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Podocytes
Foot processes
Basement
Membrane
• Filtration Fraction
– ACEI
• Dilate efferent
• Decrease GFR
• Decrease FF
– NSAID
• Constrict afferent
• Decrease RBF
• Decrease GFR
• No change FF
Importance of Prostaglandins
Juxtaglomerular Cells
Modified Smooth
Prostaglandins Renin muscle cells
Afferent arteriole
Macula Densa
Distal tubule
Senses Na
Angiotensin I
Aldosterone Angiotensin II
Adrenal
Autoregulation
Increased afferent
arteriolar vasodilation Autoregulation
PGE2 Increased efferent
PGE2
NO arteriolar constriction
PGI2 Angiotensin II
A c u te R e n a l F a ilu r e
P r e -r e n a l
R enal
A TN
I n te r s titia l N e p h r itis
G lo m e r u lo n e p h r itis
V a s c u la r
P ost - R en al
Outpatient Acute Kidney Injury :
Etiologies
10%
Obstructive Uropathy
Acute GN
10%
Acute Interstitial
66% Nephritis
9%
22%
48%
Renal Origin : AKI
ATN
(85%)
Ischemic Toxic
(50%) (35%)
Pars
Convoluta
Pars Recta
AKI – Site of Injury
• Ischemic
– Outer Medulla
• Proximal tubule
–Pars recta
• TALH (major site)
• Toxic
– Proximal tubule (pars convoluta) >>
Distal tubule
Laboratory Evaluation of ARF
Pre- renal ATN
Azotemia
Urine Sodium < 20 > 40
• Initiating Phase
– Time of exposure to hemodynamic or
toxic insult
• Oliguric Phase
– Period of oliguria (67%)
• Urine volume < 400 cc/day
Duration of AKI at this point : 10 –14 days
Phases of AKI
• Diuretic phase
– Increasing urine output (non-oliguric)
– No change in renal function
• Recovery phase
– May last 3 – 12 months before full
functional recovery occurs
• Acid base / Water homeostasis
CKD
• Acidosis
– Impaired ammoniagenesis –inability to secret H+ -
initially non anion gap then in advanced CKD/ESRD –
high anion gap
• Supplement HCO3
• Anemia
– Lack of erythropoietin – made in interstitium
• Inject erythropoietin
• Hyperparathyroidism
– Trade off hypothesis – increased Phos, decreased calcium
(low vitamin D) followed by increased PTH=
osteodystrophy
• Treat with phos binders
Initiation of RRT
• Laboratory indicators:
– Unmanageable hyperkalemia
– Severe Metabolic acidosis
– Uremic Symptoms / Encephalopathy
• (ie. nausea, vomiting, altered mental acuity,
seizures, anorexia)
– Pericaridal rub
– Unmanageable volume overload
Telescopic Urine
Nephrotic Syndrome
Adults Children
Minimal Change 10 - 15 75
Membranous 20 - 30 <5
Membranoproliferative 10 - 15 15 - 20
NORMAL
Oxalate crystals
Anion Gap Metabolic Acidosis:
Phases of Ethylene Glycol Toxicity
Ethylene Glycol Stage 1
Alcohol Dehydrogenase
Glycoaldehyde
Aldehyde Dehydrogenase
Alcohol Dehydrogenase
Glycoaldehyde Direct
Fomepizole
Inhibition
Aldehyde Dehydrogenase
• Ethylene Glycol
AND Brand New !!!!!
• Methanol
• Salycylates
• Uremia
• Ketoacidosis
– Diabetic Iron overdose
– Alcoholic
Isoniazid
• Lactic Acid
Propylene glycol
Methanol Overdose
Formic Acid
Urease
What is this ???
Cystine
Cystinuria
Calcium Oxalate
Uric Acid
Cystine
Xanthine
Triple Phosphate
Triamterene
Calcium Phosphate
Ephedrine
Calcium Oxalate Stones : Treatment
• Hypercalciuria
– Decrease sodium intake (< 150 meq/day)
– Do not decrease dietary calcium !!!
• Increased risk of stone disease with reduced
calcium intake
• Dietary calcium supplements decreased stone
formation
Rationale
– Calcium is necessary to bind dietary oxalate in the
intestines which prevents its absorption
– Reduced intestinal calcium allows enhanced oxalate
absorption
Hypercalciuria
• Diuretics
– Thiazide diuretics reduce urinary
calcium
• Mild volume depletion
• Enhanced urinary sodium and
calcium absorption
– Do not use loop diuretics
• Increase urinary calcium
Hyponatremia : YES or NO
Osmoles
Plasma
Interstitial Intracellular
3.5 L 11.5 L 28 L
14 L
TBW
Intracellular Extracellular
2/3 1/3
Interstitial Intravascular
3/4 1/4
10% 2% Osmolality results in
Volume results
A linear increase in
in an exponential
ADH secretion
increase in ADH