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238 Cards in this Set
- Front
- Back
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Turners's Syndrome associated with what kidney disease?
Cardiac problem? |
Horseshoe Kidney
(Also aortic coarctation) |
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Most como=mon genetic cause of renal failure
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ADPKD
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How does horseshoe kidney develop?
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Trapped under mesenteric Artery at L3
Kidneys fuse. Usually only UTIs, etc. Otherwise normal kidney function |
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glomerular capillaries vs peritubular capillaries
(Pressure/reabsorption). |
Glomerular capillaries - high pressure/filtration
Peritubular capillaries - low pressure/reabsorption |
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What kind of diuretics lead to Free water clearance = 0
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Loops
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Without ADH, CH20 is what?
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It is >0, net free water excretion
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With ADH, CH20 is what?
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It is <0
Retention of Free water |
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Presentation of Nephrotic Syndrome
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Massive Proteinuria (>3.5g/day)
Hypoalbuminemia Generalized edema Hyperlipidemia/lipiduria |
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Swollen Ascites, periorbital edema, lipiduria is caused by what?
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Minimal change disease
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Most common nephrotic syndrome in children
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Minimal change disease
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Minimal change disease is due to?
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IC damage to visceral epithelial podocytes with podocyte food effacement
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What renal diseases demonstrate podocyte damage?
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Minimal change disease (podocyte effacement) and Focal Segmental Glomerulosclerosis (Podocyte loss)
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Proliferation of pod
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HIV
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Focal segmental schlerosis and hyalinosis
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FSGS
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FSGS polymorphism is what? Confers what advantage?
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APOL-1
Resistance to Tropanomyosis |
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What disorder is linked to M-Type Phospholipase A2 Receptor
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Membranous Nephropathy
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HCV, HBV infection linked to what renal disorder
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Membranous nephropathy
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diffuse capillary and GBM thickening with spike and dome on EM
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Membranous Nephropathy
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In Membranous nephropathy, where do ICs go?
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Subendothelial IC accumulation
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Basement membrane spikes on EM indicative of what?
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Membranous nephropathy
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What causes membranoproliferative glomerulonepropathy (type 1)
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IC activate classical pathway and make subendothelial deposits
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enlarged glomeruli are a sign of what Nephrotic disorder?
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Membranoproliferative
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What is the pathophysiology of Membranoproliferative Glomerulonephropathy Type II
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No ICs
Activate complement pathway and makes Intramembranous deposites |
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Difference between Type I and II membranoproliferative glomerulonephropathy
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Type I: Classical pathway, subendothelial deposits
Type II: Alternative pathway, Intramembranous deposits |
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Pathophysiology of Diabetic nephropathy
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Hyperglycemia --> glycosylation of GBM -> increased collagen type Iv thickening
Also have glycosylation of efferent arterioles --> increased GFR --> hemodynamic changes and capillary schlerosis |
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Pathological changes in Diabetic nephropathy
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mesangial expansion
GBM thickening NO ICs |
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Nodular Glomerulosclerosis
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Ch
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Christmas tree sign
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Kimmelstiel-Wilson Disease (Nodular Glomeruloschlerosis) caused by advanced diabetic nephropathy
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Characteristics of nephritic syndromes
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Hematuria
Azotemia Oliguria HTN proteinuria < 3.5g/day edema |
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Hypercellularity obliterating the capillary space =?
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PSGN
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Swollen flea bitten kidney in a child that just recovered from being ill
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PSGN
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PSGN: where are the IC deposits
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Subepithelial, intramembranous
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What type of bacteria causes PSGN
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Group A beta-hemolytic strep (12, 4, 1)
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PSGN is what type of disorder? Segmental, Global, Diffuse,
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Diffuse and Global
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Rapidly Progressive Glomerulonephritis (RPGN) is caused by?
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anti-GBM, ANA, ANCA antibodies
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Characteristics of RPGN
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Diffuse and Global
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Appearance of RPGN
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Crescent pattern from epthithelial proliferation which obliterates the glomerular space and capillaries
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Goodpasture syndrome is also seen in the?
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lungs
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Goodpasture syndrome is what kind of hypersensitivity reactions?
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Type II
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Goodpasture - what type RPGN?
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Type I
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Linear immunoflorescence for IgG or C3 is indicative of?
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Goodpasture syndrome
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Goodpasture sydnrome is caused by an Ag to what?
