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193 Cards in this Set
- Front
- Back
What RTA is characterized by high urine pH, hypercalciuria, hypocitraturia, and calcium phosphate stones?
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Type I RTA (Distal)
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Microvillus transformation, foot process effacement --> MCD
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?
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What classes of drugs should be used to treat hypertension in:
CHF |
Thiazide diuretic, beta-blocker, ACEi, ARB, aldo antagonist
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What happens when you give an isotonic NaCl injection?
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Remains almost entirely extracellular, causing an increase in the overall ECF volume.
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What would the urinalysis reveal in:
Pre-renal ARF |
minimal protein
no cells or casts Uosm > 500 (kidneys are functioning well) FENa < 1 % |
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What substances can cause nephrotoxicity activity at:
Afferent arteriole |
NSAIDs, sulfonamides
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What glomerular disease is hepatitis C associated with?
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Membranoproliferative glomerulonephritis
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What are causes of Type I RTA?
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Mutation in proton ATPase on alpha-intercalated cells
Mutation in carbonic anhydrase Mutation in Cl-HCO3- exchanger on BL membrane |
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FSGS
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?
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What classes of drugs should be used to treat hypertension in:
Post-MI |
Beta blocker, ACEi, aldo antagonist
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What happens when you give a hypertonic NaCl injection?
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Some isotonic expansion of the ECF and some increase in osmolality, resulting in the extraction of water from the ICF.
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What would the urinalysis reveal in:
Acute tubular necrosis |
Mild protein
Casts Uosm < 350 FENa > 1% |
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What substances can cause nephrotoxicity activity at:
Glomerulus |
Metals, NSAIDs
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What is the morphology of MPGN?
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Large glomeruli, proliferation of mesangium and leukocytes. Lobular appearance. Thick GBM, often with double contour (subendothelial deposits)
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What RTA is characterized by appropriately acidified urine, hyperchloremic acidosis but in acid balance, and bicarbonaturia when alkali is administered?
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Type II RTA (Proximal)
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What classes of drugs should be used to treat hypertension in:
High CVD risk |
Thiazide, beta blocker, ACEi, calcium channel blocker
|
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FSGS
|
?
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What happens when a hypotonic NaCl injection is given?
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Some isotonic increase in ECFV, proportional increases in ICFV and ECFV with reductions in ICF and ECF osmolalities.
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What substances can cause nephrotoxicity activity at:
Proximal tubule |
Metals, pigments (protein), antineoplastics (Cis-platin), antibacterials, cyclosporine, rampamycin
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What would the urinalysis reveal in:
Acute interstitial necrosis |
Mild protein
RBCs, WBCs, Uosm < 350 FENa > 1% |
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What glomerular disease shows sausage-like immune complex deposits in mesangium and capillary loops?
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MPGN
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What causes Type II RTA?
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Impaired HCO3- reabsorption in proximal tubule (sometimes associated with Fanconi syndrome)
Caused by faulty Na-HCO3- cotransporter on BL membrane |
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What classes of drugs should be used to treat hypertension in:
Diabetes mellitus |
Thiazide, beta-blocker, ACE-i, ARB, CCB
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What happens when you give IV mannitol?
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Stays in ECF, acts like NaCl. Used to relieve cerebral edema.
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Collapsing glomerulonephropathy
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?
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What substances can cause nephrotoxicity activity at:
Distal tubule |
cis-platin, glycols (deposition)
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What would the urinalysis reveal in:
Glomerulonephritis |
Protein, blood
RBC casts Uosm > 500 (this is weird) FENa > 1% |
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What entities can cause crescentic GN?
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Anti-GBM (idiopathic or Goodpasture’s), immune complex (idiopathic, SLE, post-infx, HSP, IgA, MPGN), or pauci-immune (idiopathic, Wegener’s granulomatosis, or microscopic polyarteritis)
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What happens if you give bicarb to someone with:
Distal RTA (Type I) Proximal RTA (Type II) |
Distal: serum HCO3- goes up, urine pH doesn't change much
Proximal: can't reabsorb any more HCO3-, so urine pH goes up, and serum HCO3- doesn't change much |
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What classes of drugs should be used to treat hypertension in:
Recurrent stroke prevention |
Thiazide, ACEi
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What causes generalized edema? Localized?
