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PHA 521 > Glomerular and Cystic Kidney Disease > Flashcards

Glomerular and Cystic Kidney Disease Flashcards

1
Q

Functional Role of the Kidney

A

control the balance of water in the body

control red blood cell production (erythropoietin)

control acidity of the blood

filter blood and pass waste products for excretion

control blood pressure (RAAS)

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2
Q

What is the average urine PHYSIOLOGIC protein excretion in adults

A

~80mg/day

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3
Q

What level of protein excretion qualifies as PATHOLOGIC proteinuria

A

150mg or greater over 14 hours

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4
Q

Albumin

A

smallest plasma protein

20-40% of physiologic proteinuria

filtered more readily than other globulins/plasma proteins

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5
Q

Microalbuminuria

A

excretion of 30-300 mg/day of albumin

too small to be detected by routine dipstick screening

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6
Q

Macroalbuminuria

A

excretion of albumin >300mg/day

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7
Q

Nephrotic range proteinuria

A

daily excretion of 3.5+g of protein

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8
Q

Glomerular Disease

A

MCC of pathologic proteinuria

alteration of glomerular permeability –> injury to podocytes, BM, capillary endothelium, mesangium –> pathologic proteinuria

initially: excess albumin
eventual progression to larger proteins

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9
Q

Overflow Proteinuria

A

overproduction of smaller proteins overwhelms reabsorptive ability of proximal tubule –> pathologic proteinuria

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10
Q

Tubular Proteinuria

A

tubulointestinal disease –> diminished reabsorptive capacity of the proximal tubule –> pathologic proteinuria

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11
Q

Classifications of Glomerular Disease

A

nephritic or nephrotic

primary or secondary

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12
Q

Glomerular Disease

A

cause some degree of glomerular damage

urinary loss of proteins –> hypoalbuminemia

DEFINITIVE DIAGNOSIS/GOLD STANDARD: biopsy

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13
Q

Nephritic Syndrome: definition

A

inflammatory process w/ associated immunologic response –> renal glomeruli damage –> blood cell passage

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14
Q

Nephritic Syndrome: clinical presentation

A 
edema (IS THIS EXTREMITY OR FACE)
hematuria (coca cola urine) (dysmorphic RBC and casts)
occasional WBC
subnephrotic proteinuria
HTN 
azotemia
rising creatinine
oliguria
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15
Q

Rapidly Progressive Glomerulonephritis

A

severe injury to glomerular capillary wall, GBM, Bowman’s capsule

most severe of the nephritic spectrum

progresses to renal failure in wks/mos

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16
Q

Nephritic Syndrome: Primary

A

post infectious glomerulonephritis
IgA nephropathy
Henoch Schonlein purpura
Pauci immune glomerulonephritis (ANCA assn)
anti glomerular BM glomerulonephritis (good pastures)

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17
Q

Post Infectious Glomerulonephritis

A

group A beta hemolytic streptococci

immune mediated glomerular injury - deposition of immune complexes

1-3wk after strep infxn (pharyngitis, impetigo)

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18
Q

Post Infectious Glomerulonephritis: clinical presentation

A

oliguria
edema
variable hypertension

coca cola urine

UA: RBCs, red cell casts, proteinuria

ASO titer high (unless blunted by abx)

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19
Q

Post Infectious Glomerulonephritis: prognosis

A

children: good
adults: less favorable (severe disease RPGN, develop CKD)

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20
Q

Post Infectious Glomerulonephritis: Treatment

A

treat underlying infxn

supportive

  • anti hypertensives (ACE-I, ARB)
  • salt restriction
  • diuretics (loop)

**steroids are of no benefit

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21
Q

IgA Nephropathy

A

aka Berger’s disease

IgA deposition in glomerular mesangium –> inflammatory response

MC primary glomerular disease world wide

children, young adults
M>F

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22
Q

IgA Nephropathy: clinical presentation

A

variable
follows URI or GI infxn

hematuria (coca cola urine 1-3d from illness onset)
proteinuria
INC IgA levels
NORMAL complement levels

