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82 Cards in this Set

  • Front
  • Back
blunting of the calyces
pyelonephritis; get blunted under the scarred/contracted tissue
fever, rash, oliguria, pyuria (esosinophils) after a pt is put on a drug (methicillin)
acute drug induced interstitial nephritis

stop the drug (combo type I and IV hypersensitivity)
caused by chronic hypertension which causes hyaline arteriosclerosis in the kidney
pt w headache, blurry vision,

paiplladema, malignant htn
"flea bitten kidney" red and black

This is called a flea-bitten kidney and is associated with glomerular damage, glomerulitis, arteriolitis and hemorrhage in a case of malignant hypertension.

onion skinning arteriosclerosis, petechiae (ruptured blood vesels); petechial lesions on cortex
in a pt w irregular irregular pulse
Multiple pale renal infarcts
Note the irregular white areas on the cortical surface. Most infarcts occur from embolic disease from the left heart.
pt w a renal mass. Pt is a smoker and obese.

labs show polycythemia and hypercalcemia
renal cell carcinoma (VHL on chromosome 3, polyognal clear cells full of glycogen, paraneoplastic syndromes (ectopic EPO = polycythemia, PTHrP = hypercalcemia)
kid with unilateral flank mass and hypertension
wilms tumor

htn bc tumor is making renin

chromosome 11
aniridia (absent iris) and one limb greater than the other
wilms tumor; chromosome 11
painless hematuria
bladder cancer (transitional cell)
baby w potters facies (flattened nose, low-set ears, and recessed chin)
hx of HTN, abnormality of ultrasound in the renal pelvis,
and had click murmur (therefore MVP) – dx?
pt with HTN, abnormality on ultrasound in renal
area, lost 600 mls of blood all of a sudden, leading to hematochezia (MCC hematochezia =

associated w ADPKD
how does an increase or decrease in capillary oncotic pressure affect GFR
increase = decreases GFR (reaches equilibrium faster)
decrease = increases GFR (takes longer to reach equilibrium)
how does an increase or decresae in Kf affect GFR
increase Kf = increseased GFR (more can filter across bc o fincreased permeability)
decreased Kf = decreased GFR (less can filter across)
how does afferent dilation or constriction affect hydrostatic pressure and renal plasma flow
afferent dilation = increased hydrostatic pressure, increased renal plasma flow
afferent constriction = decreased hydrostatic pressure, decreased renal plasma flow
affects of efferent constriction and dilation on cap hydrostatic pressure
e. c. = increased hydrostatic pressure
e. d. = decresaed hydrostatic pressure
salicylate poisoning
dense calcification of kidney
compication of chronic pyelonephritis
differentiate acute vs chronic pyelonephritis other than time frame
APN = fever, spares cortex

CPN: assymetrical scarring, blunted calyces, thyroidization of kidney (eosinophilic casts)
primary pathogen capable of causing UTI + liver abscess and pneumonia in otherwise healthy people.
klebsiella pneumoniae
K capsular antigen
electron dense deposits composed of Ig and complemtn within the basement membrane
MPGN II (dense deposit disease)
does MPGN type I or II involve complement activation
subepithelial deposits
acute GN (post streptococcal = subendothelial humps)
Epimembranous deposits
Membranous GN
Subendothelial deposits
lupus glomerulonephritis (diffiuse proliferative)
deposits in mesangium
IgA nephropathy/Henoch-Schonlein GN
fibromuscular dysplasia
stenotic renal artery; mc in YOUNG WOMEN
embryonic glomerular structures
Wilms tumor (deletions involving WT1 located on c11)
enlarging abdominal mass w normal VMA
Wilms tumor (deletions involving WT1 located on c11)
WAGR complex
Wilms tumor, aniridia, genitourinary malformation, mental motor retardation
19 y/o male w dysuria and yellow green urethral discharge; play odds
nongonococcal urethritis (more common than gonococcal)

i.e. chlaymdiae (intracellular)
High fractional excretion of sodium indicates what
Post renal (can't reabsorb sodium)


>40 urine Na
Low fractional excretion of sodium indicates what


<10 urine Na
leukocytes and neutrophils
tubulointerstitial nephritis
pulmonary congestion
due to fluid overload in acute glomerulonephritis
uniformly progresses to chronic renal failure if untreated
diffuse proliferative glomerulonephritis (SLE)

mcc of death in SLE
why would a pt be hypocalcemic in chronic renal failure
decreased calcitriol synthesis -> hypocalcemia
secondary hyperparathyroidism -> hypercalcemia, phosphauria
management of hyponatremia
water restriction
management of hyperphosphatemia
phosphate binders (niital)
management of hypervolemia
decreased salt and water intake + loop diuretics
this dz is due to hyperparathyroidism and is associated w myopathy
Osteitis fibrosa
Adynamic bone disease
oversuppression of PTH
Suppressor of PTH production
1,24 dihydroxyvitamin D? not sure
hematuria time frame in APSGN vs IgA nephropathy
IgA = fast, very close