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NC1 domain on Collagen IV alpha 3 chain
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Type II RPGN = ?
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Post-strep or Lupus
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Type II RPGN = what type of hypersensitivity reaction?
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Type III
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What is the appearance of Type II RPGN on immunoflorescence?
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Granular
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Type III RPGN
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Vasculities: Wegener's (C-ANCA), microscopic polyangitis (p-ANCA)
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Immunoflorescence for Type III RPGN
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There is none - ANCA instead
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Pathophysiology of IgA Nepropathy
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Respiratory infection --> abnormal IgA secretion --> Attacks mesangium
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What pathways is activated in Berger's Disease
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Alternative complement pathway
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Pruned Tree appearence unders immunoflorescence?
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IgA nephropathy = Berger's Disease
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Sign of IgA nephropathy?
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Purpura, Hematuria
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What is the most common glomerular disease worldwide?
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IgA nephropathy
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LM signs of IgA nephropathy
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mesangial proliferation
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What is Alport syndrome?
Genetics? |
Abnormal Collagen IV, Alpha 3,4,5 chain
X-linked |
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Split basement membrane
Lamina densa thickened or split |
Alport syndrome
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Minimal Change Disorder - LM findings
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There are none! See only w/ electron microscope (podocyte effacement)
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Volume of distribution = ?
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Vd = Dose/Co
Co = concentration at zero time |
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Bioavailability = ?
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Bioavailability = AUCpo/AUViv x100
AUC = area under the curve |
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Steady state Clearance =?
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Css = Ko/Cltotal
Cl = clearance Ko = infusion rate constant |
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Loading dose =
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Loading Dose = Css x Vd
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Average Steady state clearence =?
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Css (Average) = f(D/t) / Cltotal
For oral doses |
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FSGS risk factors
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- Black race
- HIV infection - IV drug abuse (eg, Heroin) - Sickle-cell disease |
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Responce to corticosteroids for FSGS?
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poor
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Dosage Adjustment factor = ?
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1-fe [1-Clu/Cln]
Where Cl = creatinine clearence |
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Calculating dosage for renal failure patients. How do you do that?
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Du = Ku/Kn x Dn
Where Ku/Kn = 1-fe [1-Clu/Cln] |
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Calculating dosing interval for renal pts
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Tu=tn x kn/Ku
Where Ku/Kn = 1-fe [1-Clu/Cln] |
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young child post respiratory infection with proteinuria but good renal function
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minimal change syndrome
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lipid-laden proximal tubular cells
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minimal change
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thick GMB with tram-track appearence
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Membranoproliferative glomerularnephritis
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Schistosomiasis is associated with what kidney disorder
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Membranoproliferative glomerularnephritis type I
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Difference between IgA and PSGN
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PSGN:
no recurrent 1-2wks (instead of 1-2day) post infection IgG instead of IgA Decreased Serum C3 levels (IgA has normal levels) |
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IgA nephropathy is associated with:
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Henoch Schönlein purpura
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most common cause of non-infectious gross hematuria
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transitional cell carcinoma
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most common cause of microscopic hematuria in males
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BPH
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hematuria and dysmorphic RBC
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glomerulonephritis
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what is an important space for kidney tumors
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sinus space
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How many nephrons/kidney
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1.5 million
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Renal artery is longer on the ___
Renal vein is longer on the ____ |
Artery = longer on right
Vein = longer on left |
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vasa recta can only be found in
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juxtaglomedullary glomeruli
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One anatonomical abnormality that can predispose to UTI
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if ureter doesn't enter into bladder with an oblique course
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Narrow diameter with darker nuclei = _____ convoluted tubule
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distal
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which as a thicker wall - afferent or efferent arteriole
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afferent arteriole
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layers of glomerular complex
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fenestrated capillary with endothelium
Basel lamina - basement membrane Podocyte processes - epithelium |
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When does the proneprhos, mesonephros and metanephros develop?
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4th week
late 4th week 5th week |
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What forms the wolffian duct
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mesonephric
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what forms the mullerian duct
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paramesonephric duct
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the metanphros requires what for its development
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contact between the ureteric bud and the metanephric mesoderm
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What duct does the uteric bud arise from?
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Mesonephric duct
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When does renal agenesis result?