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23
Q

IgA Nephropathy: prognosis

A

1/3: spontaneous remission
20-40%: CKD
remainder: chronic microscopic hematuria + stable creatinine

most unfavorable prognostic indicator:
proteinuria > 1g/d

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24
Q

IgA Nephropathy: Treatment

A

corticosteroids (if proteinuria 1-3.5g/d)

ACE-I or ARB (if severe proteinuria)

target BP: <130/80

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25
Henoch Schonlein Purpura
systemic small vessel associated w/ IgA deposition in vessel walls children assn w/ inciting infxn (group A strep)
26
Henoch Schonlein Purpura: clinical presentation
palpable purpura in LE and buttock arthralgias abdominal sx (nausea, colic, melena) dec GFR (w/ nephritic presentation -- some may have enough damage that leads to nephrotic)
27
Henoch Schonlein Purpura: treatment
no definitive treatment **some successful indications w/ plasma exchange (plasmapheresis) and DMARDs DMARDs: disease modifying antirheumatic drugs
28
Pauci-Immune Glomerulonephritis
ANCA associated seen w/ small vessel vasculitis - granulomatosis w/ polyangiitis - eosinophilic granulomatosis w/ polyangiitis - microscopic polyangiitis
29
Pauci-Immune Glomerulonephritis: clinical presentation
fever malaise weight loss purpura granulomatosis w/ polyangiitis: - respiratory tract sx - nodular lesions that can bleed
30
Pauci-Immune Glomerulonephritis: diagnostics
Labs: - ANCA positive (antineutrophil cytoplasmic antibodies) - hematuria - proteinuria
31
Pauci-Immune Glomerulonephritis: treatment
high dose corticosteroids DMARDs
32
Anti-Glomerular Basement Membrane Glomerulonephritis
aka goodpasture syndrome glomerulonephritis + pulmonary hemorrhage BM injury from anti GBM antibodies 1/3: no lung injury 2/3: lung injury
33
Anti-Glomerular Basement Membrane Glomerulonephritis: epidemiology
bimodal peak incidence 2nd-3rd decade 6th-7th decade
34
Anti-Glomerular Basement Membrane Glomerulonephritis: clinical presentation
preceded by URI hemoptysis dyspnea RPGN
35
Anti-Glomerular Basement Membrane Glomerulonephritis: diagnostics
Labs: - hemosiderin laden macrophages in sputum - anti-GBM antibodies CXR: -pulmonary infiltrates
36
Anti-Glomerular Basement Membrane Glomerulonephritis: treatment
plasma exchange therapy (plasmapheresis) -removes circulating antibodies immunosuppresive drugs (corticosteroids, DMARDs) - prevents formation of new antibodies - controls inflammatory response
37
Nephrotic Syndrome
significantly inc BM permeability
38
Nephrotic Syndrome: essentials of diagnosis
urine excretion 3.5+g/24hr hypoalbuminemia (serum albumin <3g/dL) bland urinary sediment (oval fat bodies) peripheral edema hyperlipidemia
39
Nephrotic Syndrome: clinical presentation
PERIPHERAL EDEMA: - serum albumin <2 g/dL - Na retention - initially presents in dependent areas of the body (LE) DYSPNEA: - pulmonary edema - pleural effusion - diaphragmatic compromise from ascites
40
Nephrotic Syndrome: urinalysis findings
proteinuria oval fat bodies (associated w/ marked HLD)
41
Nephrotic Syndrome: blood chemistry findings
dec serum albumin (<3 g/dL) dec total serum protein (<6g/dL) HLD (inc proteinuria --> fall in oncotic pressure --> inc lipid production --> dec VLDL clearance --> hypertriglyceridemia dec vitamin D, zinc, copper
42
Nephrotic Syndrome: protein loss considerations
daily total dietary protein intake should replace the daily urinary protein losses to avoid negative nitrogen balance protein malnutrition can occur w/ urinary protein loss >10g/d
43
Nephrotic Syndrome: edema considerations
dietary salt restriction utilize thiazide and loop diuretics (combination, high dose)
44
Nephrotic Syndrome: HLD considerations
encourage dietary modifications and exercise aggressive pharmacologic thearpy
45
