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68 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Relative to the nephron as a whole, where are the glomeruli and collecting ducts located?
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Glomeruli - cortex
Collecting ducts - medulla |
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Which kidney is taken during donor transplant and why?
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Left kidney is taken during transplant because it has a longer renal vein.
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Where in the glomerulus apparatus are the juxtaglomerular cells? The macula densa? What do they each do?
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Each is part of the JGA.
JG cells line the afferent arteriole and release renin in response to decreased renal blood pressure Macula dense cells are in the distal convoluted tubule and direct the JGA to secrete renin in response to decreased Na delivery to distal tubule |
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What stimulates the JGA to release renin?
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1. Decreased BP sensed by JG cells
2. Decreased Na sensed by macula densea 3. Increased sympathetic tone (beta 1) |
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How do the ureters course?
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Ureters: water under the bridge:
Ureters under the uterine artery and ductus deferens |
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How much of the total body weight is water? What different compartments is this divided into?
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60% of body weight is water:
- 1/3 ECF and 2/3 ICF Of the ECF: 1/4 is plasma and 3/4 is interstitial fluid |
60-40-20 rule:
60% total body weight 40% ICF 20% ECF |
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How do you measure ECF and plasma volume?
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ECF - inulin
Plasma - radiolabeled albumin |
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What is average osmolarity?
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Avg osmolarity - 290 mOsm
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What are the portions of the glomerular filtration barrier and what does each do?
Which barrier is lost in nephrotic syndrome? |
1. Fenestrated capillary endothelium (size barrier)
2. Fused BM with heparan sulfate (negative charge barrier) 3. Epithelial layer with podocyte foot processes |
Charge barrier is lost in nephrotic syndrome.
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What is the formula for clearance?
How does the relation of clearance and GFR reflect overall movement of substance? |
Cy = Uy x V / Py
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Cy > GFR is net tubular secretion
Cy < GFR is net tubular reabsorption |
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What substance is ideal for calculating GFR? What substance is more often used?
How is this calculated? |
Inulin is idea for calculating GFR bc it is freely filtered and neither reabsorbed nor secreted. Creatinine is a close second, but slightly overestimates GFR bc it is lightly secreted .
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GFR = Ui x V / Pi
= Clearance of inulin = Pressure difference between glomerular capillary and Bowman's space minus the oncotic difference between the two. The oncotic pressure at Bowman's space is usually 0. |
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What is PAH used to calculate?
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PAH = Effective renal PLASMA flow
- PAH is filtered and nearly fully secreted. (It underestimates by ~10%). |
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What is RPF as opposed to renal blood flow (RBF)?
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RBF = RPF / (1-Hct)
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How is filtration fraction calculated?
What is normal FF? What is filtered load? |
FF = GFR / RPF
Normal FF = 20% |
Filtered load = GFR x plasma concentration
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What is the path of blood flow into and out of the kidney (looking forward and back a few vessels)?
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Renal artery --> interlobar artery --> interlobular arter -->
Afferent arteriole--> efferent arteriole --> vasa recta --> interlobular vein --> interlobar vein --> renal vein |
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What is free water clearance? What is the formula for calculating it?
How does it controlled? |
Free water is total urine - water occupied with solute.
You have to calculate the solute concentration which = Urine osm x urine flow rate / plasma osm |
Free water is controlled by ADH
- With ADH - retention of free water (>0) - Without ADH - excretion of free water (<0) - Isotonic urine (=0) seen with loop diuretics |
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Where in the nephron is glucose reabsorbed? Under what type of transport?
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Glucose is reabsorbed at the proximal tubule under Na/glucose cotransport (GLUT-2)
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Where are amino acids reabsorbed and via what type of transport?
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Amino acids are reabsorbed in the proximal tubule by Na-dependent transporters (3 diff ones).
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What is Hartnup's dz?
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Hartnup's dz:
- Deficiency of neutral amino acid (tryptophan) transporter resulting in decreased niacin and pellagra (3D's) |
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How does PTH affect the proximal tubule?
How does ATII affect the proximal tubule? |
PTH --> inh Na/phosphate cotransport which leads to phosphate excretion
AT II --> stimulates Na/ H exchange which leads to Na and water reabsorption. |
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Where in the nephron is ammonia generated?
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Ammonia is generated and secreted in the proximal tubule to buffer secrete H+.
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Where is urine made most concentrated? How is this done?
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The thin descending loop of Henle is impermeable to Na and in the renal medulla which is hypertonic. Therefore, water is reabsorbed and Na is left in the lumen, creating a hypertonic urine.
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What occurs in the thick ascending loop of Henle? What transporter directs this?
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Thick ascending loop:
Na-K-2Cl pump (can be affected by loops) actively reabsorbs each and induces passive reabsorption of Mg2+ and Ca2+. Thick ascending loop is impermeable to water, so lumen becomes less concentrated. |
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What happens in the distal convoluted tubule?
