RENAL SYNDROMES - WALL - IMPORTANT!! Flashcards Preview

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Flashcards in RENAL SYNDROMES - WALL - IMPORTANT!! Deck (53)
1

What are the four key diagnostic factors to examine for abnormal kidney function?

Changes in SCr Concentration
Abnormalities in UA
Altered renal homeostatic mechanisms
Abnormal kidney imaging

2

What are the key questions to ask when looking at kidney disease?

Acute or Chronic
Prerenal, Intrinsic, Postrenal
Glomerular, Tubular or Vascular
Inflammatory or Non-inflammatory
Systemic Disease Associated

3

What are the three categories of intrinsic renal disease?

glomerular
intrinsic
vascular

4

What are the five glomerular syndromes?

nephrotic syndrome
nephritic syndrome
mixed nephritic nephrotic syndrome
mesangial nephritic syndrome
chronic glomerular disease

5

What are three categories of tubular syndromes?

inflammatory tubular interstitial disease
non-inflammatory tubular interstitial disease
chronic interstitial disease

6

What are the four categories of vascular syndromes?

prerenal azotemia
renal artery stenosis (uni or bilateral)
hypertensive nephrosclerosis
vasculitis

7

Describe nephrotic syndrome

abnormal permeability to the glomerular capillary wall to protein, presenting with proteinuria/albuminuria >3g/day. Lipiduria

Neg. dipstick w/ heavy proteinuria means it's not albumin.

3-4+ Dipstick for protein, Low serum albumin
Peripheral Edema, typically normal GFR and normal BP

8

What are clinical examples of nephrotic syndrome?

minimal change disease (children)
membranous glomerulopathy (white ppl)
FSGS (black people)
Diabetic Nephropathy: overall most ocmmon cause of nephrotic syndrome

9

What are volume changes present in nephrotic syndrome?

renal tubular retention of salt and water (esp. dt and CD) - edema, normal BP
expanded tbNa and tbw - Edema ISF
Expanded ISF
Relatively normal plasma volume (normal BP)

10

What is the basic pathology of nephritic syndromes?

inflammatory changes within glomerulus
infiltration of glomerulus by inflammatory cells
endothelial cell swelling
complement activation, often present

11

What are urinary findings of nephritic syndrome?

hematuria (always present)
dysmorphic RBCs in urine
RBC casts
non-nephrotic ranged proteinuria (<2
1/2+ protein dipstick

12

Why do you have mild proteinuria in nephritic syndrome that doesn't reach nephrotic levels?

Although you have the glomerular injury, the GFR is reduced in nephritic syndromes. So protein is leaked into the urine, but the decreased GFR prevents high proteinuria

13

What proteins are responsible for creating RBC casts?

tams-horsfall proteins

14

What are the clinical features of nephritic syndrome?

HTN, reduced GFR, hematuria

15

why do you have reduced gfr in nephritic syndrome?

inflammatory changes have pro-inflammatory cytokines and mediates, comlement activation and proliferation of mesangial cells, with infiltration of glomerulus by inflammatory cell (mononuclear and PMNs), and endothelial cell swelling. This reduces the surface area for glomerular filtration, leading to decreased GFR

16

What volume changes are associated with nephritic syndrome?

renal retention of salt and water (bc reduced gfr)
reduced gfr
expanded tbNa and tbw
expanded ecfv, expansion of ecfv and icfv
HTN and possibe pulmonary edema

17

What are clinical examples of nephritic syndrome?

post-streptococcal glomerulonephritis
RPGN

18

What are SAlbumin levels in nephritic syndrome?

they are normal because no severe albumin loss because of decreased GFR

19

What is the basic pathology of mesangial nephritic pattern?

glomerular inflammatory changes restricted to mesangial area of glomerulus
glomerular capillary wall remains unaffected (normal GFR and minimal proteinuria)
hematuria is hallmark
normal BP and Na retention
Glomerular RBC casts

20

What are clinical examples of mesangial nephropathy?

IgA nephropathy (most common GN worldwide)
SLE with immune deposits limited to mesangium

21

How do you tell between post-strep GN and IgA nephropathy?

while both are associated with previous respiratory infections, the timing is different.

Post-strep is 5-6 days after infxn
IgA Nephropathy is 1-2 after infxn

22

What is the basic pathology of mixed nephritic and nephrotic syndrome?

Evidence for inflammatory glomerular disease (hematuria, reduced GFR)
Nephrotic Range proteinuria (low serum albumin, and edema formation)

23

What are clinical examples of mixed nephritic nephrotic syndrome?

diffuse proliferative glomerulonephritis related to SLE
Membranoproliferative Glomerulonephritis most often related to Hep C (tram tracks)!!!!

24

What is the general pathology of chronic glomerular disease?