Nephrotic Syndrome: hypercoaguable state considerations
serum albumin < 2 --> hypercoaguable low antithrombin III, protein C, protein S --> inc platelet activation prone to renal vein thrombosis
46
Nephrotic Syndromes
minimal change disease membranous nephropathy focal segmental glomerulosclerosis
47
Minimal Change Disease: pathogenesis
inc levels of glomerular permeability foot process effacement
48
Minimal Change Disease: epidemiology
MC in children boy>girl adults: M=F
49
Membranous Nephropathy
MCC of primary nephrotic syndrome in adults idiopathic immune mediate glomerulopathy immune complex deposition in glomerular capillary walls --> inc permeability
50
Membranous Nephropathy: clinical presentation
variable asymptomatic EDEMA W/ FROTHY URINE high incidence of venous thromboembolism
51
Membranous Nephropathy: diagnostics
Labs: | subnephrotic (<3.5 proteinuria) to classic nephrotic (>3.5 proteinuria) syndrome
52
Membranous Nephropathy: treatment
ACE-I or ARB (if BP >125/75) (reduces urine protein levels) Corticosteroid therapy (nephrotic syndrome only) (if failure to improve w/ 6 mo of conservative treatment)
53
Focal Segmental Glomerulosclerosis
inc permeability due to podocyte injury primary or secondary renal disease
54
Focal Segmental Glomerulosclerosis: primary renal disease
idiopathic some genetic altered podocyte formation african descent children
55
Focal Segmental Glomerulosclerosis: secondary renal disease
``` obesity HTN chronic urinary reflex HIV infection analgesic exposure biphosphonate exposure ```
56
Focal Segmental Glomerulosclerosis: clinical presentation
proteinuria | most w/ overt nephrotic syndrome
57
Focal Segmental Glomerulosclerosis: treatment
diuretic (edema) ACE-I or ARB (proteinuria, HTN) statin (HLD) high dose corticosteroid (primary, overt nephrotic)
58
Renal Cyst Development
genetic (autosomal dominant polycystic kidney disease) and non-genetic process childhood and adulthood diseases (acquired renal cysts secondary to chronic renal failure)
59
Renal Cyst Categorization
``` size location septations calcifications contents enhancement ```
60
Simple Renal Cyst
65-70% of all renal masses observed in normal kidneys MC incidental finding little clinical significance incidence inc w/ age M>F no clinical manifestations
61
Simple Renal Cyst: characteristics
develop in cortex and medulla solitary/multiple unilateral/bilateral <1cm->10cm round/oval lined by single epithelial layer fluid filled clear to straw colored fluid
62
Simple Renal Cyst: potential complications
obstruction of calyxes or renal pelvis rupture (flank pain, hematuria) infection --> renal abscess (insidious fever, vague lumbo-abdominal pain, +/-hematuria or pyuria) hypertension (compression of renal parenchyma --> angiotensin dependent HTN)
63
Simple Renal Cyst: US criteria for simple cyst
sharply demarcated w/ smooth thin walls no echoes (anechoic) w/in mass enhanced back wall indicating good transmission through the cyst
64
Simple Renal Cyst: US criteria for complex cyst
thick walls and/or septations calcifications solid components mixed echogenicity vascularity
65
Simple Renal Cyst: diagnostics
first line: US CT w/ and w/out contrast if US is equivocal or c/w complex cyst
66
Bosniak Classification of Renal Cysts: Category I
sharply demarcated w/ smooth thin walls homogenous fluid no contrast enhancement simple cyst benign image in 6-12 months
67
Bosniak Classification of Renal Cysts: Category II
``` closely resemble simple cyst few thin septa few calcifications <3cm diameter, well marginated no contrast enhancement ``` complex cyst benign imagine in 6-12months
68
Bosniak Classification of Renal Cysts: Category IIF
more complicated than II multiple thin septa thickened walls, calcifications >3cm diameter complex cyst likely benign (5% malignant) repeat imaging in 3-6months
69
