Quiz 5- Renal Flashcards

1
Q

History of renal patient

A

pain: flank or lower back
PMHx: lupus, DM, HTN
FHx: PKD, AI nephropathies, nephrolithiasis
Exposures: heavy metals and chemicals, radiographic contrast media
Meds: analgesics, antibiotics, NSAID’s, diuretics

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2
Q

ROS for renal patient

A
general: fever, WT loss, fatigue
CV: dyspnea, chest pain, edema
GI: anorexia, N/V, cramp-like abd pain
LUTS: polyuria, dysuria, hematuria
musculoskeletal: joint pain or swelling
skin: rask, pruritis
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3
Q

complete PE for renal patient

A

observation:
severely ill patients with renal disease can looks pale, sallow
drowsiness, slurred speech may suggest acute renal failure
deep breathing suggests metabolic acidosis
Lung/heart: high BP, heart failure, pericardial rub, pleural rub, edema
Neurological: encephalopathy,
Fundoscopic: retinal changes from diabetes or HTN
Abdominal: renal mass, renal artery bruit, ascites, CVA tenderness
Skin: xerosis, pallor, petechiae, ecchymosis

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4
Q

History of urologic patient- pain

A

pain:
ureters: R or L sied spasms (stone) may radiate to thigh or genitalia
bladder: suprapubic pain
urethral: dysruia
Red flags: sudden onset of flank pain and fever

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5
Q

History of urologic patient- voiding sx

A

voiding:
irritative: dysuria, frequency, urgency
obstructive: hesitancy, straining, decreased caliber
incontinence: unable to hold urine
enuresis
nocutria
Red flags: fever, back pain, lower extremity weakness

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6
Q

History of urologic patient- discharge

A

amount
color
consistency
concomitant sx: fever, chills, rash, hematuria, dysuria

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7
Q

PE for urologic patient

A

Assess for CVA tenderness: pyelonephritis, calculi, UTI
Abdomen: dullness in suprapubic area may suggest bladder distention (pt may feel urge to urinate when pressing), may see distention
Gynecologic exam
Male genitalia exam

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8
Q

UTIs that involve the lower urinary tract can be called?

A

urethritis, cystitis, prostatitis

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9
Q

SX of lower UTI?

A

dysuria, urgency, frequency, suprapubic pain, cloudy urine, strong odor to urine, hematuria

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10
Q

UTIs that involve the upper urinary tract can be called?

A

pyelonephritis, ureteritis

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11
Q

SX of upper UTI?

A

may include fever ( ≥103° F), chills, flank pain, tender CVA, GI sx (diarrhea, N&V), may be dysuria

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12
Q

Urinary Frequency

A

need to urinate many times during the day. –often accompanied by Urgency (sensation of urgent need to urinate with only small amt of urine passing)

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13
Q

in a pt with urinary frequency make sure to ask:

A

Fluid consumption
Flow symptoms (pain, hesitancy, sensation of incomplete voiding, nocturia)
Fever, hematuria, sexual activity
Missed menses, breast swelling, morning sickness (pregnancy)

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14
Q

what’s your ddx for a pt with urinary frequency?

A

UTI, pregnancy, compression/ prolapsed uterus, foreign bodies, stones, excessive fluid intake, substances (coffee, alcohol, diuretics), DM, food sensitivity, BPH, prostatitis, spinal cord injury, urethral stricture, incontinence

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15
Q

red flags for a pt with urinary frequency?

A

Fever, back pain, lower extremity weakness

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16
Q

Dysuria
definition
causes

A

painful or uncomfortable urination (burning, aching).

From irritation, inflammation, infection (eg cystitis, urethritis/STI), perineal lesions exposed to urine

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17
Q

in a pt with dysuria ask patient re:

A

Discharge, chills/fever, hematuria, sexual activity
Timing of pain in relation to urination
Location of pain: urethra, suprapubic (bladder), flank (renal), abdominal (ureter)

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18
Q

DDx for a pt with dysuria

A

cervicitis, cystitis, epididymitis, prostatitis, urethritis, contact irritant/allergen, foreign body, interstitial cystitis, reactive arthritis, atrophic vaginitis

