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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
cold agglutinin disease
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
cryoglobulinemic GN Type II and III
glomerulonephridity associated with autoimmune diseases such as SLE, Sjogren's syndrome, and viruses such as Hepatitis C and HIV
27
MPGN type 1
= 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
which three glomerulopathies is hep C associated with?
1. immune complex mediated MPGN (type 1) 2. mixed cryoglobulinemia GN (nephritis) 3. membranous nephropathy/glomerulopathy (nephrotis)
29
MPGN type 2
"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
treatment for nephritic diseases?
``` #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 ``` 3. add methyprednisolone for proteinuria that is over 1 gm/dl and high GFR 4. add cyclophosphamide or mycophenolate mofetil for GFR <70, and prediction of progression to ESRD
31
see ANCA, with systemic necrotizing vasculitis
microscopic polyangitis
32
see ANCA with respiraotyr necrotizing granulomas
Wegner's gramulomatosis
33
when do you see anti-GBM antibodies?
no lung hemorrhage = anti-GBM GN lung hemorrhage = Goodpasture synxrome
34
see ANA's
Lupus GN, type of immune complex Glomerular nephritis
35
3 types of nephrotic diseases?
MCD - in kids FSGS MG
36
african american, HIV, heroin, periorbital edema, HTN, UA shows oval fat bodies. renal biopsy shows, podocyte injury
FSGS | - idiopathic disease that may be related to abnormalities in APOL1 gene
37
HIV nephropathy?
FSGS
38
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
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
what antigen is seen in MG?
antigen against PLA2 receptor on podocyte membrane, results in fusion of foot processes and supeithelial deposits
40
secondary causes of MG?
infections: Hep B and C, endocarditis, syphillis AI: SLE, MCTD, thryoiditis carcinomas drugs: NSAIDs
41
electrophoresis of nephrotic syndrome
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
amyloidosis
nephrotic syndrome due to amorphic, eosinophilic PAS negative substances found in glomeruli
43
what does diabetes result in?
diabetic nephropathy, nephrotic spectrum
44
68 y/o man presenting with polyuria and oliguria and proteinuria, most likely due to?
prostatic obstruction
45
chronic tubulointerstitial disease
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
Type 1 RTA
impaired distal acidification, nephrocalcinosis urine pH greater than 5.3 (alkaline) causes: amphoteracin B, HyperparaT, Sjogrens syndrome, Medullary sponge kidney
47
Type 2 RTA
reduced proximal bicarb excretion, can acidify urine to <5.3, causes: myeloma protein, drugs (tenovofir, toluene, acetazolamide)
48
Type 4 RTA
- decreased ALDO secretion effect - urine usually less than 5.3 - increased plasma potassium causes: diabetics, ACEIs, obstruction, interstitial nephritis, HIV, NSAIDS
49
what is the cause of low anion gap hyperchloremic metabolic acidosis and occult metabolic alkalosis seen in pt. w/ multiple myeloma?
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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