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Renal II, Exam 3 > Chronic Renal Disease > Flashcards

Chronic Renal Disease Flashcards

1
Q

what do you see with acute renal disease?

A

sudden increase in BUN/Cr

oliguria, hypovolemia, hypervolemia

nausea, vomiting, malaise

azotemia w/ confusion, asterixis, pericardial effusions

hyperkalemia, acidosis, hyperphostphatemia

bleeding and clotting

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2
Q

stages of CKD

A
  • stage 3 for 3 months is considered CKD
    1: kidney damage w/ normal or increased GFR >90 ml/min
    2. kidney damage w/ mild decreased GFR: 60-89
    3. moderate decrease in GFR: 30-59
    4. severe decrease in GFR: 15-29
    5. Kidney failure w/ GFR <15, dialysis
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3
Q

most often causes of CRD?

A

70% due to diabetes/HTN with GN and cystic diseases, prostatic obstruction and tubulointerstitial diseases being the rest

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4
Q

What are the sx of CRD?

A
  1. HYPERTENSION!!!
  2. edema, CHF
  3. bone disease
  4. anemia
  5. broad waxy casts
  6. acidosis/hyperkalemia/progressive azotemia
  7. parastehsias
  8. small bilateral kidneys

decreased GFR –> sympathetic NS –> stimulates PT reabsorption of sodium –> HTN, edema, CHF

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5
Q

why does CKD cause osteodystrophy?

A
  1. phosphorus increases due to inability to excrete it, resulting in decrease in free Ca2+ –> PTH stimulation –> osteoclast remodeling –> weak bones
  2. renal disease also results in decreased 1alpha hydroxylast activity in kidney –> decreased production of active 1,25 (OH)vitamin D –> decreased Ca2+ reabosrption from the gut

** both low calcium levels and low 1,25 Vit D levels stimulate production of PTH **

continuously elevated PTH drives osteoblasts to produce RANKL and thus more osteoclast activity w/ bone resoprtion, causing osteitis fibrosa cystica, low vitamin D levels produce osteomalacia (softening)

  1. Mg dysregulation: both hypo/hyper magnesemia results in decreased PTH secretion and thus hypocalcemia
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6
Q

why does CKD cause anemia?

A
  • decreased EPO production
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7
Q

what type of casts are seen in CKD?

A

broad waxy casts respresentataive of tubular destruction

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8
Q

why do you acidisosis in CKD?

A

hyperchloremic production (vs. anion gap)

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9
Q

what are sx. of progressive azotemia of CKD?

A

<60 ml/min for 3 mos

see fatigue, weakness, malaise, nausea, vomiting

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10
Q

why are parasthesias seen in CKD?

A

uremic toxins result in peripheral neuropathies

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11
Q

what change is seen in kidneys w/ CKD?

A

bilateral small kidneys with fibrosis

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12
Q

Postinfectious glomerulonephritis

A

= immune complex GN
= Nephritic glomerular disease
- see subepithelial humps of IgG and C3, low serum complement levels

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13
Q

IgA nephropathy

A

Nephritic glomerular disease

see mesangioproliferative GN with IgA, periorbital edema, urine shows blood and protein, normal complement level

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14
Q

Henoch-Schonlein

A

Nephritic glomerular disease

mesangioproliferation of IgA, arthralgias, nausea, palpable rash, normal complement levels

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15
Q

Anti-GBM GN

A

Nephritic glomerular disease

see linear anti-basement membrane antibodies targetting the alpha-3 chain of type IV collagen

ex. Goodpasture’s syndrome

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16
Q

Type I cryoglobulinemic GN

A

Nephritic glomerular disease

  • occurs at the same time as cancers of the blood and immune system
  • ex: multiple myeloma, chronic lymphocytic leukemia, Waldenstroms macroglobulinemia
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17
Q

see mesangioproliferative GN with IgA, periorbital edema, urine shows blood and protein, normal complement level

A

Renal IgA nephropathy called Berger’s disease: synpharyngitic hematuria

  • hematuria that develops in older children after respiratory, GI or UTI
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18
Q

mesangioproliferation of IgA, arthralgias, nausea, palpable rash, normal complement levels?

A

Henoch-Schonlein Purpura (HSP) = occurs when IgA chains get caught in skin, joint, bowels, and blood vessels
- systemic childhood disease thats onset often follows URI

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19
Q

what systemic disease may you see IgA nephropathy/mesangial proliferations in?