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if there is no contact between uteric bud and metanephric mesoderm
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When does renal dsyplasia occur
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incomplete or abberent juxtaposition between ureteric bud and metanephric mesoderm
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What joins during the 8the week
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metanephric tubules join the collecting tubule (from uteric bud) to form the Uriniferous tubules
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Is development more advanced closer to the medulla or the cortex?
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Closer to the medulla
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When does nephron formation end
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35th week
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What do renal arteries originally branch from?
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Iliac arteries
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How does the Hilar region rotate?
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from anterior to medial facing
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Efferent ductles of the testis are from?
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mesonephric tubules
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bladder epithelium from?
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endoderm of UG sinus
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Bladder extrophy is a problem resulting from?
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bad migration of mesoderm from umbilical region to form anterior abdominal wall
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Renal agenesis: mutation in what gene?
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RET
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renal agenesis: what side/sex affected
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Males, left
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If we see only ONE umbilical artery, then think
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renal agenesis
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Potter sequence
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Oligohydramnios --> insufficient amniotic fluid --> low set ears, receding chin, limb deformities, pulmonary hypoplasia
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Whats the difference between Potter's sequence and Potter's Syndrome
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When Potter's sequence is associated with bilateral renal agensis then its called a syndrome
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Why do potter's sequence babies die
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pulmonary hypoplasia
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Renal tubular dysgenesis is?
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the absence of the formation of the proximal convoluted tubule
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maternal ace inhibitor use causes
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Renal tubular dysgenesisi - no proximal convoluted tubule
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Causes of renal tubular dysgenesis
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Maternal ACE inhibitor use
Neonatal hemochromatosis Hypocalvaria Chronic fetal hypotension Consanginous marriage |
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renal tubular dysgenesis genetic
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AR
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Beckman Wiedemann Syndrome
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renal hypertrophy
HEmihypertrophy Omphalocele Wilms Tumor |
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Most common congenital kidney disorder
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horseshoe kidney
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When kidney is fused at lower pole, it is trapped behind which artery
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inferior mesenteric artery
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pelvic kidney is what?
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kidney doesn't migrate during development and there is incomplete division of the ureteric bud. If they fuse then only a discoid kidney
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Bifid ureter causes
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sumpernumary kidney
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Two utereric buds causes
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supernumerary kidney
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How frequent are additional renal arteries
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25%
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What is the essential histological feature in diffuse and mulitcystic rena dysplasia
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primitive ducts surrounded by loose mesynchme with cartilage presente
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Occipital encephalocele, polycystic kidneys, cleft palate, pulmonary hypoplasia
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Menkle's Syndrome - AR
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unilateral, large, prominent kidney cysts
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multicystic renal dysplasia
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what is usually seen with multicystic renal dysplasia
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unilateral
ureter absent, atretic or stenotic |
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smooth kidneys with cylindrical dilatation of tubules at right angles
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ARPKD
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signs of nephritic syndrome
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hematuria
mild to moderate proteinuria decreased GFR but with renal tubular function intact oliguria azotemia hypertension periorbital edema |
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Atherosclerosis at origin of renal artery is common or uncommon? What demographics is it seen in?
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Uncommon
diabetic men |
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when do you do a renal biopsy
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indicated in any parencymal disease in which histopathology is essential for either diagnosis or management:
1. acute or subacute decline in GFR 2. Heavy or nephrotic proteinuria 3. Multisystem illnesses 4. Assessment of efficacy of treatment (lupus) or prognosis |
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What is the difference between edema formation in nephrotic vs nephritic syndrome
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Nephritic: decreased GFR/filtration -> sodium retention -> increased plasma volume --> increased Hydrostatic pressure --> Edema (also seen in nephrotic)
Nephrotic: a) proteinuria --> hypoalbuminemia --> decreased oncotic pressure --> decreased plasma volume --> renin angiotensin --> volume retention --> edema |
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tubular proteinuria is a sign of?
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proximal tubule issues -> these small proteins usually reabsorbed in the proximal tubule. Tubulointerstitial diseases cause this. Fanconi syndrome
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Hyponatremia w/ high SG = ?
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Diluting defect - (i.e. SIADH)
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Hypernatremia w/ high SG = ?
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See if this is a water intake problem
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Hypernatremia w/ low SG
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concentrating defect such as nephrogenic or central DI
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In the presence of high ADH, the specific gravity will be?