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Drop in plasma oncotic pressure. Increase in interstitial oncotic pressure.
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Spikes and holes --> membranous GN
|
?
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What substances can cause nephrotoxicity activity at:
Collecting duct |
Obstruction by anticholinergics, bromocriptine, quinolones, sulfonamides
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What would the urinalysis reveal in:
Post renal ARF |
minimal protein
varied microscopy Uosm < 350 FENa > 1% |
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What are the two main features of pauci-immune GN?
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Fibrinoid necrosis and crescents
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What classes of drugs should be used to treat hypertension in:
Benign prostatic hypertrophy |
Alpha-blockers
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How does CHF result in edema?
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Reduced CO and systemic BP from left heart --> retention of NaCl and water. Expand vascular volume, mostly on venous side, increasing Pc.
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Spikes and holes --> membranous GN
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?
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How does toluene result in nephrotoxicity?
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Causes myoglobinuria --> acute tubular necrosis
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What are the two types of ANCA associated with?
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C-ANCA - proteinase 3 – Wegener’s, occasionally idiopathic or MPA
P-ANCA – myeloperoxidase – MPA and idiopathic, occasionally Wegener’s So basically this tells you nothing. |
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What is a lab hallmark of pre-renal ARF?
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Elevated urea concentration out of proportion to creatinine elevation
because more filtrate is reabsorbed proximally, where urea is permeable |
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What RTA is characterized by acidic urine, hyperchloremic acidosis, and hyperkalemia?
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Type IV - Hyporenin-Hypoaldosteronism
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What is the mechanism of:
Spironolactone |
Aldosterone antagonist in cortical collecting duct
(Aldo's effects are to increase Na/K ATPase, K+ secretion, mitotic growth factor, upregulation of ENaC) |
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How does glomerulonephritis result in edema?
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Retention of NaCl and water is primary (due to decreased GFR). Expand vascular space, resulting in (1) increased venous return from veins--> increased EDV --> increased BP --> inhibits renin release (2) Blood accumulates on venous side --> increased Pc --> transudation --> edema. Increased venous pressure stimulates release of ANP --> inhibit sodium reabsorption and promote diuresis
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Spikes and holes (see red deposits in GBM) --> membranous GN
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?
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How does acetaminophen cause nephrotoxicity?
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metabolite is a free radical that produces damaging protein adducts in liver and kidney
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What is the therapy for pauci-immune GN?
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Immunosuppressive
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What drugs can cause reduced perfusion, resulting in ARF?
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NSAIDs, ACEi, cyclosporine
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How does hypoaldosteronism lead to acidosis?
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Hypoaldo --> hyperkalemia --> inhibits glutaminase and NH3 generation --> lack of buffer to accept protons --> backleak --> acidosis
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How does liver disease cause edema?
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(1) cirrhosis – fibrosis leads to increased R --> increased Pc in acini --> ascites
(2) other liver disease – reduced production of albumin--> lowers oncotic pressure --> fluid leaks out of capillaries |
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What are the adverse reactions to:
Spironolactone |
Hyperkalemia
Metabolic acidosis Gynecomastia |
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How do aminoglycosides cause nephrotoxicity?
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Magnesium and potassium wasting due to tubular damage
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What kind of proteinuria is there in MCD?
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Selective – albumin
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Acute post strep GN
See neutrophils, some obliterated capillary lumina |
?
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What drugs can cause direct tubular toxicity, resulting in ARF?
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Aminoglycosides, contrast, pigment, heavy metal
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How do diuretics lead to metabolic alkalosis?
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Loss of NaCl -> decreased EABV --> AII and aldo
AII--> increased HCO3- reabsorption in PT because there's a Cl- deficiency Aldo --> increased H+ secretion in CCD |
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How is the therapeutic index calculated?
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TD50/ED50
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How does the nephrotic syndrome result in edema?
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Loss of urine protein > 3.5 g/day ‡ decreased plasma oncotic pressure ‡ fluid leaks into interstitium
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What aldo blocker does not cause gynecomastia?
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Eplerenone
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What is the mechanism of MCD?
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T-cell mediated and cytokines. Mutated nephrin.
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Humps - pathognomonic for acute post strep GN
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?