APSGN = 10 days or more after infection (often a cutaneous infection)
pathologic features of predominant small artery involvement w intimal proliferation and sometimes thrombosis also termed "thrombotic microangiopathy" is found in which renal dzs
HUS, TTP, scleroderma, sickle cel nephropathy, malignnat htn

the primary process is endothelial damage
why dont give loop diuretic sin nephrotic syndrome
high dose loop diureics can precipitate renal failure in nephrotics bc the intravascular volume cannot be defende dby hypoalbuminemia (thus you accelerate hypoalbuminemia worsening fluid status)
causes of euvolemic hyponatremia
causes of hyponatremia w low urine sodium
CHF (decreased renal perfusion = decreased perfusion)
pt w hypertension, alkalosis, hypokalemia
Hyperaldosteronism (Conns syndrome)
diagnosis of medullar sponge kidney
function of the urine anion gap
differentiates renal from nonrenal causes of nongap acidosis
associated w elevated lipids, glucose or plasma proteins
causes of hypervolemic hyponatremia
CHF, cirrhosis and nephrotic syndrome, massive edema of any cause
causes of isovolemic hyponatremia
SIADH, cerebral trauma
selective proteinuria
minimal change dz
prognosis of minimal change
good; responds to steroids
prognosis of ASGN
often resolves spontaneously
prognosis of RPGN
prognosis of DPGN
bad (lupus)
what should you not use to tx malignant htn
ACe inhibitor (can bottom out GFR = renal failure)
stones in alkaline urine
ammonium magnesium phosphate (struvite)
lithium association
nephrogenic diabetes insipudus
how to differentiate nephrogenic diabetes insipudus from central diabetes isnipudus?
desmopressin injection

if central, will increase urine conc
if nephrogenic, no effect
sitmulates production of cAMP -> insertion of aquaporins on apical surface of collecting ducts
waxy casts w very low urine flow
WBC casts in urine
acute pyelonephritis or cystitis
vasculitis from exposure to endotoxin causing glomerular thrombosis
Schwartzman reaction (following second exposure to endotoxin)
Urethritis, conjunctivitis, arthritis in a male
Reiter's syndrome (reactive arthritis associated w HLA-B27)
Streak ovaries, congenital heart disease, horseshoe kidney
Turner syndrome (XO, short stature, webbed neck, lymphedema)
renal cell carcinoma, hemangioblastomas, angiomatosis, pheochromocytoma
VHL disease (dominant tumor suppressor gene mutation)
Red urine in the morning
paroxysmal nocturnal hemoglobinuria
Polyuria, acidosis, growth failure, electrolye imbalances
Faconi's syndrome (proximal tubular reabsorption defect)
Palpable purpura, joint pain, abdominal pain (child)
Henoch-Shonlein purpura (IgA vasclitis affecting skin and kidneys)
Hypertension, hypokalemia, metabolic acidosis
Conn's syndroem (primary hyperaldosteronism)
deep, labored breathing/hyperventilation
Jussmaul breathing (diabetic ketoacidosis)
free water clearance
Defined as the volume of distilled water that would have to be added to or subtracted from the volume of urine produced in one minute so as to make that urine isomotic with plasma.

(-) free water clearance = concentrated urine
(+) free water clearance = dilute urine
(0) free water clearance = isomotic urine
Cockcroft-Gault Prediction of Creatinine Clearance
CCr = 140 - AgxWt/Plasma creatinine x 72

for women multiply by .85
clinical examples of neurogenic flaccid bladder
The bladder frequently becomes distended,
the wall thins, and bladder tone decreases. However, some residual contractions remain
because of the intrinsic contractile response of smooth muscle to stretch. As a rule,
residual volume is present after urination. Incontinence is present, and urinary retention
occurs. Perianal sensation, and the anal and bulbocavernous reflexes are abolished. Bladder
volume is increased, but bladder pressure is decreased
flaccid neurogenic bladder
Bladder volume is often
reduced and reflex hyperactivity may lead to a state of spastic neurogenic bladder,
in which the bladder fills to a set point, and then spontaneously empties whether it is
convenient for the patient or not. Perianal sensation is preserved, and the anal and bulbo-
cavernous reflexes are normal. Bladder intravesical pressure is increased but bladder volume is decreased.
spastic neurogenic bladder; frequent UTis bc of residual volume

In addition, during the
period of overflow incontinence before the voiding reflex is re-established, these patients
must be catheterized frequently, further predisposing them to urinary tract infections.
The level of the lesion is between the lower brainstem or spinal cord above the level of the conus medullaris.
what do the anal or bulbocavernous reflex measure
These reflexes measure the integrity of S2, 3, and 4.