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High
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Name 3 causes of high urine pH
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1) Urea splitting bacteria
2) Metabolic Alkalosis via HCO3- administration with metabolic acidosis 3) Metabolic Acidosis (Type 1 RTA) |
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Low pH of Urine caused by
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Paradoxical aciduria in pts with volume depletion and metabolic alkalosis
Or normal finding from due to organic acid excretion |
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Renal Tubule Acidosis Type 1
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Problem with tubular cells in the distal tubule - prevents H+ excretion, HCO3- production
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Renal tubular Acidosis Type 2
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Problem with proximal tubular cells - process impairing HCO3- reabsorption
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Renal tubular Acidosis Type 4
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Hypoaldosteronism or lack of collecting tubule response to aldosteronism ---> associated with hyperkalemia
Hyporeninemia Hypoaldosteronism |
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dipstick tests will detect what type of protein
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Albumin
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4+ protein urine =
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>500 mg/dl
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When do you see glucose in urine? Name 3
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1) Diabetics
2) Any disorder affecting proximal tubule (Fanconi, multiple myeloma) |
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Nitrate in urinanalysis is an indication of what?
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Gram negative bacteria (also false negative if urine not in bladder for at least 4hrs)
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White blood cells in urine with no bacteria = ?
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Acute interstitial nephritis
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Leukocyte esterase can be positive for what infectious disease
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TB
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How many RBC in a HPF would indicate pathology
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>1-2
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Differential for RBC in urine sample
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UTI
Stones Glomerular nephritis Bladder pathology Tumor |
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What is the maximum number of leukocytes you should see in the urine?
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>4/HPF
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Red cell casts imply
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Glomerulonephritis with defects in glomerular capillary walls
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White cell casts are seen when?
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- Pyelonephritis
- Acute interstitial nephritis |
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Broad casts are seen with?
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chronic glomerulonephritis
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Waxy casts are seen with?
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Chronic glomerulonephritis
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Muddy brown casts are seen with?
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severe ischemia to tubules in setting of hypertension or toxic injury
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Crystals in the urine are related to?
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Nephrolithiasis = stones
Ethylene Glycol toxicity Cooled urine |
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acute renal failure + Ca oxalate crystals = ?
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ethylene glycol ingestion
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Foaming of urine means?
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Presence of protein!
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What should you think if dipstick urine blood is positive but no RBC on HPF?
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Hemoglobinuria from RBC lysis (reaction to a transfusion) OR myoglobinuria due to excess skeletal muscle breakdown such as in Rhabdomyolysis (crush injuries, cocaine)
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Yellow brown urine seen in
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Bilirubin = cirrosis or cell lysis
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Orange urine seen with?
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Rifampin
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Green urine with?
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amitryptaline and propofol
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Hematuria
Flank Pain enlarged kidneys on both sides |
ADPKD
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Filtration Fraction =
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GFR/RPF
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If RBF decreases and FF increases then....
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Na+ and H20 resabsorption would increase (due to increased filtration, decreased hydrostatic prssure but increased oncotic pressure in the peritubular capillaries)
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In conditions of hypovolemia and HF, what happens to reabsorption of Na?
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It increases, mostly because of hydrostatic pressure decrease and oncotic pressure increase
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Autoregulation of RBF is composed of what?
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Afferent arteriole dilation or constriction
Happens between 80 and 180mmHG |
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Autoregulation of GFR happens when? How?
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when <80mmHg...during renal hypoperfusion, GFR maintained by increasing efferent resistance (renin, angiotensin) and decreasing afferent (NO and PGs) resistance
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How could drugs interfere with autoregulation?
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NSAIDs inhibit prostoglandins - making dilation hard
Angiotensin II inhibition makes constriction hard |
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Angiotensin II antagonists do what to GFR?