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What drugs can cause allergic interstitial nephritis, leading to ARF?
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Antibiotics, NSAIDs, phenytoin
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How does hyperaldosteronism lead to metabolic alkalosis?
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Aldo stimulates intercalated cells to excrete H+
This is not Cl responsive! |
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How is the margin of safety calculated?
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LD1/ED99
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How does the nephrotic syndrome result in edema?
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Loss of urine protein > 3.5 g/day --> decreased plasma oncotic pressure --> fluid leaks into interstitium
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What is the mechanism of:
Loop diuretics |
Inhibits Na/K/2Cl transporter in TALH
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How do you differentiate between MCD and other renal disorders?
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Good response to corticosteroids.
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What drugs can cause tubular obstruction, resulting in ARF?
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Acyclovir, sulfa
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Freebie
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Thanks.
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IgA nephropathy
See mesangial hypercellularity, normal capillary loops on left. Right - more severe, with some endocapillary and extracapillary proliferation (crescents) |
?
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How does acetaminophen induce toxicity?
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Metabolte free radical produces damaging protein adducts in liver and kidney.
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How is urea handled in the nephron?
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Freely filtered at glomerulus. 1/2 is passively reabsorbed in proximal tubule. The rest is impermeable except for the deepest part of the CD, where permeability is increased when ADH is present.
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In what conditions is spironolactone used?
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High aldo states (CHF, cirrhosis, hyperaldosteronism)
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Where are the deposits in membranous GN?
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SubEPIthelial
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What are the mechanisms of decreased GFR in ATN?
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Tubular cell damage
Obstruction from cell debris --> increased Pt Loss of cell polarity and disruption of cell jxns --> backleak Activation of tubuloglomerular feedback because of decreased proximal reabsorption of Na |
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Double contours (not specific for IgA)
|
?
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How do COX inhibitors cause toxicity?
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Vasodilate afferent arteriole, compete with aldosterone --> hyperkalemia
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How is creatinine handled in the nephron?
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Freely filtered at glomerulus.. Not reabsorbed. Some is secreted. Estimates GFR because the secretion makes up for overestimation of plasma creatinine inherent in measurement methodology.
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In what conditions are loop diuretics useful?
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CHF, nephrotic syndrome, cirrhosis
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What is the EM appearance of membranous GN?
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Subepithelial deposits along GBM, separated by spikes
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MPGN - see GBM thickening, abnormal lobulation of glomerulus, capillary lumens may be occluded
|
?
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How do aminoglycosides and sulfonamides cause toxicity?
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Aminoglycosides: magnesium and potassium wasting due to tubular damage
Sulfonamides: poor sulubility causes obstruction, also hypersensitivity vasculitis |
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How do you calculate GFR from creatinine levels?
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GFR= (Ucr x urineflow)/Pcr
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What are the ADRs of loop diuretics?
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Hypokalemia, metabolic alkalosis, deafness
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What is the IF appearance of membranous GN?
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Granular deposits of Ig and complement along GBM
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Double contours - in this case, it's MPGN, but it could also be IgA)
|
?
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How is glucose handled in the nephron?
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Freely filtered at glomerulus, actively reabsorbed in proximal tubule by a mechanism that has a transport maximum, which is about 370 mg/min --> glucose does not normally appear in urine if plasma glucose is normal
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What are examples of loop diuretics?
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Furosemide (Lasix), bumetanide, torsemide, ethacrynic acid
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What kind of proteinuria is in FSGS?
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Non-selective
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MPGN - sausage-shaped (semi-linear) deposits of IgG and C3
|
?
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What are three effects of PTH?
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1) Promotes osteoclastic activity, mobilizing Ca2+ from bone
2) Increases activity of renal vitamin D3 1a-hydroxylase, which is required for synthesizing calcitriol, which increases intestinal reabsorption of Ca2+ 3) Increases Ca2+ reabsorption from nephron and reduces the maximal transport for Pi, increasing Pi excretion |
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What is the mechanism of thiazide diuretics?
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Inhibits Na/Cl transporter in distal convuluted tubule
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Does FSGS recur after transplant?
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Yes – suggests circulating factor.
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MPGN - subendothelial and rare subEPIthelial deposits
|
?
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Summarize the handling of Na+.
