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SS- Renal > Disorders > Flashcards

Disorders Flashcards

1
Q

Bartter’s syndrome

A

AR: Na wasting
thick ascending loop of Henlee
defect in NaK2Cl transporter
Sx: hypokalemia, elevated renin and aldosterone, hypochloremic metabolic acidosis, increase PGE2, failure to thrive
some: hypomagnesemia, hypercalinuria
neonatal: polyhydramnios (fetal polyuria)
SALT CRAVING, DEAF
mutations: Na/K/2Cl, ROMK, CLCNKA, CLCKB, barttin
Tx: K and Mg if needed, COX inhibitors

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2
Q

Gittleman’s syndrome

A

AR: Na wasting
DCT
mutation in Na/Cl cotransporter: presents later in life
Sx: hypokalemia, hypochloremic metabolic alkalosis, hypocalciuria

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3
Q

glucosuria

A

cause: pregnancy, DM, familial renal glucosuria
Sx: thirst, nocturia due to osmotic diuresis

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4
Q

familial renal glucosuria

A

mutation in SGLT1

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5
Q

renal failure

A

loss of ability to balance salt and water

edema causes increase work load of heart leading to HF and pulmonary edema + acidemia and hyperkalemia

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6
Q

diabetic nephropathy

A

MOST COMMON: ESRD
AA, native american, mexican
nephrotic: glomerular capillary wall deposition
pore size increased and charge difference reduced: proteinuria
chronic
Sx: HTN, increased then decreased GFR, microalbuminemia to macro
HE: increase measangial matrix, glomerular collapse, glomerulosclerosis; normal or increased glomeruli initially
risk: increases sig. when 1st relative of Type 1 DM has diabetic nephropathy
type 1: 10 years before develops
type 2: can’t tell how long
Tx: reduce BP and proteinuria; ACEI/ARB
3 types: glomerular, papillary, tubulointerstitial

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7
Q

nephritic syndrome

A

endothelial cell
inflammation
UA: 1-2+ proteinuria, hematuria, RBC casts, dysmorphic RBC
spot urine protein creatinine ratio: 1
Sx: periorbital swelling, HTN, elevated BUN and Cr, oliguria
sub endothelial or mesangial: post-infectious glomerulonephritis, lupus nephritis, IgA nephropathy
BM: anti-GBM disease
necrotizing injury and inflammation: ANCA

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8
Q

nephrotic syndrome

A

visceral epithelial cell (podocyte)
noninflammatory
EM: fusion of pedicels (effacement)
UA: 3+ to 4+, greater than 3.5 g/day, greater than 40 mg/hr/m2 in children, proteinuria, fatty cast
spot urine protein creatinine ratio: 10
Sx: pitting edema, hypercholesterolemia
podocyte injury: MCD, FSGS
sub epithelial complexes: membranous nephropathy
capillary wall: amyloidosis, light chain deposition disease, diabetic nephropathy
Tx: ACEI/ARB, tx hyperlipidemia, corticosteroids, Calcineurin inhibitors

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9
Q

proteinuria

A

presents as foamy urine

due to barrier failure: large pore or loss of charge selectivity or abnormal circulating protein

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10
Q

Diabetes Mellitus

A

impairment of insulin secretion and peripheral resistance to insulin
Sx: hyperglycemia (thirst, polyuria, weight loss, vision)
microvascular: CAD, cerebrovascular disease, PVD
Macro: nephropathy, neuropathy, retinopathy
increased thickness of BM and damaged capillaries: reduced Kf
macroalbuminuria: more likely to die than develop ESRD
renal complications: pyelonephritis, emphasematous pyelonephritis, type 4 RTA, neurogenic bladder

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11
Q

lower urinary tract obstruction

A

stones, BPH

increases PBS and decreases GFR

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12
Q

frequent emptying of bladder

A

decrease PBS and increases GFR

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13
Q

low capillary flow

A

increases FF and therefore πG increases and GFR decreases

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14
Q

Addison’s

A

absence of aldosterone

increased urinary excretion of NaCl

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15
Q

Conn’s syndrome

A

aldosterone secreting tumor

increased Na reabsorption and K secretion: hypokalemia, hypernatremia, hypertension