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19
Q

red flags for a pt with dysuria

A

fever, flank pain, recent instrumentation, immunocomp, recurrence

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20
Q

Nocturia

etiology

A

excessive fluid late in evening, urine retention, BPH, interstitial cystitis, GU allergies

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21
Q

Nocturnal enuresis

definition

A

Involuntary bedwetting after age 5 yrs.
More common in boys and in those with family history (70% if both parents)
Normally prevented by: ADH secretion at sunset
Normally prevented by: Ability to wake up when the bladder is full.
Normally uncommon after age 4 (

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22
Q

Nocturnal enuresis

etiology

A
  1. primary – ~90% of cases, child never achieved continence for > 6mos
    - neurological-developmental delay
    - genetics
  2. secondary – incontinence develops after 6 mos of achieving urinary control
    - neurological-developmental issues (eg autism, Down’s)
    - diabetes mellitus, diabetes insipidus, hypoglycemia, sickle cell disease
    - functionally small bladder
    - sleep apnea, sleep walking
    - bladder irritability (UTI, constipation)
    - ADHD
    - psychological stress: sexual abuse, bullying, birth of sibling, social isolation, divorce/separation, loss of parent/ grandparent or pet
    - food allergies/ sensitivities (dairy, wheat, apples, oranges)
    - parasites (pinworms)
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23
Q

urinary incontinence
definition
3 types

A

Inability to hold urine
3 types
-overflow- distended bladder from obstruction (BPH, pelvic tumor, fecal impaction)
-stress- sudden increase in intra-abdominal pressure from cough, sneeze, exercising etc. which apply pressure to bladder, leading to urine leak OR results from loss of sphincter tone due to childbirth, aging, obesity
urge- decreased parasymp inhibition leads to detrusor ms hyperreflexia stroke, MS, Parkinson’s, tumors etc.

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24
Q

Polyuria

defintion

A

excessive output of urine (> 3000 ml/day)
lost fluids and solutes need to be replaced (hypotension and CV collapse)
need to distinguish from urinary frequency

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25
Q

in a pt with polyuria ask the re:

A

Fluid consumption, abrupt/gradual onset
Polyphagia, polydipsia (increased appetite, thirst)
Dry eyes/mouth, weight loss/night sweats
Family history, drug history

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26
Q

polyuria

etiology

A

a. an appropriate response to osmolar, sodium or fluid loads or may occur secondary to diuretics, sodium loads from increased sodium intake, excessive water and sodium through IV feedings or rapid resorption of edema fluid

b. inappropriate response to a pathological state
i) diabetes insipidus- hypothalamic- pituitary disorder due to deficiency of vasopressin (ADH) creating polydipsia, polyuria
ii) nephrogenic diabetes insipidus- urinary concentrating defect that is unresponsive to ADH. May result from chronic renal failure (nephrons can’t conc. urine), recovery from acute renal failure or acute pyelonephritis, also in hypercalcemia, hypokalemia, congenital tubular disorders and drug induced disease
iii) compulsive drinking excessive amounts of fluid: psychogenic polydypspia; overdose of lithium may cause
iv) osmolar load: glucose osmotically active—spilling leads to Na & H20 excretion

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27
Q

red flags for a pt with polyuria

A

abrupt onset, night sweats, cough, weight loss, psychiatric disorder

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28
Q

Oliguria and Anuria
definition
etiology

A

oliguria: decreased urine output (

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29
Q

Hematuria

A

Microscopic hematuria = excretion of >3 RBCs/hpf in centrifuged urine or gross
the presence of any RBCs >1 occasion should be investigated
microscopic hematuria commonly renal cause
Gross hematuria commonly uroepithelial (if painless, R/O tumor)
Pediatrics – consider GN, child abuse
Geriatric – suspect UTI, sometimes occult

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30
Q

in a pt with hematuria ask re:

A

Habits: smoking, drug use
Medications (analgesics, Coumadin)
Occupational exposures
Obstructive symptoms (incomplete emptying, difficulty starting/stopping stream)
Irritative symptoms (irritation, urgency, frequency, dysuria)
Recent infections, family history, drug history

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31
Q

in a pt with hematuria ask about pain pattern

A

Painless urination: consider tumors of Bl, Ki, Prostate until proven otherwise! staghorn calculi, polycystic Ki, sickle cell, hydronephrosis, acute GN
Dysuria: consider infection
Flank pain: consider Ki/ureteral stone, PN, trauma or tumor