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Oh goody.
Proximal tubule: 70% of Na is actively reabsorbed, Cl and water follow passively Ascending limb of loop of Henle: 20% is reabsorbed by the Na/K/2Cl cotransport (impermeable to water) Distal tubule: 5% Na is reabsorbed (Na/Cl cotransport), impermeable to water Collecting duct: 3-5% reabsorbed by electrogenic Na channel pumps that are aldo regulated (ENaC). Variably permeable to water with regulation by ADH If there is low aldo (from high blood pressure) – you get decreased Na reabsorption in CD |
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What are the ADRs of thiazides?
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Hypokalemia,
metabolic alkalosis, gout (more UA absorbed with Na in proximal tubule under influence of AII), glucose intolerance (hypokalemia impairs insulin release) |
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What is the morphology of FSGS?
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Increased mesangial matrix, collapsed GBMs, deposition of hyaline masses and lipid droplets
IgM in the areas of hyalinosis |
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Idiopathic pauci-immune
Fibrinoid necrosis without proliferation Also crescents |
?
|
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What are the effects of hypoaldosteronism?
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Na loss, hypovolemia, decreased CO, decreased RBF
K+ retention, hyperkalemia, cardiac arrhythmias H+ retention, metabolic acidosis |
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What are examples of thiazides?
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Hydrochlorothiazide
Chlorthalidone Metolozone |
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What is the morphology of acute post-strep GN?
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LM- uniform increase in mesangial and endothelial cells, inflammatory infiltrate, thrombi in capillaries. Crescents – bad prognosis
EM – humps IF – IgG and complement, subENDOthelial |
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This is anti-GBM, because you don't see immune complex deposits in pauci-immune.
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If you're thinking of either idiopathic pauci-immune GN or anti-GBM, what does this tell you?
|
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What is diabetes insipidus?
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Either no synthesis of ADH (central) or ADH receptors in CD are resistant (nephrogenic)
Leads to inability to reabsorb water, leading to diuresis |
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What is the mechanism of acetozolamide?
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Carbonic anhydrase inhibitor (decreased ability to exchange Na for H+) --> diuresis
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What nephropathy occurs 1-2 days after a nonspecific upper respiratory infection?
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Berger’s disease (IgA nephropathy)
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Malignant hypertension
Top - Fibrous thrombosis Bottom - Mucoid intimal hyperplasia and onion skinning |
?
|
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What are the clinical signs of diabetic nephropathy?
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Microalbuminemia, grdual increase in proteinuria. Eventually Cr increases, renal failure. Retinopathy is indicative.
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How is H+ handled in the nephron?
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Very low concentration in plasma. H+ is actively secreted by nephron, mostly in proximal tubule, 10% in CD. Most titrates HCO3- in tubular fluid, some reacts with ammonia, and some with other buffers (e.g. phosphates)
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What are the ADRs of acetozolamide?
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Metabolic acidosis (decreased HCO3- absorption)
Hypokalemia |
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What are the clinical manifestations of Alport’s syndrome?
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Nephritis with nerve deafness and eye disorders, hematuria and proteinuria.
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What are the pathological features of diabetic nephropathy?
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Mesangial glomerulosclerosis - increased thickness in capillary walls, increase in mesangial matrix.
|
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How is H+ secretion stimulated?
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a) Respiratory acidosis leads to increased H+ secretion and therefore increases plasma HCO3- (renal compensation)
b) Aldo-increased Na reabsorption in CD causes H+ secretion to maintain electrical balance c) Na+ reabsorption is balanced wither by passive K+ secretion or active H+ secretion. If K+ is in short supply, H+ secretion is stimulated. |
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What are other examples of K+ sparing diuretics?
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Amiloride
Triamterene (Block ENaC in collecting duct) |
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What is the morphology of Alport’s?
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LM – segmental glomerular proliferation or sclerosis, increased mesagngial matrix. Foam cells. Tubular atrophy, interstitial fibrosis.
EM – thin BM, thickens with age. Basket weave appearance. |
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Diabetic nephropathy - this is nodular glomerulosclerosis, a Kimmelsteil-Wilson lesion. Notice also hypocellularity.
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If this also stained brown on silver stain, what would this be?
