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RCS > L5- Renal Pathology > Flashcards

L5- Renal Pathology Flashcards

1
Q

list some of the many normal functions of the kidney

A
  • 1700L blood/day –> 1L urine
  • fluid / electrolyte / acid-base balance
  • excretion of nitrogenous wastes (urea)
  • EPO synthesis, renin synthesis, PG synthesis, VitD activation
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2
Q

give the equation for creatinine clearance and what it is used for

A

CL(Cr) = U(Cr) / P(Cr) * (vol/time)
U = [Cr] in urine; P = [Cr] in plasma
-overestimates GFR up to 15%

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3
Q

what are the common inaccuracies of using creatinine for calculating GFR

A
  • Under collection: false low CrCl in elderly, acute renal disease, chronic renal disease
  • Over collection: false high CrCl in pregnancy, diabetic glomerulonephritis
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4
Q

plasma levels of creatinine represent….

A

function of muscle mass (not a good indicator of renal function)

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5
Q

list the clinical manifestations of Glomerular Renal Diseases (hint- 3 common ones)

A
  • Acute nephritic syndrome: hematuria, proteinuria, HTN
  • Nephrotic syndrome: proteinuria, edema, lipiduria, hypoalbuminemia, hyperlipidemia
  • Asymptomatic: w/ proteinuria, hematuria
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6
Q

list the clinical manifestations of Tubular Renal Diseases (hint- 3 common ones)

A
  • UTI: bacteria, pyuria
  • Nephrolithiasis: colic, hematuria
  • Renal tubular defects: polyuria, nocturia, electrolyte disorders
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7
Q

list the clinical manifestations of glomerular/tubular renal diseases (acute and chronic)

A
  • Acute: oliguria, anuria, azotemia (high N levels in blood)

- Chronic: prolonged symptoms of uremia (high blood urea)

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8
Q

list the general causes of renal failure and appropriate related diseases

A

1) Renal (primary kidney disease): congenital, acquired (glomerular / tubulointerstitial)
2) Pre-Renal (inadequate blood supply): HF (low CO), low perfusion, hypovolemia, sepsis, hemorrhage
3) Post-Renal (bilateral urinary obstruction): tumors, BPH

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9
Q

describe the clinical classification of renal dysfunction in glomerular disorders

A
  • heavy proteinuria
  • RBC + RBC casts (microscopic amounts of blood in urine)
  • oval fat bodies (lipiduria)
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10
Q

describe the clinical classification of renal dysfunction in tubulointerstitial disorders

A
  • mild proteinuria
  • functional tubular defects
  • WBCs (pyuria)
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11
Q

list some classic descriptors used to classify types of glomerulonephritis

A
  • Focal (few glomeruli) v Diffuse (all)
  • Proliferative (>100 nuclei in glomerulus) v Membranous (thick GBM) v Membranoproliferative
  • focal segmental (fibrosis of glomeruli segment)
  • crescentic (parietal epithelial cell proliferation)
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12
Q

what are the 2 mechanisms for pathogenesis of primary glomerular diseases

A

1) immune mechanisms (most common): Ab mediated, cell-mediated, complement activation (alternative pathway)
2) nonimmune mechanisms: reduction in renal mass

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13
Q

in Ab-mediated immune-mediated glomerular disease, how/why are Abs formed/available (in response to……)

A

Response to Ag type:

  • Endogenous: tumor Ags, Ags w/in kidney
  • Exogenous: drugs, organisms (viral, fungal)
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14
Q

briefly describe the method Ab-Ag complexes deposit in the kidney and result in glomerular renal disease

A
  • Ab-Ag complex forms either in periphery or in situ => IC (immune complex)
  • IC is localized in various parts of glomerulus => complement activation
  • complement => influx of inflammatory cells (neutrophils, macrophages) –> injury to glomerular filtration membrane
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15
Q

describe the various types of ICs (immune complexes) in the kidney causing glomerular membrane damage

A
  • In Situ IC: i) fixed Ags (intrinsic), ii) Planted Ags (exo-/endo-genous)
  • Circulating IC: endogenous (DNA), exogenous (infectious protein)
  • Cytotoxic Abs: direct cell injury w/o IC deposits
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16
Q

immune mechanisms of glomerular kidney disease involves (1) activation and (2) sensitization for its progression

A

1- alternate complement pathway activation (mostly nephritic syndrome, C3 convertase)
2- T cell sensitization (GBM damage)

17
Q

list the changes to glomeruli seen on light microscopy in glomerular renal disease caused by nonimmune mechanisms (hint- 7)

A
  • cell proliferation: endothelial, epithelial, mesangial, parietal (crescent) cells
  • leukocytic infiltration
  • necrosis
  • thrombi (fibrin)
  • GBM thickening
  • hyalinization glomerulosclerosis (segmental, global)
  • deposits (amyloidosis)
18
Q

what are the 4 terms used to describe the distribution of glomerular alterations in glomerular renal disease

A
  • diffuse: all glomeruli
  • focal: some glomeruli
  • global: entire glomerulus
  • segmental: part of glomerulus
19
Q

list the changes to glomeruli seen on electron microscopy in glomerular renal disease caused by nonimmune mechanisms

A
  • GBM irregularities
  • mesangium expansion
  • electron dense deposits: i) locations (mesangium, GBM, mixed); ii) pattern (dense granular, fibrillary)
20
Q

list the 4 ways glomerular deposits are described on electron microscopy

A
  • effacement (absence) of foot processes (minimal change disease)
  • subendothelial deposits
  • subepithelial deposits
  • intramembrane deposits (–> GBM destruction)
21
Q

list the changes to glomeruli seen on immunofluorescence studies in glomerular renal disease caused by nonimmune mechanisms

A

(fluorescein isothiocyanate)

  • Stains for Ags (IG deposits): Ig-G/A/M, C3, λ/κ chains
  • Distribution: i) GBM, mesangium, both; ii) patchy, diffuse
  • Pattern: granular, linear (fine, coarse)
22
Q

Nephritic syndrome is glomerular injury due to (1) with the following clinical presentation: (2)

A

1- neutrophils

2- HTN; oliguria, hematuria (dysmorphic RBC) + RBC casts, WBC (neutrophils), proteinuria <3.5g

23
Q

Nephrotic syndrome is glomerular injury due to (1) with the following clinical presentation: (2)

A

1- CKs –> podocyte damage –> podocyte fusion + lack of negatively charged GBM
2- pitting edema (generalized), proteinuria >3.5g + fatty casts, hypercholesterolemia, hypoalbuminemia, hypercoaguable state (loss of antithrombin III)

24
Q

what is the purpose of kidney biopsy, and why might it be contraindicated

A

1) make diagnosis / monitor Tx effects and disease progression

2)

  • advanced renal disease (small, echogenic kidney on US)
  • young child (nephrotic syndrome)
  • associated to systemic findings
  • orthostatic proteinuria
  • normal complement, creatinine, BP, and limited proteinuria
25
Q

list the 3 major consequences of reductions in renal mass leading to glomerulosclerosis

A

i) systemic HTN –> mesangial cell hyperplasia, ECM deposition
ii) intraglomerular HTN –> intraglomerular coagulation
iii) glomerular hypertrophy –> epithelial/endothelial injury

all => glomerulosclerosis
iii) => proteinuria

26
Q

explain the changes to GBM in intramembranous deposition

A
  • destruction of GBM
  • areas of thinning and thickening of GBM
  • lamination of lamina densa (it splits into 2 layers)

RCS (29 decks)

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