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32
Q

in a pt with hematuria ask about timing of gross blood seen

A

Start of micturation: anterior urethral lesions (urethritis, stricture, meatal stenosis)
End of micturation: suggests bladder trigone, prostate, bladder neck, posterior urethra
Throughout micturation: suggests Bl, ureteral or renal pathology
Cyclically with menstruation: endometriosis of the urinary tract
Blood between voidings (on underwear): suggests bleeding on either end of the urethra

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33
Q

ddx for hematuria

A

Pseudohematuria {dehydration, dyes (sudan red), foods (beets, rhubarb, berries}, vaginal source of bleeding, genital/perineal trauma, rifampin

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34
Q

red flags for hematuria

A

Gross hematuria, persistent microscopic hematuria in elderly, Age>50, hypertension and edema

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35
Q

work up for pt with hematuria

A

dipstick/complete UA, urine culture and sensitivity, CBC, coagulation screen, renal function test, prothrombin time, PSA, urine cytology, Imaging

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36
Q

Renal colic
defintion
etiology

A
  • usu. unilateral, severe crescendo-decrescendo pain originates in the flank, radiates from CVA across the abdomen., along the course of the ureter, into the region of the genitalia and inner side of the thigh
  • most often caused by passage of renal calculi
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37
Q

concomitant sx in a pt with renal colic that suggests renal stones?

A

N/V, chills/fever (if infected), gross hematuria suggests passage of stone or bleeding cysts, frequency

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38
Q

in a pt with renal colic what are the red flags?

A

fever, oliguria or anuria

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39
Q

sx of edema

A

unexplained weight gain, tightness of rings and shoes, puffiness of face, swollen extremities, abdominal distention, pitting on digital pressure

40
Q

etiology of generalized edema

A

i. heart dz.- CHF, pericarditis
ii. liver dz.- jaundice, ascities, spider nevi, red nose, palmar erythema, nausea/ vomiting, enlarged & tender liver, history. of heavy alcohol use
iii. kidney disease.- nephrotic syndrome, glomerulonephritis, any other cause of chronic renal failure. (DM, hypertension)
iv. myxedema (hypothyroid)- periorbital edema caused by infiltration of mucopolysacch. hyaluronic acid & chrondroitin sulfate, pretibial-swelling on anterior leg, non-pitting, firm
v. lymph edema- e.g. mastectomy, removed lymph nodes —> swollen arm

41
Q

labs for uronephro stuff

A
  1. URINE EOSINOPHILS (Wright’s stain)
    Eosinophiluria seen in acute interstitial nephritis, RPGN, acute prostatitis, Renal atheroembolism
  2. CBC- anemia (decrease in RBC production from dec epo, blood loss), infection
  3. URINE CYTOLOGY
    Screen and test for uroepithelial/bladder cancer: at-risk population, painless hematuria
  4. Work up for refractory HTN: plasma renin, aldosterone cortisol, ACTH
  5. PROSTATE SPECIFIC ANTIGEN (PSA)
    Increases with age, BPH, Prostate cancer. Used to screen and monitor CaP
  6. STI testing: Urine NAAT PCR, gram stain, etc
42
Q

imaging tests for uronephro

A

a. X-ray- (KUB) plain film (for size, shape, position), radiopaque renal calculi (kidney-ureter-bladder)
b. U/S- masses, cysts, hydronephrosis, aid for a biopsy; polycystic kidneys, cystic from solid mass. Doppler U/S used for renal arteries and prostate, testicular and penile blood flow.
c. IVU (IV urography – dye injected, some people react, replaced by CT)- to visualize kidney & lower UT. Used in cases of recurrent UTI, obstruction producing hydronephrosis, vesicoureteral reflux, hypertension, renal calculi
d. Retrograde urography- detailed exam of lumen of ureters, bladder
e. Cystourethrography: incontinence, strictures, reflux
f. CT- carcinoma, stones (helical without contrast), following US for masses
g. Angiography- most invasive of all procedures- for vascular lesions such as aneurysm, some tumors
h. MRI- extent of tumor invasion, hemorrhagic vs infected cyst, vasculature of kidney
i. Renal scan (radionucleotide scan); renal emboli, renal parenchymal scarring

43
Q

procedures for uronephro stuff

A

a. Catheterization: for urinary retention
b. Cystoscopy: visualize bladder wall (bladder cancer, interstitial cystitis)
c. Biopsy (renal, bladder, prostate)
d. Urethral dilation for strictures

44
Q

UTI

bugs

A
e. coli
klebsiella
pseudomonas
staph
chlamydia trachomatis
45
Q

what are some host defenses against a UTI?