A

hepatic cirrhosis, HIV, CMV, and Celiac disease as well as part of HSP

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20
Q

patient w/ palpable purpura, fever, w/l, hematuria. hx is negative for asthma or eosinophilia. RBC casts seen on UA, blood test shows P-ANCA present

A

renal biopsy shows rapidly progressive GN

= type I Pauci-Immune RPGN called microscopic polyangitis

21
Q

Microscopic Polyangitis

A

type of Pauci-Immune RPGN where pt presents with P-ANCA - see renal failure w/ palpable purpura, fever, w/l, hematuria

22
Q

P-ANCA

A

Pauci-Immune RPGN

  • seen in microscopic polyangitis
  • MPA does not have granulomatous inflammation and does not involve the upper respiratory tract as does Wegners
  • antibodies to strong cations (anti-MPO abs) react when MPO is exposed on neutrophil membrane
23
Q

C-ANCA

A
  • Pauci-Immune RPGN
  • granulomatosis with polyangitis (formerly called Wegner’s franulomatosis)
  • Abs to neutral proteins of weak cations react (PR3) react when PR3 is expressed on neutrophil membrane
24
Q

essential mixed cryoglobulinemia

A
  • a disease where pt. forms antibodies against antibodies (in this case Hep C antibodies)
  • cryoglobulins act on large particles, get caught in skin, joints, kidneys
    = a medical condition in which the blood contains large amounts of cryoglobulins - proteins (mostly immunoglobulins themselves) that become insoluble at reduced temperatures. This should be contrasted with cold agglutinins, which cause agglutination of RBCs.
  • -> crescentic pattern on biopsy
  • arthralgias, hematuria, hepatosplenomegally
  • spent time in cold
  • serum complement levels are depressed and RF is positive
  • RBCs present in urine
  • pt. positive for Hepatitis C
25
Q

cold agglutinin disease

A

Cold agglutinin disease is an autoimmune disease characterized by the presence of high concentrations of circulating antibodies, usually IgM, directed against red blood cells.[

26
Q

cryoglobulinemic GN Type II and III

A

glomerulonephridity associated with autoimmune diseases such as SLE, Sjogren’s syndrome, and viruses such as Hepatitis C and HIV

27
Q

MPGN type 1

A

= disease where discrete immune complexes are found in mesangium and supeptihelial space. ICs are combos of antigens, antibodies and complement that bind an become lodged in the kidney –> activating inflammation and damage to kidney itself
* low C3 and C4 levels*

pt. presents w/ recent URI, gross hematuria, mild proteinuria
- see IF of Ig and C3 deposits in mesangium and subepithelial capillary wall
- LOW C3 AND C4 LEVELS
- EM shows “tram tracking”

  • best tx = ACE inhibitors (always first tx for CKD unless Cr is over level 3)
28
Q

which three glomerulopathies is hep C associated with?

A
  1. immune complex mediated MPGN (type 1)
  2. mixed cryoglobulinemia GN (nephritis)
  3. membranous nephropathy/glomerulopathy (nephrotis)
29
Q

MPGN type 2

A

“dense depsit disease” = intramembranous deposits in GBM

  • immuoglobulin staining for only C3
  • EM shows dense ribbon-ike deposits found in BM, glomeruli, tubules, and bowman’s capsule
  • ** C3 IS LOW***
  • see profound hypocomplementemia due to C3NEF factor always being activated
  • seen in children and young adults
30
Q

treatment for nephritic diseases?

A 
#1 is ACE inhibitors for treating HTN
2. treat proteinuria w/ ACE inhibitors: will dilate the efferent result ing in glomerulus putting out less protein - proteinuria eventually causes CKD thus need to stop this from ocurring
  1. add methyprednisolone for proteinuria that is over 1 gm/dl and high GFR
  2. add cyclophosphamide or mycophenolate mofetil for GFR <70, and prediction of progression to ESRD
31
Q

see ANCA, with systemic necrotizing vasculitis

A

microscopic polyangitis

32
Q

see ANCA with respiraotyr necrotizing granulomas

A

Wegner’s gramulomatosis

33
Q

when do you see anti-GBM antibodies?

