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38 Cards in this Set

  • Front
  • Back
clearance formula
C = UV / P

if C < GFR then there is net tubular reabsorption
if C > GFR, then there is net tubular secretion
if C = GFR than there is no secretion or reabsorption
components of glomerular filtration barrier
fenestrated capillary endo (size barrier)
fused basement membrane w/heparan sulfate (negative charge barrier)
epithelial layer of podocyte foot processes
GFR formula
inulin can be used to calculate GFR b/c is freely filtered and neither reabsorbed nor secreted

GFR = UV/P of inulin

also = Kf (Pgc-Pbs) - (Pi gc - Pi bs)

pi bs normally = 0
ERPF formula
can be estimated using PAH (b/c is filtered and secreted in proximal tubule)


RBF = RPF / (1-Hct)
filtration fraction

** angiotenin II constricts efferent arteriole=>
low RPF, high GFR, so FF increases
(so an ACE-I leads to decreased FF)

high plasma protein = low FF
and vice versa
constricted ureter = low FF
free water clearance
C water = V- C osm

V = urine flow rate
C osm = UV/P osm
NSAIDs can cause acute renal failure how?
in high vasoconstrictive states... by inhibiting the renal production of prostaglandins
(prostaglandins vasodilate afferent arteriole to increase GFR)
winter's formula
Pco2 = 1.5 (HCO3) + 8 +/- 2

(use to determine compensation for metabolic acidosis)
compensation for metabolic alkalosis
PCO2 should increase by 0.7 for every 1 increase in bicarb
toxicity of loop diuretics

ototoxicity, hypokalemia, dehydration, allergy [sulfa], nephritis [interstitial], gout
ethacrynic acid
same action as furosemide

but is NOT a sulfa drug
toxicity of thiazides

glycemia, lipidemia, uricemia, calcemia

also sulfa allergy, hyponatremia, hypokalemic metabolic alkalosis
effects of diuretics on pH
acidosis: CAIs, K sparing

alkalosis: loops, thiazides
potter's syndrome
= bilateral renal agenesis
when ureteric bud doesnt form from the mesonephric duct
limb, facial deformaties
pulmonary hypoplasia
not compatible with life
Fanconi's syndrome
hereditary or acquired dysfxn of the proximal renal tubules
glycosuria, hyperphosphaturia, aminoaciduria, acidosis
____ autoregulates RBF
the renal vasculature

keeps RBF constant even when arterial pressure varies from 100-200 mmHg

*RBF = 25% of cardiac output
types of RTA
(normal anion gap)
type 1 [distal]: failure to excrete titratable acid, NH4
type 2: renal loss of HCO3
type 4: hypoaldosteronism (poor excretion of NH4 and hyperkalemia)
prerenal ARF
low CO
increased systemic vasc resistance
drugs (COX inhibitors and ACE-Is)
renal ARF
renovesicular obstruction
HUS, TTP, DIC, SLE, ATN, scleroderma
postrenal ARF
bilateral ureteric obstruction
prostatic hyperplasia
bladder neck obstruction
WAGR syndrome
wilm's tumor [WT-1 on chrom 11p]
aniridia [absence of the iris]
genital anomalies
mental retardation
treatment of SIADH
lithium or demeclocycline

block the effects of ADH (prevents excessive water retention)
central DI treatment
desmopression (ADH analogue)

**not useful in nephrogenic ADH, when kidneys don't respond to ADH
kidney vasculature most susceptible to damage from a sickle crisis
vasa recta
->due to the very high osmo of the renal medulla
->ischemia can cause patchy papillary necrosis, proteinuria, and cortical scarring
membranous glomerulonephritis
PAS positive electron dense deposits distributed along epithelial side of the capillary basement membrane
nodular glomerularsclerosis [Kimmelstiel Winston disease]
ass'd with DM
ovoid hyaline masses in the periphery of the glomerulous

also see widespread capillary basement membrane thickening and diffuse glomerulosclerosis
renal hemodynamics in pregnancy
increased GFR, increased circulating plasma volume

'normal' creatinine can be less than 1.0
there is a specific association between _________ [renal disease] and HIV
seen with IVDU/HIV
does not respond to steroids, poor Px
also see hyalinization with focal deposits of IgM and C3
P-osm equation
(total body osm - urine osm)/
(total body water - urine vol)

TBW = (body wt) x 0.6 (0.5 in F)
total body osm = (intial P osm x total body osm)
median umbilical ligament
adult derivative of the urachus
->derivative of the allantoic duct
->normally the duct fuses
->but if it remains patent, a young patient can have urine discharge from umbilicus
effectiveness of diuretics is dependant on the pts creatinine clearance
loops: work down to 10 mL/min

thiazides and potassium sparing: work down to 40 mL/min
only site in the kidney where epithelial cells have a 'brush border'

(allows enhancement of ability reabsorb plasma constituents)
derived from the ureteric bud
collecting system and renal pelvis

(other parts like loop of Henle, bowman's capsule, glomerular tuft: are from metanephric mesoderm)
segment of kidney with lowest osmolarity
early distal tubule

is usually <150 [called the diluting segment]
benign nephrosclerosis
finely granular surface
multifocal loss of glomeruli in the superficial cortex

**malignant hypertension will cause a mottled, hemorrhagic appearance
ureter is anterior to which anatomic level
bifurcation of the common iliac artery
retroperitoneal fibrosis
causes progressive compression of ureters and subsequent hydronephrosis
loop diuretics cause this type of alkalosis
contraction metabolic alkalosis