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Renal > Renal Syndromes: Test Review > Flashcards

Renal Syndromes: Test Review Flashcards

1
Q

What are the 4 ways to diagnose abnormal kidney function?

A
  1. Changes in serum creatinine concentration
  2. Urinalysis abnormalities
  3. Altered renal homeostatic mechanisms
  4. Abnormal kidney imaging studies
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2
Q

What are the 5 types of glomerular syndromes?

A
  1. Nephrotic
  2. Nephritic
  3. Mixed nephrotic/nephritic
  4. Mesangial nephritic
  5. chronic glomerular disease
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3
Q

What are the 3 types of tubular syndromes?

A
  1. Inflammatory tubular interstitial disease (infectious or noninfectious)
  2. Non-inflammatory tubular interstitial disease
  3. Chronic interstitial disease
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4
Q

What are the 4 types of vascular syndromes?

A
  1. Prerenal azotemia
  2. Renal artery stenosis (uni- or bilateral)
  3. Hypertensive nephrosclerosis
  4. Vasculitis
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5
Q

What is the second most common cause of ESRD?

A

HTN

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6
Q

What is the hallmark of nephrotic syndrome?

A

Heavy proteinuria >3g/day, dipstick will be 3+ or 4+.

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7
Q

What are the other features of nephrotic syndrome?

A

Low serum albumin, lipiduria, peripheral edema, normal GFR, normal BP.

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8
Q

Why is there peripheral edema in nephrotic syndrome?

A

The low serum albumin results in low plasma oncotic pressure. ECFV expands but mainly in the interstitial compartment.

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9
Q

What are the 4 clinical examples of nephrotic syndrome?

A
  1. Diabetic nephropathy
  2. Minimal change disease
  3. Membranous glomerulopathy
  4. Focal segmental glomerulosclerosis
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10
Q

What is the overwhelmingly most common etiology of nephrotic syndrome?

A

Diabetic nephropathy b/c there are so many diabetics. 40% of diabetics develop diabetic nephropathy.

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11
Q

Minimal change disease occurs most commonly in what patient population?

A

Children

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12
Q

What nephrotic syndrome is most common in whites?

A

Membranous glomerulopathy

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13
Q

What nephrotic syndrome is most common in blacks?

A

Focal segmental glomerulosclerosis

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14
Q

What volume changes take place in nephrotic syndrome?

A

Renal tubules increase retention of salt and water thus total body sodium and total body water elevated BUT with normal serum Na concentration. The expanded interstitial fluid volume accounts for the edema. Plasma volume is relatively normal and thus normal BP.

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15
Q

What happens in nephritic syndrome?

A

Glomerulus infiltrated by inflammatory cells leading to endothelial cell injury. Endothelial cells swell. Complement activation is often present.

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16
Q

What are the urinary findings in nephritic syndrome?

A

Hematuria (microscopic or gross). Dysmorphic RBCs. RBC casts. Proteinuria <2g/day (dipstick 1+ or 2+).

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17
Q

What is pathomnemonic for nephritic syndrome?

A

RBC casts in the urine

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18
Q

What leads to the HTN seen in nephritic syndrome?

A

The damaged cells retain salt and water.

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19
Q

What is the GFR in nephritic syndrome?

A

Reduced

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20
Q

What are the volume changes seen in the nephritic syndrome?

A

Retention of salt and water w/ reduced GFR. Total body Na and TBW are elevated but serum Na concentration normal. Thus, ECFV and ICFV expanded. Leads to HTN and possible pulmonary edema.

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21
Q

Why is there more edema in nephrotic than nephritic?

A

Since nephrotic proteinuria is greater than nephritic, there is more of a change in plasma oncotic pressure.

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22
Q

What is the given clinical example of nephritic syndrome?

A

Post-streptococcal glomerulonephritis

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23
Q

What is mesangial nephritic syndrome?

A

Glomerular inflammatory changes are restricted to the mesangial area of the glomerulus.

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24
Q

What are the features of mesangial nephritic syndrome?

A

Normal GFR, normal BP, minimal proteinuria, hematuria (micro or gross), possible RBC casts.

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25
Q

What is the hallmark of mesangial nephritic syndrome?

A

Hematuria

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26
Q

What happens to the glomerular capillary wall in mesangial nephritic syndrome?

A

Nothing, it is unaffected. Explains the normal GFR and minimal proteinuria.

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27
Q

What are the 2 clinical examples of mesangial nephritic syndrome?

A
  1. IgA Nephropathy

2. SLE w/ immune deposits restricted to the mesangium

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28
Q

What is the most common glomerulonephritis worldwide?

A

IgA nephropathy

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29
Q

Since post-strep glomerulonephritis is IgA mediated too, how do you distinguish it from IgA nephropathy?

A

IgA nephropathy has a much faster onset than post-strep GN.