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decrease it bc you lose autoregulation
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A mutation in ___, causes Finnish Nephrotic Syndrome
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Nephrin, holds together podocyte foot processes
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Clearance equation
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Clearance = Ux x V / px
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Creatinine is which of the following:
filtered reabsorbed secreted Does it over or under estimate GFR |
It is freely filtered and NOT reabsorbed
It overestimate GFR bc it is secreted a little bit |
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When GFR decreases, what happen to plasma creatinine and creatinine excretion
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1) Plasma creatinine rises
2) Creatinine excretion decreases, but then returns to normal level PLASMA creatinine stays at higher level |
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PAH is which of the following:
filtered reabsorbed secreted |
PAH is freely filtered and secreted but not reabsorbed
PAH is a measurement for RPF IT undersestimates RPF by around 10% |
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RBF =
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RPF/(1-hematocrit)
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Net tubular reabsorption -
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Filtered load - excretion rate
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Net tubular secretion
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Excretion rate - filtered load
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K+ homeostasis is maintained by
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Cellular shift (insulin, catecholamines and K+ extracellually increase K+ ATPase activity, shifting K+ into cells)
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Place of tightest regulation of K+
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Cortical collecting duct
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What 5 factors increase K+ secretion
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1. High serum K+
2. High distal flow rates 3. High Na+ delivery to distal tubule 4. Aldosterone 4. Luminal Anions |
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How does aldosterone affect K+ secretion
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It increases Na-K-AtPase activity in the basolateral membrane
Increases K+ channels Increases EnAC channels |
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What pumps in intercalated cells function in K+ depleted settings?
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H+/K+ pumps
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Hyperosmilarity causes what to happen to K+
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Hyperkalemia:
water shift to ECS causes K_ to move with it due to chemical gradient/solvent drag ---> |
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Increased pH, what happens to K+
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Hyporkalemia:
Shifts into cell, H+ shifts out of cell |
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Non-anion gap metabolic acidosis - do you see hypo or hyperkalemia or nothing
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You see hyperkalemia
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In an anion gap metabolic acidosis, do you see hypo/hyperkalemia or nothing
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You shouldn't see K+ redistribution (however, remember, you will see K+ shift due to hyperosmolarity in DKA)
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What causes hyperkalemia
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1. Kidney disease -> only at onset of oliguria
2. Decreased effective circulating volume (CHF, cirrhosis) -> decreased GFR & increased Na/H20 reabsorption leads to lower urinary flow and less electrichemical gradient 3. Hypoaldosteronism (less K+ secretion) 4. Cellular shifts caused by rhabdo, beta blockers, insulin deficiency, increased serum osmolarity, non-anion gap metabolic acidosis |
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What meds cause hyperkalemia
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ACE-i
ARBs K+ sparing diuretics Heparin NSAIDS Beta blockers |
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NSAIDS inhibit the release of what?
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RENIN, PGs
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Treatment of Hyperkalemia
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Calcium
Insulin + gloucose, beta agonist, HCO3- Removal of excess K+ --> Kayexalate, IVF, diuretics |
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What removes excess K+ from body
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Kayexalate
IVF Diuretics |
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What causes hypokalemia
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1. Diarrhea, laxative abuse
2. Increased Aldosterone 3. Loop/Thiazide diuretics 4. Bartter's and Giltelman's syndrome 5. Anions in lume (DKA, metabolic acidosis, Penicillin derivatives) 6. Vomiting (HCl loss and volume depletion) 7. cellular shift from catecholamine surg, beta agonists, cell production |
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What do you lose with vomiting that causes you to become _____kalemic
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You lose HCl and Na+ --> causes you to become hypokalemic
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What would catacholamines and beta agonists do to K+
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Cause a shift of K+ into cell causing hypokalemia
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what part of the nephron is Na+ load dependent
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The thick ascending limb and early distal tubule
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Countertransport of H+ into urine occurs where?
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IN proximal tubule
In intercalated cells of collecting duct |
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Function of ANP
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in hypervolemic states it constricts efferent arterioles (increasing GFR)
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Sympathetic neural activity controls GFR how?
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In hypovolemic states it constricts afferent arterioles (decreasing GFR) and increasing Na+ reabsorption
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Filtered Load =
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Px x GFR
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Fractional Excretion =
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Excreted x / Filtered load
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FeNa =
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FeNa = (Una/Pna) / (Ucreat/Pcreat)
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Tubular injury does what to FeNa?
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Makes it greater than 1% since tubules lose capacity for Na reabsorption
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Basic urine pH could be due to what disorder affecting proximal tubule
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Fanconi syndrome
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What are the characteristics of Bartter's syndrome?
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High urine chloride
Hypokalemia Metabolic alkalosis No ELEVATED BP |
|
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Amiloride and Tirampterene MOA
|
Inhibit ENaC channels
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What can increase ENaC numbers
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Aldosterone
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What is the breaking phenomena?