A

no lung hemorrhage = anti-GBM GN

lung hemorrhage = Goodpasture synxrome

34
Q

see ANA’s

A

Lupus GN, type of immune complex Glomerular nephritis

35
Q

3 types of nephrotic diseases?

A

MCD - in kids
FSGS
MG

36
Q

african american, HIV, heroin, periorbital edema, HTN, UA shows oval fat bodies. renal biopsy shows, podocyte injury

A

FSGS

- idiopathic disease that may be related to abnormalities in APOL1 gene

37
Q

HIV nephropathy?

A

FSGS

38
Q

non-hodgkins lymphoma, peripheral edema, 40 lb. w/g, hx of recurrent infections, patients abdomen is prominent, dyspneic.

seum vitamin D levels are low, kidney biopsy shows thickened GBM w/ “spike and dome” pattern of subepithelial deposits

A

Membranous glomerulopathy (associated w/ lymphoma, carcinoma, pencillamine, thryoiditis, HepB/C, syphilis, endocarditis)

“subepithelial deposits have lumpy bumpy spike appearance” rather than linear (seen in anti-GBM)

  • often results in renal vein thrombosis:
39
Q

what antigen is seen in MG?

A

antigen against PLA2 receptor on podocyte membrane, results in fusion of foot processes and supeithelial deposits

40
Q

secondary causes of MG?

A

infections: Hep B and C, endocarditis, syphillis
AI: SLE, MCTD, thryoiditis
carcinomas
drugs: NSAIDs

41
Q

electrophoresis of nephrotic syndrome

A

In nephrotic syndrome there is loss of albumin AND antithrombin III, protein C and S, as well as increased fibrinogen, increased production of alpha 1 lipoprotein-a (HDL) and increased platelet aggregation (with the latter three being due to low albumin).

  • nephrotic syndrome results in even large proteins, alpha2, VLDL, LDL getting through slightly and resulting in hyperlipiduria and oval fat bodies, but high lipid levels in blood
  • albumin in the blood drops dramatically, but alpha2 macroglobulin, and beta cannot get through, thus they increase relatively on plasma electrophoresis
  • loss of antithrombin results in inability to deactivate thrombin –> nephrotic patients to have increased clotting
42
Q

amyloidosis

A

nephrotic syndrome due to amorphic, eosinophilic PAS negative substances found in glomeruli

43
Q

what does diabetes result in?

A

diabetic nephropathy, nephrotic spectrum

44
Q

68 y/o man presenting with polyuria and oliguria and proteinuria, most likely due to?

A

prostatic obstruction

45
Q

chronic tubulointerstitial disease

A

characterized by:
- isothenuria (same concentration as plasma) w/ polyuria, moderate proteinuria, very few cells, type I, II or IV RTA, broad waxy casts, small kidneys

Proud American Veterans Love GM:
Prostate (obstructive uropathy)
Analgesics (NSAIDS)
VU reflux
Lead (heavy metals)
Gout
Myeloma
46
Q

Type 1 RTA

A

impaired distal acidification, nephrocalcinosis

urine pH greater than 5.3 (alkaline)

causes: amphoteracin B, HyperparaT, Sjogrens syndrome, Medullary sponge kidney

47
Q

Type 2 RTA

A

reduced proximal bicarb excretion, can acidify urine to <5.3,

causes: myeloma protein, drugs (tenovofir, toluene, acetazolamide)

48
Q

Type 4 RTA

A
  • decreased ALDO secretion effect
  • urine usually less than 5.3
  • increased plasma potassium

causes: diabetics, ACEIs, obstruction, interstitial nephritis, HIV, NSAIDS

49
Q

what is the cause of low anion gap hyperchloremic metabolic acidosis and occult metabolic alkalosis seen in pt. w/ multiple myeloma?

A

The light chains of MM (Bence Jones protein) have damaged the proximal tubule causing it to leak HCO3 as in the Fanconi syndrome.

“Myeloma Kidney”
= hypercalcemia, hyperuricemia, amyloidosis, B cell infiltration, hyperviscosity

high calcium b/c it’s a bone disease, malignancies are always assoc. w/ hyperuriemia due to high protein turnover, AL is light chains (same as bence proteins, but different type of light chains), B cell infiltration due to plasma cells invading the kidney, hyperviscosity due to too much protein in the blood

Renal II, Exam 3 (9 decks)

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