How does PTH affect this segment? |
Distal convoluted tubule:
Na-Cl channels (thiazides) actively reabsorb Na and Cl and passively reabsorb water. This makes a hypotonic urine. |
PTH causes increased Ca-Na exchange and net Ca reabsorption.
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What happens in the collecting tubules?
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Na is reabsorbed in exchange for K and H (regulated by aldosterone). This is why K-sparing diuretics block aldosterone.
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How do aldosterone and ADH affect the collecting tubule?
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Aldosterone - leads to insertion of Na channel on luminal side --> greater Na exchange for K and H.
ADH acts on V2 receptors to insert aquaporins on luminal side (reabsorption of water) |
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What are the 6 effects of AT II?
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1. Acts on vascular SMC to cause vasoconstriction and raise BP>
2. Constricts efferent arteriole which raises FF (lowers RBF and raises GFR) 3. Stimulates aldosterone syn which leads to more Na exchanged for H and K at the collecting tubules |
4. Stimulates ADH secretion from post pituitary which leads to increased aquaporin insertion into the principal cells of the collecting tubules
5. Increases Na/H exchange at proximal tubule 6. Stimulates hypothalamus to cause thirst |
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Which cells of the kidney release erythropoietin?
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Endothelial cells of peritubular capillaries release EPO in response to hypoxia
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How do NSAIDS affect the kidney?
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NSAIDS --> decreased prostaglandin syn --> less vasodilation of afferent arterioles --> decreased GFR and decreased RPF so FF remains constant
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What effects does PTH have on the kidney?
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PTH:
1. Proximal tubule: inh Ph reabsorption (inh Na/Ph cotransport) 2. Distal convoluted tubule: increased Ca reabsorption (Ca/Na exchange) |
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What enzyme in the kidney is involved in vit D syn?
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25-OH vit D ---> 1,25-(OH)2 vit D via 1a-hydroxylase
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How does ANP affect the nephron?
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ANP --> increases GFR and increases Na filtration without increasing Na reabsorption at distal nephron
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What causes K shift intracellularly?
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These push K into cells:
1. Insulin (Na/K ATPase increased) 2. B-adrenergic agonists (Na/K ATPase increased) 3. Alkalosis (K/H exchanger) 4. Hypo-osmolarity |
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What is the Henderson-Hasselbalch equation?
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pH = pKa + log [HCO3-] / (0.03 x P CO2)
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How do pH, P CO2 and [HCO3-] look in:
resp acidosis met alkalosis |
resp acidosis:
decreased pH, increased P CO2 and increased [HCO3] to compensate met alkalosis: increased pH, increased P CO2 (compensatory) and increased [HCO3-] |
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How do you quantify respiratory response in compensation for a metabolic acidosis?
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First: metabolic acidosis --> decreased respiration and thus increased pCO2.
pCO2 = 1.5 (HCO3) + (6 to 10) |
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What are normal values for pCO2 and HCO3-?
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nl pCO2 = 35-45
nl [HCO3-] = 22-26 |
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What are the main causes of resp acidosis?
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Respiratory depression --> resp acidosis:
- Airway obstruction, COPD, acute lung dz - Opioids, narcotics, sedatives - Weakening of resp muscles |
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What are the main causes of resp alkalosis?
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Resp alkalosis - hyperventilation (e.g. early altitude exposure) or aspirin (early effect)
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What are the main causes of metabolic alkalosis?
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Metabolic alkalosis:
- Diuretic use - Vomiting - Antacid use - Hyperaldosteronism |
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What are the main causes of normal anion gap metabolic acidosis?
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Normal anion gap met acidosis:
- diarrhea - glue sniffing - renal tubular acidosis - hyperchloremia |
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MUD PILES
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MID PILES are the anion gap metabolic acidoses:
M - Methanol (formic acid) U - Uremia D - DKA P - Paraldehyde or phenformin I - Iron tablets of INH L - Lactic acidosis E - Ethylene glycol (oxalic acid) S - Salicylates |
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How do you measure anion gap?
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Anion gap:
Na - (Cl + HCO3) nl = 12 |
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What are the different types of renal tubular acidosis (RTA)?
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RTA's:
Type I (distal) - Defect in collecting tubule to excrete H+ (ass w/ hypokalemia and risk of calcium stones Type 2 (proximal) - Defect in proximal tubule HCO3- reabsorption (ass w/ hypokalemia and hypophosphatemic rickets) Type 4 - Hypoaldosteronism or lack of response leading to hyperkalemia and inh of ammonia excretion in proximal tubule (leads to decreased urine pH due to decreased buffering capacity) |
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RBC casts
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RBC casts - glomerulonephritis, ischemia, malignant HTN
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WBC casts
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WBC casts - tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
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Granular or muddy brown casts
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Granular or muddy brown casts - acute tubular necrosis
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Waxy casts
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Waxy casts - advanced renal dz / CRF
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Hyaline casts
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Hyaline casts - non-specific
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What is seen in the urine of a patient with bladder cancer or kidney stones?
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Bladder cancer and kidney stones both cause RBCs to be excreted in urine but not as casts.