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reduction in urinary sodium loss a few days after start of diuretics
- stimulation of aldosterone - augmented Na reabsorption in early distal tubule - reduced GFR and filtered Na load - Augmented proximal reabsorption of Na |
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ANP mechanisms
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Vasoconstriction of efferent arterioles
Decreased Na reabsorption in collecting duct Decreasees secretion of vasopressin, aldosterone, renin |
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Macula densa senses what?
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NaCl
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Juxtaglomerular apparatus sense what?
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afferent arteriole pressure drop
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How does ADH work
|
Via V1 receptor activating phosphotidyl inositol pathway (vasoconstrictive)
Via V2 receptor - adenylate cyclase pathway -> CAMP -> protein kinase A -> aquaporin genesis and water reabsorption |
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ADH is regulated by:
Primarily Others |
primarily plasma osmolarity
also: Pain, stress, drugs, pO2, Blood volume |
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When ADH is turned off, collecting duct is
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impermeable to water
|
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Posm =
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2(pNa) + Glucose/18 + BUN/2.8
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Free water clearance =
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V(1-Uosm/Posm)
If CH20 is negative - water reabsorbed If CH20 is positive - water is cleared |
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What happens to sodium with aldosterone deficiency?
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Na loss in urine in distal tubule and CCD
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Treatment of hypervolemia
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Dietary Na restriction, diuretics
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Causes of edema: protein related
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Hypoalbuminemia -> decreased oncotic pressure from malnutrition/liver disease, nephrotic syndrome,
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Can hypoalbuminemia lead to pulmonary edema
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not usually (although may be a pulmonary effusion)
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causes of edema, pressure related
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Increased hydrostatic pressure (hypervolemia) or venous obstruction
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What happens during the early state of obstruction? What time period is considered the early stage?
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First few hours
Increased BS pressure -> decreased GFR -> afferent vasodilation to overcome BS pressure |
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What happens during the middle stage of obstruction?
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4-5hrs
Kidney realizes it can't compensate enough to overcome obstruction and decides to avoid damage from high intraglomerular pressure by afferent vasoconstriction. Reduced GFR ->reduced distal delivery of Na -> Thromboxane A2, AT-II and endothelin -> afferent vasoconstriction -> decreased GFR |
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What happens during the late state of obstruction
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physical changes to drop collecting system pressure to normal ->
hydronephrosis increased lymphatic drainage Reduced GFR |
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What happens to urinary sodium in obstruction
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sometimes it can be decreased but it is NOT due to hypovolemia. don't add fluids
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What are the side effects of obstruction
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hyperkalemia
metabolic acidosis (if can't secrete dietary acids) RTA (nonanion gap) |
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Can you see polyuria with obstruction
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Yes, from impaired ADH response
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Can you use creatinine or GFR to determine if obstruction is present?
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NO!
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Colicky pain, hematuria
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Kidney stone
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Bilateral obstruction can look like?
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Volume depletion with elevated BUN and creatinine but increased BUN/Creatinine ratio
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Difficulty urinating, flank tenderness, pelvic fullness
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Obstruction
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Severe flank pain + gross/micorscopic hematuria
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kidney stone
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Most common kidney stone?
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Calcium oxalate
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what four factors inhibit stone formation
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urinating
citrate Mg Macromolecules |
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Conditions that predispose one to stones
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Horseshoe kidney
Medullary sponge kidney Polycystic kidney disease |
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Risk factors for calcium oxalate stones
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High crystalloid/h20 ratio
Hyperuricosuria high Na+ diet (promotes urinary Ca2+ excretion) low carb diet (high protein -> high uric acid) Hypercalciuria -> hyperparathyroid, RTA, Sarcoidosis Hyperoxaluria (Vit C, congenital problem) Low urine volume |
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Treatment for Calcium Oxalate Stone
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Increased fluid intake
Thiazides (decrease Ca excretion) Potassium citrate Low oxalate diet Calcium supplements |
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Uric Acid stones - can you see on x-ray
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No, radiolucent
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What is often seen with uric acid stones
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gout
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What medicine should you not use for gout
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PRobenecid (causes stones!)
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Uric Acid stone treatment
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restrict dietary purines
Will dissolve spontaneously |
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Infected stones: what type of bacteria?
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urease positive (Proteus) -> increased pH favors stone formation
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How do you treat Cystine stones
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Penicillamine or Tiopronin
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What percentage of stones pass spontaneously?
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90%
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Aldosterone: increases or decreases K+ secretion
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INCREASES
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