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16
Q

Liddle syndrome

A 
AD
pseudo hyperaldosteonism
gain of function of beta or gamma ENac
Sx: HTN, low renin and aldosterone, hypokalemia, metabolic alkalosis
Tx: salt restriction
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17
Q

metabolic alkalosis

A

increased pH, PCO2, HCO3

causes: loop/thiazide diuretics, vomiting, antacids, hyperaldosteronism

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18
Q

non-anion gap metabolic acidosis

A 
decrease pH, PCO2, HCO3
causes: HARDASS
Hyperalimentation
Addison Disease
Renal tubular acidosis 
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
mild to mod. renal insufficiency
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19
Q

increased anion gap metabolic acidosis

A 
decrease pH, PCO2, HCO3
causes: MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets or Isoniazid
Lactic Acidosis (shock)
Ethylene glycol
Salicylates (Aspirin)
renal failure: decreased NH4 excretion
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20
Q

respiratory acidosis

A

increase pCO2, HCO3
decrease pH
causes: hypoventilation; hypercapnia: airway obstruction, acute lung disease, chronic lung disease, opioids, sedatives, weak respiratory muscles
Cl: changes inversely and equally to bicarb

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21
Q

respiratory alkalosis

A

increase pH
decrease pCO2, HCO3
causes: hyperventilation: hysteria, hypoxemia, salicylates (early), tumor, pulmonary embolism
Cl: changes inversely and equally to bicarb
*preganancy: chronic

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22
Q

type 2 renal tubular acidosis

A 
proximal: loss of bicarbonate
Faconi
FEHCO3: greater than 10%
urine pH: less than 5.5
Sx: hypokalemia
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23
Q

type 1 renal tubular acidosis

A

distal: decreased acid secretion
Sx: hypokalemia, hypercalciuria, stones, failure to thrive
FEHCO3: less than 5%
urine pH: greater than 5.5

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24
Q

type 4 renal tubular acidosis

A 
aldosterone deficiency
decreased acid excretion
FEHCO3: less than 5-10%
urine pH: greater or less than 5.5
Sx: HYPERkalemia
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25
Q

acute respiratory disorders

A

acidosis: increase pCO2 by 10 results in increase of bicarb by 1
alkalosis: decrease pCO2 by 10 results in decrease of bicarb by 2
* greater change in pH

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26
Q

chronic respiratory disorder

A

acidosis: increase pCO2 by 10 results in increase of bicarb by 4
alkalosis: decrease pCO2 by 10 results in decrease of bicarb by 5

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27
Q

Cl responsive metabolic alkalosis

A

urine Cl less than 20 mEq/l (usually less than 10 mEq/l)

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28
Q

Cl resistant metabolic alkalosis

A

urine Cl greater than 20 mEq/l (usually greater than 50 mEq/l)

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29
Q

hyperkalemia

A

Sx: weakness, ileum, EKG: peaked T wave; then wide QRS, short QT, long PR; absent P wave; V tach
causes:
1. increase intake
2. decrease renal excretion: renal failure, decreased tubular flow, distal tubular dysfunction, hypoaldosteronism
3. internal redistribution: insulin deficiency, B2 blocker, hypertonicity, acidosis, cell lysis
Tx:
1. stabilize heart: calcium gluconate
2. move K into cell: insulin, albuterol, bicarb
3. move K out of body: diuretics, kayexalate, dialysis

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30
Q

hypokalemia

A

Sx: weakness, rhabdomyolysis, ileus, HTN, nephrogenic diabetes insipidus, EKG: flat T wave; prominent U wave, depressed ST
chronic: asymptomatic
causes:
1. inadequate K intake
2. external loss: GI, cutaneous, renal
3. internal redistribution: insulin, catecholamine, alkalemia, cell proliferation
Tx: K, K sparing diuretics

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31
Q

hypokalemia normotensive disorders with metabolic alkalosis

A 
loop and thiazide diuretics
vomiting
nasogastric suction
Bartter's syndrome
Gitelman's syndrome
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32
Q

hypokalemia normotensive disorders with metabolic acidosis

A

renal tubular acidosis (1 and 2)

ureteral diversion

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33
Q

hypokalemia hypertensive disorders

A

hyper-reninemia: renal artery stenosis, renin secreting tumor
primary hyperaldosteronism: Conn’s syndrome, adrenal hyperplasia or tumor, Cushing’s syndrome (glucocorticoids can bind aldosterone receptor)

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34
Q

hyponatremia

A

Sx: lethargy, hyporefelxia, mental confusion
1. decrease ECFV: diarrhea, vomiting
2. NO CHANGE ECFV: HF, liver failure
renal Na loss: Una greater than 20 mEq/L
extrarenal Na loss: Una less than 20 mEq/L
Tx: isotonic saline infusion (slow)

