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CLIN MED PA 581: GU > Glomerular Dz > Flashcards

Glomerular Dz Flashcards

Objectives

1
Q

Nephrotic Syndrome Epidemiology

A
  • 15x more common in kids than adults
  • In children, 2-7 cases per 100,000
  • MCC = Minimal Change Disease (lipoid nephrosis)
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2
Q

Nephrotic Syndrome risk factors

A
  • Because nephrotic syndrome is not itself a disease, risk factors for it are diseases that cause it except when it is idiopathic
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3
Q

Nephrotic Syndrome Etiologies

A
  • MCD (lipoid nephrosis)
  • Diabetes mellitus
  • Membranous nephropathy: hepatitis B, gold, penicillamine, syphilis, carcinomas
  • SLE
  • Focal glomerulosclerosis: heroin, AIDS
  • Amyloidosis
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4
Q

Nephrotic Syndrome signs and symptoms

A
  • Generalized edema
  • Heavy proteinuria (>3.5 gm/24 hrs)
    • Foamy urine
  • Hypoalbuminemia
  • Hyperlipidemia
  • Lipiduria
  • NO HTN (unless pre-existing)
  • Hypercoaguability (loss of anticoag proteins in the urine e.g. prot C, prot S)
    • PE,DVT
  • Infections (loss of immunoglobulins in urine)
    • More susceptible to bacterial infections
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5
Q

Maltese cross

A
  • oval fat bodies
  • seen from lipiduria
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6
Q

Nephrotic Syndrome complications

A
  • Cardiovascular ds bc of hyperlipidemia
    • atherlosclerosis
  • DVT, PE bc of hypercoaguability
  • Infections bc of hypoimmunoglobulinemia
    • Especially bacterial
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7
Q

Nephrotic Syndrome Dx

A
  • Easy to diagnose nephrotic syndrome, important thing is to find cause
    • H&P
    • UA, 24 hr urine collection
      • make sure min of 3.5g/min
    • Renal biopsy
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8
Q

Nephrotic Syndrome management

A
  • Steroids most useful for MCD or SLE
  • Treat underlying cause
  • General measures
    • control HTN if present
    • early treatment of infection
      • So it doesn’t turn into pyelonephritis
    • avoid nephrotoxic agents
      • NSAIDs
      • Aminoglycosides
      • contrast dye
        • If must use it, consult radiologist for alternative option
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9
Q

Nephrotic Syndrome prevention

A
  • ACE inhibitors or ARBs in DM with HTN
    • Microalbuminuria is 1st sign of DMà nephrotic syndrome
  • Can be Idiopathic
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10
Q

Diabetic Nephropathy Epidemiology

A
  • MCC of end stage kidney disease in the US
  • ¼ of diabetics have it
  • Onset is usually 10-15 years after dx
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11
Q

Diabetic Nephropathy Risk Factors

A
  • inc. incidence of nephropathy in DM patients with
    • Poor glucose control
    • Uncontrolled HTN
    • Type 1 DM, with onset < 20yo
    • Past or current smoking
    • FH of diabetic nephropathy
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12
Q

Diabetic Nephropathy Pathophys

A
  • long-standing poorly controlled BG → changes in nephrons
  • 1st efferent arteriole constriction and afferent arteriole dilation → glomerular capillary HTN and hyperfiltration
  • gradually changes to hypofiltration
  • concurrently, there are changes within glomerulus
    • BM thickening
    • widening of podocyte slit membranes
    • inc. number of mesangial cells and↑ mesangial matrix
    • matrix invades glomerular capillaries and produces deposits (Kimmelstiel-Wilson nodules)à true cause of complications
    • mesangial cells and matrix progressively expand and consume entire glomerulus, shutting off filtration
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13
Q

Diabetic Nephropathy Signs and symptoms

A
  • MC 1st symptom is nocturia
  • 1st sign is microalbuminuria
  • fatigue, malaise, anorexia
  • HA
  • N&V
  • urinary frequency
  • pruritis
  • edema
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14
Q

