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Flashcards in Day 7 5/20/15 Deck (32):
1

BUN Creatinine Ratio

The ratio of serum BUN to creatinine is usually between 10:1 and 20:1. An increased ratio may be due to a condition that causes a decrease in the flow of blood to the kidneys, such as congestive heart failure, early stage post-renal failure or dehydration.

2

Crockoft Gault Equation for Creatinine Clearance (GFR)

Creatinine Clearance (or GFR) = [(140-age) x weight kg] / [serum creatinine x 72] x0.85 for females
-slightly overestimates GFR because creatinine is moderately secreted by renal tubules

3

Fractional Excretion of Na (FeNa) Equation

FeNa = 100 [(Na urinary x Cr plasma) / (Na plasma x Cr urinary)]

1% = damage to kidney itself

4

nocturia

-need to urinate waking one from sleep

5

Urinary loss of albumin results in:

-dec. oncotic pressure leading to edema
-hallmark of nephrotic syndrome

6

Nephrotic Syndrome
-blood albumin leve
-blood gammaglobulin level
-blood coagulation state
-blood lipid and cholesterol level

-hypoalbuminemia- edema
-hypogammaglobulinemia
-hypercoagulable state- loss of antithrombin III
-hyperlipidemia
-hyperchoesterolemia

7

Nephrotic Syndromes

-minimal change disease
-focal segmental glomerulosclerosis (FSGS)
-membranous nephropathy
-membranoproliferative glomerulonephritis (MPGN)
-diabetes mellitus

8

Minimal Change Disease Causes

-nephrotic
-common in children
-idiopathic or Hodgkin lymphoma related
-loss of foot processes due to cytokines

9

Minimal Change Disease Lab Findings

-normal glomeruli on H&E stain
-effacement of foot processes on EM
-negative IF, no immune complexes

10

Minimal Change Disease Protein Loss

-selective proteinuria
-loss of albumin
-normal immunoglobluin

11

Minimal Change Disease Treatment

Excellent Response to Steroids

12

FSGS Causes

-nephrotic
-usually idiopathic
-HIV
-heroin use
-sickle cell disease
-most common nephrotic syndrome in hispanics and african americans

13

FSGS Labs

-segmental sclerosis on H&E
-effacement of foot processes on EM
-negative IF; no immune complexes

14

FSGS Treatment

-minimal response to steroids; progresses to chronic renal failure
-usually doesn't respond to treatment

15

Membranous Nephropathy Causes

-nephrotic
-most common cause of nephropathy in caucasians
-usually idiopathic
-HEP B/C
-solid tumors
-SLE
-drugs (NSAIDS, penicillamine)

16

Membranous Nephropathy Labs

-H&E: thick glomerular basement membrane
-granular IF: due to immune complex deposition
-EM: subepithelial (level of podocyte) deposits with spike and dome appearance

17

Two Types of MPGN & Causes

-nephrotic
-type 1: subendothelial, associated with HBV and HCV, more often associated with formation of tram-tracks
-type 2: intramembranous, associated with C3 nephritic factor autoantibody

18

MPGN Labs

-H&E: thick capillary membranes, often tram-track appearance in type 1 most commonly
-IF: granular due to immune complex deposition
-can also sometimes be nephritic

19

DM Nephrotic Syndrome Causes

-high serum glucose causes basement membrane to become leaky and causes hyaline arteriolosclerosis (thickening of blood vessel wall)
-efferent arteriole is most affected, leading to high glomerular filtration pressure
-hyperfiltration injury results in microalbuminuria and progresses to nephrotic syndrome

20

DM Treatment for Kidney

-ACE inhibitors prevent additional contraction of efferent arterioles in kidney, preventing further injury

21

Nephritic Syndrome Hallmarks

-limited proteinuria (

22

Nephritic Syndromes

-post strep glomerulonephritis (PSGN)
-rapidly progressive glomerulonephritis
-IgA nephropathy
-alport syndrome
-benign familial hematuria (thin basement membrane disease)
-focal/necrotizing/crescentic GN
-lupus GN

23

Post Strep Glomerulonephritis (PSGN) Causes

-nephritic
-arises after group A beta hemolytic strep infection of skin (impetigo) or pharynx
-occurs with nephritogenic strains that carry M protein virulence factor

24

Post Strep Glomerulonephritis (PSGN) Presentation

-hematuria (cola colored urine)
-oliguria
-hypertension
-periorbital edema
-usually seen in children but can occur in adults

25

Post Strep Glomerulonephritis (PSGN) Labs

-H&E: hypercellular, inflamed glomeruli
-IF: granular, mediated by immune complex deposition
-EM: subepithelial humps

26

Post Strep Glomerulonephritis (PSGN) Treatment

-supportive
-children rarely progress to renal failure
-some adults develop rapidly progressive glomerulonephritis (RPGN)

27

Rapidly Progressive Glomerulonephritis (RPGN) Lab Differentiation

-H&E: crescents in bowmans space, comprised of fibrin and macrophages
-IF:
-linear: goodpastures
-granular: post strep glomerular nephritis (PSGN), or diffuse proliferative GN
-negative IF: pausi-immune: cANCA means wegners granulomatosis, pANCA means microscopic polyangiitis or churg straus

28

IgA Nephropathy Causes

-nephritic
-IgA immune complex deposition in mesangium of glomeruli
-most common nephropathy worldwide

29

Alport Syndrome Causes

-nephritic
-inherited defect in type 4 collagen
-most commonly X linked
-results in thinning and splitting of glomerular basement membrane

30

Alport Syndrome Presentation

-isolated hematuria
-sensory hearing loss
-ocular disturbances

31

Renal Clearance Equation

C = (U x V) / P

C- clearance of X (mL/min)
U- urine concentration of X (mg/mL)
P- plasma concentration of X (mg/mL)
V- urine flow rate (mL/min) (1440 min per day)

32

Glomerular Filtration Rate Equation

-inulin clearance can be used to calculate GFR because it is freely filtered and not reabsorbed or secreted

GFR= Kf [(Pgc - Pbs) - (pgc - pbs)]
-gc- glomerular capillary
-bs- bowman space
-pbs normal equals 0
-normal GFR = 100 mL/min