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What is seen in urine of a patient with acute cystitis?
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Acute cystitis causes WBCs to appear in urine, but not as casts.
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How is nephritic syndrome defined?
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Nephritic syndrome is inflammatory and is associated with hematuria and RBC casts, but less than 3.5 g/day of proteinuria.
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What type of renal syndrome is seen post-strep? What characterizes it?
What is seen on LM, EM and IF? |
Post-strep glomerulonephritis is a nephritic syndrome characterized by peripheral and periorbital edema. It resolves spontaneously/
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Post strep imagery:
LM - glomeruli enlarged and hypercellular with PMNs EM - subEPIthelial immune complexes IF - granular |
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Which nephritic syndrome has the worst prognosis?
What diseases can cause this condition? |
Rapidly progressing or crescentic glomerulonephritis has the worst prognosis (RPGN)
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Crescentic or RPGN causes:
1. Goodpasture: linear IF, type II hypresensitivity, anti-GBM (also involves lungs) 2. Wegener's granulomatosis: c-ANCA 3. Microscopic polyarteritis: p-ANCA |
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What is the most common cause of death in SLE patients?
What is seen on imaging in this disease? |
SLE patients most commonly die of diffuse proliferative glomerulonephritis.
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Diffuse proliferative glomerulonephrits:
Subendothelial DNA-anti-DNA IC's --> wire-looping of capillaries IF - granular |
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What is Berger's Disease?
What is seen on imaging? |
Berger's disease - IgA glomerulonephropathy (similar to Henoch-Schonlein purpura of children). Often presents with URI or acute gastroenteritis.
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Berger's imaging:
LM and IF - IC's deposit in mesangium (IF will ping for IgA) |
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Biopsy of kidney shows split basement membrane on EM. Is this a nephritic or a nephrotic syndrome? What is the name of this condition?
What other disorders accompany this condition? |
Alport's syndrome: mutation in collagen type IV that leads to split basement membrane and causes nephritic syndrome.
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Alport's syndrome is often accompanied by nerve disorders, ocular disorders and deafness.
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What is the definition of a nephrotic syndrome? What signs indicate it? And what is it associated with in terms of other complications?
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Diabetic nephropathy is proteinuria > 3.5g/day which will cause frothy urine, hyperlipidemia, fatty casts and edema. It is associated with increased risk of thromboembolism and infection (loss of Ig)
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What is the most common adult cause of nephrotic syndrome?
What is seen on imaging? |
Membranous glomerulonephritis (diffuse membranous glomerulopathy) is the most common adult nephrotic syndrome. It can be caused by drugs, infections, SLE, and solid tumors.
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Imaging of membranous glomerulopathy:
LM - diffuse capillary and GBM thickening EM - spike and dome appearance with subEPIthelial deposits IF - granular |
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What is the most common cause of nephrotic syndrome in children?
What is lost in this disorder and what is seen on imaging? |
Minimal change disease is the most common nephrotic syndrome in children. It can be triggered by illness or immune stimulus and responds to corticosteroid therapy.
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In minimal change disease, also known as lipoid nephrosis, there is a selective loss of albumins (no globulins) due to GBM polyanion loss.
LM - normal EM - foot process effacement |
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What type of glomerular damage does amyloid deposition cause in the nephron?
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Amyloid --> nephrotic syndrome (ass. w/ MM, TB, RA) and can be seen with congo red stain.
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How does diabetes affect the nephron?
What is seen on imaging? |
Diabetes causes non-enzymatic glycosylation which causes increased permeability and thickening, increased GFR and mesangial expansion.
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Diabetic glomerulonephropathy imaging:
LM - mesangial expansion, GBM thickening, nodular sclerosis (Kimmelstiel-Wilson) |
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What is the most common glomerular disease seen in HIV patients?
What is seen on imaging? |
HIV --> focal segmental glomerulosclerosis
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Focal segmental glomerulosclerosis imaging:
LM - segmental sclerosis and hyalinosis |
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In what disorder is seen a "tram-track" appearance to GBM? What causes this and what is seen on all the imaging?
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Membranoproliferative glomerulonephritis Type I causes tram-track appearance on EM an subendothelial ICs with granular IF. Tram track appearance is due to GBM splitting caused by mesangial growth.
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What are the two types of membranoproliferative glomerulonephritises (MPGN) and what is associated with each?
How does MPGN progress? |
MPGN type I - HBV > HCV
MPGN type II - C3 nephritic factor (this prevents deactivation of the complement pathway by factor H) |
MPGN can also present as a nephritic syndrome (diffuse proliferative glomerulonephritis) and usually slowly progresses to CRF.
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Subendothelial humps
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Subendothelial humps - lupus glomerulonephritis
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Wire looping
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Diffuse proliferative glomerulonephritis or membranous glomerulonephritis (both can be caused by lupus)- wire looping
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Spike and dome
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Spike and dome - membranous glomerulonephritis (aka diffuse membranoud glomerulopathy)
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