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How can you tell the difference between metabolic and respiratory acid-base disturbances just by looking at H+ and bicarb?
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If they change in same direction, it is RESPIRATORY
If they change in opposite directions, it is METABOLIC |
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What are the ADRs of ACE-inhibitors?
|
hyperkalemia
cough angiedema teratogenic be cautious with renal insufficiency (decreases GFR initially) |
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Diabetic nephropathy - thick GBM, foot process effacement secondary to hyperfiltration
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What is this?
|
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When might renal compensation for metabolic alkalosis not be complete?
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If there is accompanying severe volume depletion, because that will result in high also levels, which will result in increased H+ secretion.
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What are examples of ACE-inhibitors?
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Captopril, lisinopril
|
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Which amyloidosis is primary? Secondary?
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AA -secondary
AL -primary |
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How does autoregulation work?
|
1) Myogenic response in afferent arteriole – increased pressure opens stretch-activated Ca2+ channels, Ca enters smooth muscle cell, binds to calmodulin, activates MLCK, stimulates contraction, constricting arteriole
2) Tubuloglomerular feedback – macula densa monitors tubular fluid, signals to afferent and efferent arterioles through renin |
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What is the mechansim of Angiotensin II Receptor Blockers?
|
Blocks AI receptor of AII
|
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Amyloidosis. This is also paler pink than Diabetic Nephropathy's nodular glomerulosclerosis.
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If this is also silver-negative, what is this?
|
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What is the effect of the sympathetic nervous system on the kidney?
|
Sympathetic only.
Alpha receptors – stimulate contraction, more of afferent than efferent (more muscle on aff) Beta receptors – on JGA of afferent arterioles, release renin when stimulated, resulting AII constricts efferent arteriole, mainly. GFR is maintained while RBF is reduced |
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What are examples of ARBs?
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Losartan
Valsartan |
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Amyloidosis w/congo red stain and polarized light.
|
?
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What are the effects of angiotensin II?
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Greater constriction of the efferent arteriole than afferent ‡ increase GFR
|
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In what conditions are beta blockers used?
|
Arrhythmias, angina, heart failure, high renin
|
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How can you distinguish btw AA and AL amyloidosis?
|
AA loses congo red affinity when treated with KMnO4.
Also, secondary immunostains with SAA in mesangium |
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What stimulates the release of renin from the JGA?
|
a) Beta-1 receptors
b) Reduction in perfusion pressure (direct effect on JGA) c) Reduction in Na+ delivery to macula densa (tubuloglomerular feedback) |
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What is the mechanism of action of beta blockers?
|
Decreased renin secretion
|
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What are the clinical features of adult polycystic disease?
|
Normal renal fxn until middle age, when they present with renal insufficiency, hematuria, flank pain, HTN.
Extrarenal: liver cysts, berry aneurysms in circle of Willis, mitral valve disease, colonic diverticula. |
|
What is found in the urine in primary amyloidosis?
|
Light chains --> Bence-Jones proteinuria
|
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What are the ADRs of beta blockers?
|
Negative dromotrope, inotrope, and chronotrope
Erectile dysfunction Depression Claudication |
|
What is the histopathological appearance of the kidney in malignant hypertension?
|
Fibrinoid necrosis of arterioles (eosinophilic deposition in vessel walls) If inflammatory cells are present, it is necrotizing arteriolitis.
|
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What do elevated ANA levels indicate?
|
SLE
|
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What is an example of a non-selective beta blocker?
What are its effects? |
Propranolol
Decreases renin, CO, peripheral resistance (by decreasing SNS activity) |
|
What type of pattern does immunofluorescence reveal in anti-GBM?
|
Linear
|
|
What is an example of a beta-1 blocker?
|
Metoprolol, atenolol
Less effect on bronchial constriction, vascular dilation |
|
How do you distinguish between IgA and Type II SLE (mesangial lupus nephritis)?
|
EM looks the same (deposits in mesangium, mesangial proliferation).