Diabetic Nephropathy Dx

A
  • Screen pts with Type 1 after 5 years
  • Screen pts with Type 2 upon dx
  • Results + in 2 of 3 tests in a 3- to 6-month period confirm dx
    • transient elevations of microalbuminuria can be caused by exercise, UTI, hyperglycemia, febrile illness, severe HTN, or HF
  • 3 ways to screen for albuminuria
    • albumin-to-creatinine ratio on a spot urine test
      • ratio >30 mg albumin/1 g creatinine is considered increased
    • timed collection (e.g., 10 hrs overnight)
    • 24-hour urine collection
      • Normal <30 mg/24 hr
      • Microalbuminuria 30–299 mg/24 hr
      • Macroalbuminuria >300 mg/24 hr
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15
Q

Diabetic Nephropathy management

A
  • Can progress to overtly nephrotic levels of proteinuria (>3.5 grams/24 hr)
  • Main goal is to slow progression
    • Control blood sugar HgbA1c <7
    • Control HTN <130/80
    • ACEI or ARB
    • Low salt diet

**Diabetic nephropathy is not yet renal failure

**The goal is to slow the progression

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16
Q

Glomerulonephritis (Nephritic syndrome) incidence and risk factors

A
  • True incidence of biopsy-proven GN unknown
  • Because it is a syndrome and not a single disease entity, risk factors are diseases known to cause it
17
Q

Glomerulonephritis Etiologies

A
  • Post-infectious: MCC = strep throat
    • Autoimmune response to presence of Strep, which ends up attacking the kidney
  • Membranoproliferative GN
  • SLE
  • IgA nephropathy
  • Goodpasture’s syndrome
  • Vasculitides: PAN, Wegener’s granulomatosis
  • Henoch-Schonlein purpura, HUS (E. coli)
  • Assoc with endocarditis and visceral abscesses
18
Q

Glomerulonephritis Acute vs. Chronic

A
  • Almost any cause of acute may become chronic but post-infectious is almost always acute and self-limited
  • Chronic GN is a major cause of CRF
19
Q

Glomerulonephritis Pathophys

A
  • Inflammaiton of glomerulus often due to autoimmune damage
    • Damaged glomerulus allows leakage of red blood cells, protein, initiation of RAA which leads to fluid retention and HTN
20
Q

Glomerulonephritis signs and symptoms

A
  • mild edema
  • moderate proteinuria
  • HTN
    • Will always cause
  • hematuria (brown) and RBC casts
    • Blood can also be grey due to iron which is reduced; also called “smokey” urine
    • Having casts in urine is also called cylinduria
21
Q

RBC casts=..?

A

glomerulonephritis

22
Q

Glomerulonephritis Dx

A
  • H&P
  • UA, 24 hr urine collection
  • Renal biopsy
  • cANCA for Wegener’
23
Q

Glomerulonephritis management

A
  • Steroids, cytotoxic drugs in SLE, Goodpasture’s, Wegener’s
  • Treat underlying cause
  • General measures:
    • control HTN
    • early treatment of infection
    • avoid nephrotoxic agents
24
Q

Hypertensive nephrosclerosis

A
  • Intimal thickening and luminal narrowing of large and small renal arteries and glomerular arterioles
  • Global and focal segmental sclerosis of glomeruli
25
Q

Hypertensive nephrosclerosis Demographics

A
  • Associated with chronic HTN, especially if very high
  • More common in Blacks, even at similar BP to whites
  • More common in DM and others with underlying kidney dz
26
Q

Hypertensive nephrosclerosis Signs and Symptoms

A
  • Typically present with long history of uncontrolled HTN
  • Slowly progressive increase in BUN, creatinine
  • Mild proteinuria with benign urine sediment
    • NOT RBC
    • NOT RBC CASTS
      • If they are seen then called “active urine sediment”
  • Hyperuricemia
  • May progress to ESRD
27
Q

Hypertensive nephrosclerosis Dx

A
  • Cinical diagnosis, no specific tests
  • Renal biopsy is diagnostic but rarely needed
28
Q

Hypertensive nephrosclerosis management

A
  • CONTROL BP!!!!!
    • MAY slow progression
    • Damage may already be done
  • BUT in AASK trial, pts with lower BPs did not have significantly better outcomes

AND

  • ACEIs were only renoprotective in pts who initially presented with proteinuria

CLIN MED PA 581: GU (7 decks)

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