A

a. WBC’s in bladder mucosa
b. acidity of urine
c. mechanical action—unobstructed urine flow flushes organisms
d. local antibodies (IgA) in uroepithelium
e. Tamm-Horsfall glycoproteins in uroepithelium and renal tubules

46
Q

what are some risk factors for UTIs?

A

i. Anatomical/congenital malformations – (esp. males)
ii. DM – high CHO diet
iii. pregnancy- due to compression of GU structures leading to obstruction
iv vaginal intercourse (“honeymoon cystitis”)
v. hygiene- eg, wiping from back to front introduces E. coli bacteria to urethra. anal intercourse preceding vaginal intercourse
vi. prior antibiotic use
vii. catheterization
vii. insufficient water intake (infrequent urination/flushing)
ix. use of tampons, spermacides

47
Q

Urethritis

etiology

A
  1. Gonocccal urethritis—50% of cases
  2. NGU—(Non-Gonococcal urethritis) 50% of cases: of these
    a. most are Chlamydia trachamotis (obligate intracellular organism)
    b. ureaplasma urealyticum:
    c. trichomonas vaginalis - rare in males but consider if F partner has persistent infx
    d. E coli - seen more often in men who practice anal sex
48
Q

Urethritis

SSX

A

urgency, frequency, tingling with urination, urethral itching
progresses to burning on urination with purulent yellow, green discharge (GC) or whitish-mucoid (NGU)

NOTE: in female, GC has mild sx’s (dysuria, freq., vaginal d/c) after 7 – 21d incubation
Or often asx. may be carrier of GC & spread to partner &/or get PID

49
Q

Urethritis

Lab:

A

UA, urine culture, gram stain, urine nucleic acid testing

Confirmed cases of gonorrhea, Chlamydia reportable to public health system

50
Q

DDX recurrent UTI’s

A
Congenital abnormalities (e.g. vesicoureteral reflux)	
Bladder cancer			Prostatic    obstruction
Diabetes mellitus		Bladder Calculus
51
Q

Cystitis (Bladder infection)

A

Often asx in the elderly and kids
Females: ascending infx from the vagina, perineal area
Males: ascending from urethra or prostate; chronic bacterial prostatitis most common
cause of relapsing cystitis

52
Q

Cystitis

SSX

A

burning or painful urination, frequency, urgency, nocturia, suprapubic pain
Usually NO fever or back/flank pain

53
Q

Cystitis

Lab

A

UA: pyuria, bacteriuria, hematuria (gross or microscopic), Positive leukocyte esterase, Nitrite usu positive unless amicrobic.
Protein (trace or 1+)
NO casts (if seen, then Ki involvement)
Urine C&S IF: UA findings or sx severe and/or concomitant risk factors.
Further work-up may be warranted (U/S, CT, CMP) IF:
Pt is boy or man

54
Q

DDX for dysuria, urgency, frequency

A

Vulvovaginitis, STI causing urethritis, interstitial cystitis, herpes simplex, trauma
cystitis, eosinophilic cystitis–from food allergens, drugs, see eos in urine
Hematuria from neoplasia or calculi, PID, pyelonephritis

55
Q

Acute Pyelonephritis PN
definition
etiology

A

-acute, unilateral or bilateral, pyogenic infection of kidney tubules and interstitium
-ascending from urethra, catheterization
Organisms: E coli (75%), Klebsiella, Proteus, Enterobacter, Pseudomonas staphylococci

56
Q

Acute Pyelonephritis

SSX

A

History of LUT infection
rapid onset of chills, fever (101+), tachycardic (pt appears ill/toxic) flank pain; tender, enlarged kidney(s); CVA tenderness
N/V, anorexia
frequency and urgency in 1/3 of pts
may be abdominal guarding (R/O intraperitoneal disease)

57
Q

Acute Pyelonephritis

Lab

A

CBC: Elevated WBC with left shift
UA: numerous WBC, pos LE, nitrites
Protein is usu negative; presence is ominous sign suggesting nephron destruction
Glitter cells=PMN’s with cytoplasmic granules in state of Brownian motion
Hematuria, bacteriuria, WBC casts, may see bacterial casts
Urine culture and sensitivity
Pregancy testing may be appropriate

58
Q

complication of acute PN?