Bosniak Classification of Renal Cysts: Category III
indeterminate cystic masses thickened irregular walls or septa measurable enhancement complex cyst 40-60% malignant monitor in older patients excise in younger patients
70
Bosniak Classification of Renal Cysts: Category IV
category III + soft tissue enhancing components adjacent to cyst wall complex cyst 85-100% malignant
71
Acquired Renal Cysts
MC reason: chronic renal failure inc risk of development w/ dialysis inc incidence w/ duration of dialysis may inc RCC risk
72
Acquired Renal Cysts: diagnostic criteria
bilateral involvement > 4 cysts <0.5-2/3cm diameter
73
Acquired Renal Cysts: clinical presentation
small to normal sized kidneys asymptomatic
74
Acquired Renal Cysts: screening consideration
yearly screening after 3-5yrs of dialysis US vs. CT w/ and w/out contrast
75
Simple or Complex Renal Cyst: treatment
excision (Bosniak classification) acute/intermittent pain: - acetaminophen - NSAID persistent pain: - percutaneous aspiration w/ injection of sclerosing agent - laparoscopic unroofing
76
Autosomal Dominant Polycystic Kidney Disease: etiology
autosomal dominant - PKD1 mutation: aggressive, MC - PKD2 mutation: slow growing 5% spontaneous mutation --> obstructed tubules --> cyst formation --> fluid accumulation --> enlargement --> separate from nephron --> compression of neighboring renal parenchyma --> progressive compromise of renal function
77
Autosomal Dominant Polycystic Kidney Disease: clinical presentation
clinically silent irreversible decline in renal function (begins in 4th decade) HTN pain hematuria (microscopic) proteinuria
78
Autosomal Dominant Polycystic Kidney Disease: initial presentation
30's-40's pain (abdominal, flank, back, chest, combination) large palpable kidneys frequent UTIs or recurrent nephrolithiasis
79
Autosomal Dominant Polycystic Kidney Disease: diagnostics
US (for screening and monitoring) ``` Labs: CBC CMP UA genetic screening ```
80
Autosomal Dominant Polycystic Kidney Disease: associated manifestations
hepatic cysts (estrogen sensitive) pancreatic/splenic cysts cerebral aneurysms mitral valve prolapse colonic diverticula
81
Autosomal Dominant Polycystic Kidney Disease: treatment
no definitive treatment treat HTN - ACE-I or ARB - low Na diet - limit caffeine consumption pain management avoid nephrotoxic agents avoid contact sports manage complications ESRD - dialysis or kidney tranplant UTI - quinolones
82
Medullary Sponge Kidney
congenital disorder MC: sporadic w/ no FH rare: familial autosomal dominant not diagnosed until 4th or 5th decade
83
Medullary Sponge Kidney: clinical presentation and characteristics
asymptomatic characterized by: - dilation of collecting tubules - medullary cysts
84
Medullary Sponge Kidney: complications
``` nephrolithiasis UTI hematuria dec urinary concentrating ability renal insufficiency ```
85
Medullary Sponge Kidney: diagnostics
``` intravenous pyelography (brush/linear striations, radiating outward from calyces) ``` multidetector row CT
86
Medullary Sponge Kidney: treatment
no known therapy good hydration thiazide diuretiv (if hypercalciuria) abx (for UTI)
87
Medullary Cystic Disease
aka nephronophthisis autosomal recessive infantile, juvenile and adolescent forms progression to ESRD, generally before 20 years of age
88
Medullary Cystic Disease: characteristic findings
reduced urinary concentrating ability (bland urinary sediment, polyuria, polydipsia) chronic tubulointerstitial nephritis w/ renal cysts after age 9
89
Medullary Cystic Disease: diagnosis
clinical extrarenal manifestations (retinitis pigmentosa) genetic testing US (normal-slight dec in kidney size) (inc echogenicity w/ loss of corticomedullary differentiation)
90
Medullary Cystic Disease: treatment
no specific treatment supportive care

PHA 521 (12 decks)

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