IF - SLE stains for everything. IgA only IgA. |
|
What are the features of nephritic syndrome?
|
Proteinuria, hematuria, RBC casts, varying degrees of renal insufficiency and HTN
|
|
What are examples of alpha-1, beta adrenergic blockers?
|
Labetalol, carvedilol
Less effect on cardiac output and HR |
|
What is the most severe form of SLE?
|
Type III - diffuse proliferative GN
Neprhritic + nephrotic |
|
What are the features of nephrotic syndrome?
|
Edema, severe proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia
|
|
What is an example of an alpha-1 blocker, and what are its effects?
|
Prazosin, terazosin
Tamulosin (specific for prostate) Vasodilation w/o reflex tachycardia Used in BPH |
|
What are the morphologic characteristics of Type III SLE?
|
Hypercellularity, crescents, fibrinoid necrosis. Double contours.
|
|
Lupus - this is apparently a wire loop lesion.
|
?
|
|
What are the most common causes of nephritic syndrome?
|
Acute post-strep glomerulonephritis, glomerular diseases (including SLE)
|
|
What are examples of alpha-2 agonists? What are their effects?
|
Clonidine, alpha methyldopa
Stimulation of presynaptic alpha-2 receptors --> Decreased norepinephrine outflow from CV control centers in brain --> decreased peripheral autonomic tone |
|
Wire loop lesion --> SLE
|
?
|
|
What are the most common causes of nephrotic syndrome?
|
Lipoid nephrosis (Minimal change disease) in children and elderly, membranous glomerulonephritis in adults
|
|
What are the ADRs of alpha 1 blockers?
|
First dose orthostasis
|
|
Wire loops in upper left hand corner --> SLE
|
?
|
|
What are the features of Rapidly Progressive Glomerulonephritis (RPGN, a.k.a. crescentic GN)
|
Rapidly deteriorating renal function that accompanies glomerular injury. Nephritic urine sediment, renal failure. Accumulation of crescents (proliferation of parietal epithelial cells and migration of macrophages in Bowman space).
|
|
What are the ADRs for alpha 2 agonists?
|
Sedation, rebound HTN if stopped, dry mouth
|
|
SLE, Type V: there are deposits everywhere, thick GBM. Hematuria (RBC in urinary space)
SubEPIthelial deposits |
Oh my god, what is this?
|
|
What are the causes of RPGN?
|
Idiopathic, multisystemic disease (vasculitis or Goodpasture), or follow post-strep.
|
|
What are examples of arterial dilators?
|
Hydralazine
Minoxidil Diazoxide |
|
What are the clinical features of acute poststreptococcal GN?
|
Affects more children. Nephritic syndrome. Elevated antistreptolysin O titers, low serum complement.
|
|
What are ADRs for arterial dilators?
|
Na retention and edema --> use w/furosemide
Reflex tachycardia --> use w/B-blockers Hydralazine may also lead to headache, N/V, lupus-liks syndrome |
|
What are the pathological features of acute poststrep GN?
|
Diffuse cellular proliferation and leukocytic infiltration--> hypercellularity
Electron microscopy shows subepithelial humps of Ag-Ab complexes Granular deposits of immunoglobulins |
|
What is the mechanism of CCBs?
|
Inhibits voltage-sensitive L-type channel on smooth muscle
|
|
What are the clinical features of MCD? (lipoid nephrosis)
|
Nephrotic syndrome. Caused by food allergy, medications, or hematologic malignancies.
|
|
What are examples of CCBs?
|
Dihydropyridine (nifedipine, amlodipine)
Non-dihydropyridine (verapamil, diltiazem) |
|
What is the proposed pathogenesis of MCD?
|
Lymphokine from T cells
Fusion of epithelial foot processes --> loss of polyanionic filter, leading to proteinuria |
|
What are ADRs of CCBs?
|
Dihydropyridines: headache, edema
non: negative inotropic, conduction delay, constipation w/verapamil |
|
What is the treatment of MCD?
|
Steroids --> complete recovery
|
|
What is the mechanism and effect of reserpine?
|
Binds to central and peripheral adrenergic neuron storage vesicles --> antagonizes
|
|
What are the potential side effects of alpha methyldopa?
|
- Hemolytic anemia
- Edema - Impotence - Sedation - Increased prolactin -> lactation |
|
What are the pathological findings of MCD?
|
Light- normal
Electron – loss of foot processes, but no electron-dense deposits in GBM No immunofluorescence. |
|
What are the clinical and pathogenesis features of membranous GN?
|
Nephrotic syndrome, insidious onset. Usually idiopathic, but may be cause by infection, drugs, tumors, systemic disease.