A

if ssx don’t improve in 5 days consider
Renal Abscess
SSX: Fever/chills, flank pain, N&V, malaise
CVA and abdominal tenderness
Procedure: seen on CT, treated with draining

59
Q

DDX for acute PN:

A

PID (+CMT); Nephrolithiasis (blood, no fever, inc pain); appendicitis
(+McBurney’s, +psoas); Acute GN (RBC casts, protein); Perinephritic abscess
endometriosis (cyclic nature); acute abdomen (peritonitis, +rebound tend)

60
Q

chronic pyelonephritis

A

Often bilateral pyogenic Ki infection or congenital reflux nephropathy ➔ renal parenchymal scarring and atrophy of the calyces. Course over 20+ yrs.

61
Q

what are the risk factors for chronic PN?

A

Elderly, DM, chronic urolithiasis, low water intake/infreq urination, urine reflux, sedentary lifestyle, BPH with obstruction, chronic analgesic use, recurrent baterial UTI

62
Q

chronic PN

pathogenesis

A

Renal scarring from type 1 fimbriated E. coli is extremely common outcome of PN
Histologically, the parenchyma shows patchy interstitial fibrosis with inflammatory infiltrate. The tubules are dilated or contracted and atrophied

63
Q

chronic PN

ssx

A

usu asx, found incidentally; with progression, HTN and renal failure develop; oliguria late

64
Q

chronic PN

labs

A

UA: Bacteriuria and pyuria if active infx
Minimal proteinuria until glomerular involvement
Early: dec SG and urine osmolality may be first
Late: granular, waxy, broad casts

65
Q

chronic PN

imaging

A

KUB (kidney, ureter bladder xray) – small kidneys, irregular outline

66
Q

Glomerular disorders

A

nephritic syndrome
nephrotic syndrome
mixed nephritic and nephrotic

67
Q

Nephritic syndrome

definition and pathophysio

A

Glomerular inflammatory process causing renal dysfunction:

a. Structural changes: cellular and leukocyte proliferation, GBM thickens and scleroses, deposits laid
b. Functional changes: decreased GFR, HTN, RBCs and protein allowed to pass membrane

68
Q

Nephritic syndrome

SSX

A
PHAROH
Proteinuria 
Hematuria
Azotemia
RBC casts
Oliguria
HTN
69
Q

Nephritic syndrome
post-infectious glomerulonephritis (PIGN)
Organism

A
  • group A beta hemolytic strep
70
Q

post-infectious glomerulonephritis

SSX

A

Prior group A beta-hemolytic strep (GAS) infx: strep pharyngitis or rash
Latent period 1-3 weeks post pharyngitis
3-6 weeks after skin infx
Fever, confusion, HTN, periorbital edema, hematuria, HA, N&V, malaise

71
Q

post-infectious glomerulonephritis

Labs

A

UA: cola-colored urine, oliguria, RBCs, RBC casts (pathognomonic, but not always present)
24 hour urine protein: Proteinuria

72
Q

post-infectious glomerulonephritis

say the pt refuses tx, what must you cation the pt against?

A

if untreated may lead to nephrotic syndrome, acute kidney injury, hypertensive encephalopathy

73
Q

Rapidly Progressive Glomerulonephritis (RPGN)

definition

A

conditions that result in glomerular cresent formations (seen on biopsy) that can lead
to end-stage renal failure in weeks to months. Ages 20-50yr

74
Q

what are the various types of RPGN?

SSX for each?

