
Myeloma
Monoclonal immunoglobulin or light chain and AL amyloidosis
Filtered light chains aggregate and cause tubular obstruction, tubular damage, and inflammation
Hypercalcemia volume depletion
Diagnose cast nephropathy
Light chain in urine or serum
By electrophoresis
Dipstick negative
Light chain nephropathy
Positive AL amyloididid bc of proteinuria
Diagnose ADPCK
Between thirty and fifty nine at least two cysts in each kidney
ADPCK
HTN, normal GFR
RAAS
Give ace arb
What is common in ADPK
UTI cyst infections
RTA
Ok
When get renal calculi
Urine supersaturated with insoluble components form low urine volume, excessive or insufficient secretion of selected compounds.
Most stones
Ca based
Ca oxalate stone
Hypercalcuria, hyperoxaluria
High Na diet, loop diuretic, RTA 1, primary hyperPTH, VD excess, milk alkaloids
Hyperoxaluria
Malabsorption IBD, pancreatitis
Uric acid stone
Chemo low pH
Cystine stones
Acidic pH defect in intestinal tranpost
Obstruction insert bladder catheter and get diuresis
Obstruction below bladder neck
Insert catheter and no diuresis do US
Hydronephrosis obstruction above bladder neck
No hydronephrosis —low clinical suspicion—no work up, but high suspicion identify and relieve
Hydronephrosis
Identify site and relieve and identify cause
US
Hydronephrosis
CT IV
Site of obstruction
Tc99 MAG3
Renal scan to assess excretion before and after loop diuretic can assess function and difference between two kidneys