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30
Q

What are the features of mixed nephrotic and nephritic syndrome?

A

Hematuria and reduced GFR show evidence of inflammatory glomerular disease that is accompanied by nephrotic range proteinuria which leads to low serum albumin and edema. Think: 3+ or 4+ proteinuria plus hematuria.

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31
Q

What are the 2 given clinical examples of mixed nephrotic and nephritic syndrome?

A
  1. Diffuse proliferative GN related to SLE (stage IV)

2. MPGN

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32
Q

What does the GBM look like in MPGN?

A

Tram trak appearance

33
Q

What underlying chronic infection is MPGN most often related to?

A

Hep C. Note: in this disease, pt starts making RhF (IgM) against immune complexes that are cryoglobulins.

34
Q

What type of casts are only found in CKD?

A

Waxy casts. Any CKD dilates the tubules and leads to the formation of these big, broad, waxy casts.

35
Q

What are the features of chronic glomerular disease?

A

Chronically abnormal GFR and chronically abnormal urinalysis. There are variable degrees of proteinuria (2+ or 3+). +/- hematuria. Usually kidneys shrink in size. And obviously, waxy casts.

36
Q

What are the 2 given clinical examples of chronic glomerular disease?

A
  1. Diabetic nephropathy
  2. Long-standing intrinsic glomerular disease (membranous glomerulopathy, focal segmental glomerulosclerosis, IgA nephropathy)
37
Q

What are the 7 features of non-inflammatory tubulointerstitial disease?

A
  1. Reduced GFR
  2. Impaired ability to concentrate and dilute urine
  3. Isosthenuric urine (Uosm=300mOsm/kg, specific gravity 1.010)
  4. Impaired Na conservation (FENa >1%)
  5. U/A shows granular casts and relative absence of inflammatory cells and RBCs
  6. Minimal proteinuria (<1 g/day)
  7. No hematuria
38
Q

How do you distinguish pre-renal AKI from tubulointerstitial disease?

A

In pre-renal AKI, FENa <1% b/c the kidney is functioning and able to conserve Na.

39
Q

What is the earliest sign of non-inflammatory tubulointerstitial disease?

A

Impaired ability to concentrate the urine

40
Q

What is the specific gravity of maximally concentrated urine?

A

1.035

41
Q

What are the 3 given clinical examples of non-inflammatory tubulointerstitial disease?

A
  1. Prolonged ischemia/hypoxia (most common)
  2. ATN
  3. Direct nephrotoxins
42
Q

What are the 6 nephrotoxins?

A
  1. Aminoglycosides (the -mycins)
  2. Amphotericin B
  3. Heavy metals
  4. IV iodinated contrast media
  5. Myoglobin
  6. Free hemoglobin
43
Q

T or F. Inflammatory cells are required to produce tubular damage.

A

F: not required.

44
Q

Urinalysis of inflammatory tubulointerstitial disease shows?

A

Sterile pyuria. WBCs in the urine, often eosinophils. WBCs in the urine is the hallmark of this disease.

45
Q

What most commonly causes inflammatory tubulointerstitial injury?

A

Drugs: beta-lactams, sulfa drugs, dilantin, allopurinol. Can also be caused by viral infections.

46
Q

What stains can be used to identify eosinophiluria?

A

Hansel’s or Wright’s stain

47
Q

What are the features of acute pyelonephritis?

A

Acute bacterial infection via ascending route most commonly gram-negative bacilli. Inflammatory damage w/in the medulla. U/A: bacteria and pyuria, possible WBC casts. Urinary cultures are positive.

48
Q

Acute pyelonephritis occurs most often in which gender?

A

Females b/c they have a shorter urethra.

49
Q

How do you distinguish a bladder infection from acute pyelonephritis?

A

WBC casts will not be found with bladder infection.

50
Q

What are the features of obstructive uropathy?

A

Tubular damage leads to impaired urine concentrating ability, impaired Na conservation, and impaired K secretion. Minimal proteinuria. Can be acute or chronic.

51
Q

T or F. Imaging studies are necessary to define the etiology of obstructive uropathy.

A

T

52
Q

What are the 3 given examples of chronic obstructive uropathy?

A
  1. Benign prostatic hypertrophy or prostate cancer (bladder outlet obstruction)
  2. Gynecological malignancies w/ bilateral ureteral obstruction
  3. Nephrolithiasis
53
Q

T or F. Bilateral nephrolithiasis is required to induce AKI.

A

T

54
Q

What are the features of chronic tubulointerstitial disease?

A

Chronically decreased GFR and thus chronically elevated serum creatinine. Impaired urine concentrating ability leads to nocturia. Minimal proteinuria < 1g/day. Waxy casts. Kidneys shrink in size.

55
Q

What are the 4 given clinical examples of chronic tubulointerstitial disease?