A

Goodpastures- lung and kidney involvement (pulmonary hemorrhage—dyspnea, hemoptysis, crackles—and renal symptoms (edema, HTN))

Henoch-Schönlein purpura- CT and kidney involvement (Renal dz (hematuria, proteinuria) and purpura on arms, legs, buttocks, arthralgia, GI symptoms)

Wegener’s granulomatosis - necrotizing GN and respiratory (Renal dz (hematuria and proteinuria) as well as bleeding respiratory tract nodules—(hemoptysis, crackles)

Berger’s dz- IgA nephropathy that proceeds gastroenteritis or URI (persistent microscopic hematuria, mild persistent proteinuria, HTN;
rarely– acute or chronic renal failure)
Asymptomatic in 30-40%

75
Q

NEPHROTIC SYNDROMES

A
The end result of a variety of diseases that damage (immunological or other assaults) the GBM ➔protein wasting (from alteration of the GBM membrane charge), and increased permeability of glomerular capillaries. 
Severe proteinuria (>3.5 g/1.73 m2/24 hr) leading to systematic edema: Dec
oncotic pressure leads to increased fluid in interstitial spaces
“Foamy” urine: albumin has a soap-like effect that reduces the surface tension 
 Lipids pass as well  (lipiduria)
76
Q

Classifications of Nephrotic syndrome:

A

a. Primary—characteristic histologic patterns seen on renal biopsy
i. Minimal change disease
Kids and adults
Sudden onset proteinuria without renal dysfunction
Pattern: T-cell cytokine injury to epithelial foot process, no deposits
ii. Focal segmental glomerulosclerosis
Young adults, black men
Associated with drugs, obesity, HIV
Pattern: focal and segmental hyalinization of GBM, and sclerosis
iii. Membraneous nephropathy
adults
Associated with drugs, Hep B, syphilis, Lupus, malaria
Pattern: IgG deposits on thickened glomerular capillary walls
b. Secondary–
Poorly controlled DM (diabetic nephropathy*), Primary kidney disease and nephritic conditions, SLE, amyloidosis, HIV, pre-eclampsia, drugs (penicillamine, NSAIDs, lithium, heroin, gold compounds), Snake bite, cancer (lymphomas and leukemias), FH of congenital kidney dz

77
Q

Nephrotic syndrome

SSX

A

HTN: dec renal flow, renin secretion, increased BP in order to increase GFR
Decreased urine output
Edema, ascites, weight gain, “moon facies” (periorbital edema)
Foamy urine
Muscle wasting, weakness, malaise
Cough, exertional dyspnea
Risk of infections due to loss of immunoglobulins; risk of bleeding due to
loss of coagulation factors

78
Q

Nephrotic syndrome

Labs

A

Proteinuria >2g/m2/day (or >3.5 g/d), microalbuminuria (>30 mg/24 hr)
Hypoalbuminemia, hematuria, azotemia, lipiduria, dyslipidemia, oval fat bodies

79
Q

Diabetic Nephropathy

A

most common cause of nephrotic sydrome in US
Glomerular sclerosis and fibrosis from glycosylation of GBM proteins, cytokines, mesangial deposits and vascular endothelial damage. (over a course of years)

80
Q

when should you suspect diabetic nephropathy?

A

Suspected with patients with DM who develop proteinuria

81
Q

risk factors for diabetic nephropathy?

A

ethnicity (blacks, Latinos, Polynesians), duration/degree of hyperglycemia, HTN, dyslipidemia, smoking

82
Q

SSX for diabetic nephropathy?

A

early, asymptomatic
HTN, dependent edema, uremia (N&V, anorexia)
Diabetic neuropathy, retinopathy

83
Q

Labs for diabetic nephropathy?

A

Microalbuminuria 30-300 mg/d then progresses to proteinuria, to level of nephrotic syndrome and end-stage renal failure

84
Q

how to manage diabetic nephropathy?

