RENAL SYNDROMES - WALL - IMPORTANT!! Flashcards

(53 cards)

1
Q

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

A

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

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2
Q

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

A
Acute or Chronic
Prerenal, Intrinsic, Postrenal
Glomerular, Tubular or Vascular
Inflammatory or Non-inflammatory
Systemic Disease Associated
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3
Q

What are the three categories of intrinsic renal disease?

A

glomerular
intrinsic
vascular

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4
Q

What are the five glomerular syndromes?

A
nephrotic syndrome
nephritic syndrome
mixed nephritic nephrotic syndrome
mesangial nephritic syndrome
chronic glomerular disease
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5
Q

What are three categories of tubular syndromes?

A

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

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6
Q

What are the four categories of vascular syndromes?

A

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

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7
Q

Describe nephrotic syndrome

A

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

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8
Q

What are clinical examples of nephrotic syndrome?

A

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

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9
Q

What are volume changes present in nephrotic syndrome?

A

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)

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10
Q

What is the basic pathology of nephritic syndromes?

A

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

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11
Q

What are urinary findings of nephritic syndrome?

A
hematuria (always present)
dysmorphic RBCs in urine
RBC casts
non-nephrotic ranged proteinuria (<2
1/2+ protein dipstick
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12
Q

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

A

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

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13
Q

What proteins are responsible for creating RBC casts?

A

tams-horsfall proteins

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14
Q

What are the clinical features of nephritic syndrome?

A

HTN, reduced GFR, hematuria

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15
Q

why do you have reduced gfr in nephritic syndrome?

A

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

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16
Q

What volume changes are associated with nephritic syndrome?

A

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

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17
Q

What are clinical examples of nephritic syndrome?

A

post-streptococcal glomerulonephritis

RPGN

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18
Q

What are SAlbumin levels in nephritic syndrome?

A

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

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19
Q

What is the basic pathology of mesangial nephritic pattern?

A

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

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20
Q

What are clinical examples of mesangial nephropathy?

A
IgA nephropathy (most common GN worldwide)
SLE with immune deposits limited to mesangium
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21
Q

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

A

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

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22
Q

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

A

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

23
Q

What are clinical examples of mixed nephritic nephrotic syndrome?

A

diffuse proliferative glomerulonephritis related to SLE

Membranoproliferative Glomerulonephritis most often related to Hep C (tram tracks)!!!!

24
Q

What is the general pathology of chronic glomerular disease?

A

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