A
  1. Obstructive uropathy
  2. Analgesic nephropathy
  3. Chronic cyclosporin or tacrolimus nephrotoxicity (calcineurin inhibitors)
  4. Chronic lithium toxicity
56
Q

What are the 4 vascular syndromes?

A
  1. Pre-renal azotemia
  2. Renal artery stenosis
  3. Hypertensive nephrosclerosis
  4. Vasculitis involving the kidney
57
Q

What is the cause of pre-renal azotemia?

A

Impaired renal perfusion pressure or severely decreased renal blood flow. Basically, any disease/condition that lowers the effective arterial blood volume can cause this.

58
Q

What are the features of pre-renal azotemia?

A

Kidneys are normal and functioning. Decreased renal perfusion pressure or severely decreased renal blood flow. U/A will be normal.

59
Q

What are the labratory findings of pre-renal azotemia?

A
  1. Normal U/A
  2. BUN:Cr ratio >20
  3. Concentrated urine (Uosm > 500 mOsm/kg, specific gravity > 1.020)
  4. FENa <1%
  5. Normal kidney imaging studies
60
Q

What are the 3 given clinical examples of pre-renal azotemia?

A
  1. Low CO: CHF, pericardial tamponade, arrhythmias- anything that lowers EABV
  2. Hemorrhage
  3. ECFV deficit (vomiting, diarrhea, severe dehydration)
61
Q

Which classes of drugs make pre-renal azotemia?

A
  1. NSAIDs
  2. ACEi
  3. ARB
    Any drug that impairs the RAAS thus disrupting glomerular autoregulation.
62
Q

How do NSAIDs affect glomerular autoregulation?

A

Result in reduced renin secretion and reduced vasodilatory PG production. The afferent arteriole cannot dilate.

63
Q

How do ACEi/ARB’s affect glomerular autoregulation?

A

Results in impaired Angiotensin II production or impaired response to ATII. The efferent arteriole cannot restrict.

64
Q

What’s the major way to distinguish unilateral and bilateral renal artery stenosis?

A

No edema seen w/ unilateral. Edema present w/ bilateral. Both have HTN.

65
Q

Describe the HTN in unilateral renal artery stenosis.

A

The ischemic kidney releases renin leading to the production of ATII. Thus, this produces an ATII-dependent HTN. Pressure natriuresis occurs to offset the HTN thus, there is no edema.

66
Q

Describe the HTN in bilateral renal artery stenosis.

A

Both the kidneys are ischemic and release renin leading to the retention of Na and water resulting in a volume-dependent HTN and edema. Possible flash pulmonary edema.

67
Q

How do you treat the HTN in unilateral renal artery stenosis.

A

ACEi or ARBs. Note: these drugs will impair glomerular autoregulation in bilateral and can result in acute renal failure.

68
Q

What are the features of hypertensive nephrosclerosis?

A

Medial hypertrophy of renal arterioles. Leads to ischemic glomerular atrophy. Decreased # of nephrons results in decreased GFR. Non-inflammatory process. U/A: no hematuria or pyuria. Low grade or absent proteinuria. Both kidneys shrink in size. Can result in CKD.

69
Q

What is the second most common cause of ESRD in the USA?

A

Hypertensive nephrosclerosis.

70
Q

Hypertensive nephrosclerosis is more common in what patient population?

A

Blacks

71
Q

What are the features of malignant hypertension?

A

Severely elevated BP. Acutely damages arterioles and capillaries leading to fibrinoid necrosis. Can present w/ acute renal failure. Can result in proteinuria and microscopic hematuria. Medical emergency.

72
Q

T or F. Malignant hypertension presents similar to nephritic syndrome but with ridiculously high BPs.

A

T

73
Q

What physical finding on exam is indicative of malignant hypertension?

A

Abnormal fundoscopic exam: the extremely high BP damages retinal arteries.

74
Q

What are the features of vasculitis involving the kidney?

A

Typically presents as nephritic syndrome. Reduced GFR, hematuria, non-nephrotic range proteinuria.

75
Q

What are the 4 given clinical examples of vasculitis involving the kidney?

A
  1. HUS (hemolytic anemia, thrombocytopenia, abnormal renal fxn)
  2. Polyarteritis nodosa
  3. ANCA-associated vasculitis (c-ANCA=Wegener’s, p-ANCA=microscopic polyangiitis)
  4. Malignant HTN
76
Q

What are the 3 types of RPGN?

A
  1. Immune complex mediated
  2. Anti-GBM antibody
  3. Pauci-immune
77
Q

What is Pauci-immune?

A

Little or no immune complex deposits. IF will be negative.

78
Q

What are the features of RPGN?

A

Focal segmental necrotizing glomerulonephritis. Crescent formation. Decreased GFR over weeks to months.

Renal (33 decks)

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