A

control glucose levels, control BP, screen urine proteins
(microalbumin), HgA1c, retinal exams, diabetic foot testing
Also watch for:
infections (glucose in urine feeds bacteria e.g. PN risk)
neurogenic bladder (retention or incontinence dt neurologic damage)

85
Q

DDX for Nephrotic Syndrome: (other edema states)

A

CHF, Liver failure, PN, acute tubular necrosis (ATN), malignant HTN, multiple myeloma

86
Q

TUBULO-INTERSTITIAL DISEASES

A

Injury to renal tubules, interstitium or both; extent of damage can lead to acute or chronic renal failure

87
Q

Acute Tubular Necrosis (ATN)

Damage to renal tubular epithelial (RTE) cells from:

A

1) ischemia: shock (sepsis, anaphylaxis, hemorrhage), trauma, surgery, DIC
2) nephrotoxins: eg. aminoglycosides, amphotericin B, lithium, cisplatin, radiographic dyes, solvents, heavy metals, toxic mushrooms, NSAIDs

88
Q

Acute Tubular Necrosis (ATN)

SSX

A

depends on cause, course is variable. May lead to acute renal injury/failure
Possible: uremic pruritis, pericardial friction rub, asterixis, HTN, edema
Oliguria depending on severity and extent of tubular damage

89
Q

Acute Tubular Necrosis (ATN)

Lab

A

UA: mild proteinuria, hematuria, RTE and RTE casts with tubular fragments
CMP: elevated BUN/creatinine ratio, decreased GFR

90
Q

Acute Tubulointerstitial Nephritis (ATIN)

Inflammation of the renal interstitium, from

A

from cell-mediated immune response binding to interstitial proteins, leading to a decrease in renal function

91
Q

Acute Tubulointerstitial Nephritis (ATIN)

categories

A

a. ) Allergic Drug Reaction: (75%) Common meds: methicillin, sulfonamides, Cipro, NSAIDS, thiazide diuretics, allopurinol, phenytoin, captopril, cimetidine
b) Infections: (5-10%) Common organisms: Legionella, Leptospira, Strep, Corynebacterium diptheriae, Rickettsia, Toxoplasma, Salmonella, S.areus, Mycoplasma, TB, HIV, EBV, CMV
c) Related to systemic autoimmune dz: (10-15%) SLE, sarcoidosis, Sjögren’s, Wegener’s
d) Idiopathic

92
Q

Acute Tubulointerstitial Nephritis (ATIN)

SSX

A

acute onset of dec renal function, days to 2 weeks post admin of meds or infx
fever, rash, hematuria, oliguria, nausea, vomiting, malaise

93
Q

Acute Tubulointerstitial Nephritis (ATIN)

Lab

A

UA: hematuria, mild to moderate proteinuria, high WBCs, WBC casts, NO bacteria Eosinophiluria often present
CBC: eosinophilia
As renal function is impaired, see inc serum creatinine
FENa > 1% indicates tubular damage
Other: Depending on cause–PPD skin test, serology may be indicated
Procedure: renal biopsy if persisting symptoms

94
Q

Chronic Tubulointerstitial Nephritis (CTIN)

SSX

A

nocturia, uremia sx, small kidneys, hyperkalemia, reduced SG
Hyperchloremic metabolic acidosis from:
1. Reduced ammonia production
2. Inability to acidify the distal tubules
3. Proximal tubule bicarb wasting

95
Q

Chronic Tubulointerstitial Nephritis (CTIN)

Causes

A

a) Obstructive uropathy renal stone, prostate dz, carcinoma of cervix, colon, bladder
SSX: in partial obstruction urine output alternates from polyuria (vasopressin insensitivitiy) and oliguria (dec GFR)
Late: Azotemia and HTN

b) Reflux nephropathy “Vesicoureteral reflux” incompetent sphincter allows retrograde
SSX: HTN, renal insufficiency, hx of recurrent UTI in kids Renal scarring can lead to proteinuria and CKD.

c) Analgesic nephropathy
Common in women 50-55. Causes 3-5% of all end-stage renal failure in U.S.
SSX: many are asx (found incidentally), polyuria, HTN
Lab: hematuria, proteinuria, anemia, inc serum creatinine
Sloughed papillae can be found in the urine

d) Lead nephropathy (and other heavy metals, like cadmium)
Children 3-6mos from pica, Environmental or occupational exposure
Pb: filtered by glomerulus and transported across the proximal convoluted tubules and accumulated.

96
Q

General Work-up for CTIN:

A

Laboratory: UA, BUN, Serum creatinine, electrolytes
Abdominal U/S or IVU to investigate obstruction or reflux
Analyze history of analgesic use
CT without contrast shows small, calcified, indented kidneys
EDTA chelation test for heavy metals