Path: subepithelial immune disease deposits in GBMs ‡ damage capillary walls |
|
What are the indications for nitroprusside?
|
Severe hypertensive crisis, aortic dissection
|
|
What is the pathological appearance of the kidneys in membranous GN?
|
Swollen and pale grossly. Diffuse thickening of capillary walls.
Subepithelial deposits. Granular pattern of Ig and complement |
|
What are the adverse reactions associated with nitroprusside?
|
cyanide toxicity (lactic acidosis, arrhythmias, hypotension, hypoxia)
thiocyanate toxicity (weakness, disorientation, psychosis, muscle spasms) Reflex tachycardia |
|
What are the clinical features of membranoproliferative GN?
|
Nephrotic or mixed nephritic/nephrotic syndrome.
|
|
Which calcium channel blocker is safe in CHF?
|
Amlodipine
|
|
What is the pathogenesis of MPGN?
|
Type I: immune complex deposition in *subendothelium* and mesangium
Type II: C3 nephritic factor (an antibody against C3) with IgG antibody in serum. Dense deposits along glomerular and tubular BM |
|
What are examples of thiazide diuretics?
|
Hydrochlorothiazide (HCTZ), chlorthalidone, metolazone (increasing in potency)
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What is the pathological appearance in MPGN?
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Mesangial proliferation, BM thickening, tram-tracking
EM: Type I subendothelial deposits of C3 and IgG Type II: deposits of C3 in GBM |
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How does amiloride induce diuresis?
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K+ sparing, directly inhibits Na+ reabsorption in collecting duct.
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What are the clinical features of Focal Segmental Glomerulosclerosis?
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Nephrotic syndrome, often with hematuria, HTN, impaired GFR, and non-selective proteinuria
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What is the pathological appearance of FSGS?
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Segmental sclerosis, hyalinization of glomeruli
EM: nonsclerotic regions show loss of foot processes. Sclerotic segments show increased mesangial matrix and mesangial deposits. IgM and C3 deposits in sclerotic segments |
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What is the pathological appearance of Anti-GBM?
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Crescents and fibrinoid necrosis
EM: no deposits, but GBM disruption IF: linear pattern of Ig |
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What are the clinical features of Focal Proliferative GN?
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May be primary or secondary to SLE, Goodpasture, SBE, or Wegener’s. May be subclinical or present with hematuria/proteinuria, occasionally nephrotic syndrome.
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What is the pathological appearance in MPGN?
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Mesangial proliferation, BM thickening, tram-tracking
EM: Type I subendothelial deposits of C3 and IgG Type II: deposits of C3 in GBM |
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What are the clinical features of Focal Segmental Glomerulosclerosis?
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Nephrotic syndrome, often with hematuria, HTN, impaired GFR, and non-selective proteinuria
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What is the pathological appearance of FSGS?
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Segmental sclerosis, hyalinization of glomeruli
EM: nonsclerotic regions show loss of foot processes. Sclerotic segments show increased mesangial matrix and mesangial deposits. IgM and C3 deposits in sclerotic segments |
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What is the pathological appearance of Anti-GBM?
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Crescents and fibrinoid necrosis
EM: no deposits, but GBM disruption IF: linear pattern of Ig |
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What are the clinical features of Focal Proliferative GN?
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May be primary or secondary to SLE, Goodpasture, SBE, or Wegener’s. May be subclinical or present with hematuria/proteinuria, occasionally nephrotic syndrome.
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What are the clinical features of Berger disease (IgA nephropathy)?
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Mild proteinuria. Recurrent hematuria. Occasional nephrotic syndrome. Usually follows a respiratory infection. Common cause of GN. Related to HSP.
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What are the pathological features of Berger disease?
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Variable. May be normal. Segmental proliferation, mesangial proliferation, or crescent formation.
EM: mesangial deposits IF: mesangial IgA w/o complement |
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What are the clinical features of hereditary nephritis (Alport syndrome)?
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Hereditary abnormality of collagen ‡ renal disease, deafness, ocular abnormalities (dislocated lens, corneal dystrophy, cataracts)
Hematuria, proteinuria, slowly progress to renal failure |