Chronically abnormal GFR and abnormal UA
Variable degrees of proteinuria and hematuria
Frequently leads to decreased sized kidneys
Waxy casts (because of dilated tubules)

25

What is the sign in UA of a chronic problem?

waxy casts

26

What are clinical examples of chronic glomerular disease?

diabetic nephropathy
long-standing intrinsic glomerular disease (membranous glomerulopathy, FSGS, IgA nephropathy

27

What is the general pathology of non-inflammatory tubulointerstitial disease?

reduced GFR
Impaired concentrating ability
Isothenuric Urine, osmo 300mosm.kg, specific grav 1.010
Impaired sodium conservation
UA - granular casts, relative absence of inflammatory cells and RBCs
Minimal Proteinuria

28

What are clinical examples of non-inflammatory tubulointerstitial diseases?

ATN
Prolonged Ischemia-Hypoxia (common)
Direct Nephrotoxins (aminoglycosides, amphotericin B, heavy metals, IV iodinated contrast, myoglobin, free hemoglobin)

29

What is the general pathology of inflammatory tubulointerstitial injury?

similar to non-inflam TI disease, except active inflammatory response results in tubular damage
UA - sterile pyuria, often eosinophilia

30

Inflammation in glomerulus is likely to cause what types of cells in the urine?

rbc

31

inflammation in the tubules is likely to cause what type of cell in the urine?

wbcs

32

What are clinical examples of inflammatory tubulointerstitial injury?

Drugs (b-lactam, antibiotics, sulfa, dilantin, allopurinol)
may be associated with viral infxns

33

What is the general mechanism of acute pyelonephritis?

Acute bacterial infection, ascending route, most commonly gram-neg bacilli
Inflammatory damage within the MEDULLA (where you get to first)

34

what is on UA of acute pyelonephritis?

bacteria and pyuria, , WBC casts may be seen
Urinary cultures are positive

35

What is the general pathology of obstructive uropathy/

Leads to tubular damage
may be acute or chronic
impaired tubular function (concentrating ability, soidum conserv. k secretion)
minimal proteinuria
imaging studies are necessary

36

on imaging studies in obstructive uropathy, what are you looking for?

distended bladder, due to increased urine backup in kidney

37

what is the most common cause of obstructive uropathy in women? in men?

in women, cervical cancer
men, prostate cancer

38

What are clinical examples of obstructive uropathy?

benign prostatic hypertrophy or prostate cancer
gynecological malignancies with bilateral ureteral obstruction
nephrolithiasis

39

What is the general mechanism of chronic tubulointerstitial disease

Chronically decreased gfr (elevated scr levels)
impaired concentrating ability
minimal proteinuria
waxy casts
decreased kidney size by imaging studies, except in cystic

40

What are clinical examples of chronic tubulointerstitial disease?

obstructive uropathy
analgesic nephropathy
chronic cyclosporin or tacrolimus nephrotoxicity
chronic lithium toxicity

41

What are various vascular syndromes?

prerenal azotemia
renal artery stenosis
hypertensive nephrosclerosis
vasculitis involving the kidney

42

What is the pathology of prerenal azotemia?

frequently kidneys are normal and intact but there is impaired renal perfusion pressure or severely decreased renal blood flow

43

hwat do UA show in prerenal azotemia?

concentrated urine, low Una and FENa<1, hyaline casts

44

What are lab findings for prerenal azotemia?

normal UA
BUN/Cr ratio >20
Concentrated Urine: UOsm great than 500. Specific gravity >1.020
FENa<1%

45

What are clinical examples of prerenal azotemia?

low CO (CHF, pericaridal tampanode, arrhythmias
hemorrhage
ECFV deficit (vomiting, diarrhea severe dehydration)

46

Which drugs should be avoided when you have a pt with prerenal azotemia?

NSAIDs (they inhibit afferent dilation)
ACEi and ARBs because the inhibit efferent constriction (which you want to increase the GFR)

47

What is the pathology of Renal Artery Stenosis

Unilateral or Bilateral
Bilateral stenosis (ACE/ARB can precipitate acute renal failure by disruption glomerular auto-regulation)

48

What is the pathology of hypertensive nephrosclerosis?

medial hypertrophy of renal arterioles
leads to ischemic glomerular atrophy
decreased number of functioning nephrons results in decreased GFR
non-inflammatory process (absence of hematuria and pyuria)
Low grade proteinuria or neg for it.
2nd most common cause of ESRD

49

What is the pathology of malignant hypertension?

severely elevated BP
acutely damaging arterioles and capillaries
can present with acute renal failure
can result in proteinuria and microscopic hematuria
retinal arteries are damaged

50

What is the pathology behind vasculitis involving the kidney?

typically presents as nephritic syndrome
reduced GFR, hematuria, proteinura (non-nephrotic range)

51

what are clinical examples of vasculitis involving the kidneys?

hemolytic uremic syndrome (hemolytic anemia, thrombocytopenia, abnormal renal function)
polyarteritis nodosa
ANCA associated vasculitis
malignant htn

52

What is the pathology of rapidly progressive glomerulonephritis?

immune complex mediated
anti-gbm antibody
pauci-immune

53

what are some common things in rpgn?

focal segmental necrotizing GN
crescent formation!!!!
decreased GFR over weeks to months