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35
Q

nocturia

A

frequent urination during the night

cause: disability to concentrate urine

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36
Q

central diabetes insipidus

A 
Sx: dilute urine
cause: lack ADH
resting: high Posm, low Uosm
WD: increase Posm
ADH infusion: normal Posm, increase Uosm
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37
Q

nephrogenic diabetes insipidus

A 
Sx: dilute urine
cause: CD do not respond to AVP
congenital: x-linked V2 or AQP2 mutation
acquired: defect in medullary interstitial tonicity or cAMP, AQP down regulation, pregnancy
resting: high Posm, low Uosm, high ADH
WD: increase Posm, increase ADH
ADH infusion: no change
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38
Q

polydipsia

A 
obsessive water drinking
Sx: hyponatremia, coma, death
cause: loss of medullary hyperosmolarity
resting: low Posm, Uosm, ADH
WD: normal Posm, Uosm; increase ADH
ADH infusion: decrease Posm; increase Uosm
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39
Q

osmotic diuresis

A

cause: hyperosmotic plasma
resting: high Posm, Uosm
WD: increase Posm, Uosm, ADH
ADH infusion: Posm and Uosm remain high

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40
Q

Goodpasture’s

A

nephritic with crescentic GN
anti-GBM: antibodies against NC1 domain of alpha3 (IV) chain
young adult, white, men (thicker BM)
IF: linear, IgG, C3
Sx: glomerulonephritis with hematuria and hemoptysis, azotemia, arthritis, anemia
Tx: plasmapheresis

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41
Q

effacement of pedicels

A

nephrotic syndrome
retraction of foot processes and loss of slit pore diaphragm so that long segments of capillary are invested by cytoplasm of a single podocyte
detachment from BM and BM degradation allow proteins to leak into urinary space

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42
Q

lupus nephritis

A 
subendothelial: immune complex
HE: wire loops
rapidly progressive
IF: FULL HOUSE: IgG, IgM, IgA, C3, C4
Tx: glucocorticoids, cyclophosphamide, mycophenolate mofetil, hydroxychloroquine, aspirin
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43
Q

post-streptococcal glomerulonephritis

A 
nephrotic
subendothelial to subepithelial: 
anti-streptolysin O, anti-DNAse B
EM:  subepithelial HUMPS
HE: endocapillary proliferation, neutrophils
IF: IgG, C3 (capillary and mesangium)
Sx: tea colored urine (RBCs), recent throat or skin infection (1-6 week), HTN, azotemia
LOW C3, normal C4: alternate pathway
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44
Q

metabolic (diabetic) glomerular injury

A
  1. hyperglycemia causes non-enzymatic glycosylation of proteins resulting in thickened GBM and AGE (advanced glycation end-products)
  2. AOPP (advanced oxidation products), renin-angiotensin, TGF-beta, AGE activate NADPH oxidases producing ROS leading to mesangial matrix production, podocyte injure and apoptosis and proteinuria
    H&E: hyaline sclerosis; diffuse mesangial sclerosis
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45
Q

hemodynamic glomerular injury

A

supra-normal glomerular capillary pressures cause GBM thickening, mesangial cell hypertrophy and hyperplasia, and mesangial matrix production
causes hyaline sclerosis of afferent but not efferent arteriole: ischemic atrophy of glomerulus

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46
Q

arterionephrosclerosis

A

more common in A.A. due to apoL1

HTN leads to globally sclerotic glomeruli

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47
Q

malignant HTN

A 
black males ~40
HTN that causes end organ damage
greater than 200/120 mmHg
Sx: headache, vomiting, proteinuria, hematuria, scotoma (spots before eyes), renal failure
H&E: fibrinoid necrosis of arterioles leading to necrosis of glomeruli
onion skin
gross: flea-bitten kidney
P: can be fatal due to renal disease
MEDICAL EMERGENCY
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48
Q

diffuse glomerular disease

A

involving all or most of the glomeruli

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49
Q

focal glomerular disease

A

involving some glomeruli but not most

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50
Q

global glomerular disease

A

involving whole glomerulus

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51
Q

segmental glomerular disease

A

involving only part of glomerulus

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52
Q

proliferative glomerular disease

A

increased cell

proliferating native cells but also infiltrating inflammatory cells

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53
Q

membranous glomerular disease

A

increase GBM without increased cells

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54
Q

membrano-proliferative glomerular disease

A

increased cells and GBM

EM: TRAM TRACKS

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55
Q

membrano-proliferative glomerular disease

A

increased cells and GBM

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56
Q

pauci-immune glomerulonephritis

A

crescent: lymphocytes and monocytes in Bowman’s space
antibodies are present but not visible on immunofluorescence or EM
ANCA
Sx: arthritis, arthralgia, myalgia, fatigue

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57
Q

microscopic polyangiitis

A 
small vessel
nephritic: necrotizing injury of vascular and glomerular capillary wall
pauci-immune
P-ANCA
rapidly progressive
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58
Q

Churg-Strauss

A 
small vessel
nephritic: necrotizing injury of vascular and glomerular capillary wall
pauci-immune
P-ANCA
rapidly progressive
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59
Q

Granulomatous with polyangiitis (Wegner’s)

A

small vessel
nephritic: necrotizing injury of vascular and glomerular capillary wall
pauci-immune
C-ANCA
Sx: sinopulmonary renal syndrome, purpura
rapidly progressive
HE: normal, mesangial proliferative, segmental necrotizing, crescents (fibrin): tubulointerstitial GRANULOMAS
Tx: cyclophosphamide

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60
Q

C-ANCA

A

cytoplasmic

Anti-proteinase3

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61
Q

P-ANCA

A

perinuclear

Anti-MPO

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62
Q

IgA nephropathy

A

nephritic: mesangial
CURRENT infection
Sx: brown/red urine (macroscopic hematuria)

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63
Q

IgA nephropathy

Berger’s Disease

A 
nephritic (variable): mesangial
CURRENT infection (1-2 days)
galactose deficient IgA1
HE: variable; mesangial expansion
IF: IgA
EM: mesangial deposits
Sx: brown/red urine (macroscopic hematuria)
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64
Q

membranous nephropathy

A 
white male adults 4th-6th decade
nephrotic: subepithelial
Ab: PLA2, NEP
EM: SPIKE and DOME
immuno: IgG
HE: thick BM
2: Hep. B, syphilis, malaria, gold, penicillamine, captorpril, NSAID; lung, colon, skin cancer; SLE, sickle cell
risk for loss of renal function: male, greater than 10g/day proteinuria, HTN, azotemia, tubuointerstitial fibrosis, glomerulosclerosis
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65
Q

causes of iso-osmolar hyponatremia

A

pseudohyponatremia: severe hyperlipidemia and hyperproteinemia
post-transurethral prostatectomy, posthysteroscopic

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66
Q

causes of hypo-osmolar hypervolemic hyponatremia with decreased ECV

A

TBW and TBNa increase, TBW more than TBNa

CHF, liver disease, nephrotic syndrome, renal disease

67
Q

causes of hypo-osmolar hypervolemic hyponatremia with increased ECV

A

acute and chronic renal failure

68
Q

causes of hypo-osmolar euvolemic hyponatremia

A

increase TBW; no change TBNa
causes: SIADH, drugs, glucocorticoid deficiency, hypothyroidism, primary polydipsia, lung disorders, CNS disorders and malignancy, drug induced water retention

69
Q

causes of hypo-osmolar hypovolemic hyponatremia

A

decrease ECFand ECV
causes: diuretics, aldosterone deficit, diarrhea, vomiting, bleeding, excessive sweating with high water intake, pancreatitis, bowel obstruction, burns
severe hypokalemia

70
Q

hypernatremia

A

Uosm less than 300 mOsm/kg: diabetes insipidus
Uosm greater than 500 mOsm/kg: extra-renal water loss, Na infusion, decrease osmotic diuresis
other: primary hyperaldosteronism, Cushing’s, hypertonic hemodialysis, admin. of Na

71
Q

tubular injury UA

A

microscopic hematuria, renal tubular epithelial cells, granular casts, specific gravity 1.010, Uosm 300

72
Q

acute tubular necrosis (ATN)

A

non-inflammatory tubular injury
cause: ischemia or toxins (aminoglycosides (PT), contrast, amphotercin B)
proximal straight tubule and TALH
occlusion of tubular lumens with cells and casts
muddy brown granular casts
urine Na greater than 20
FeNa greater than 1

73
Q

allergic interstitial nephritis (AIN)

A

inflammatory tubular injury
proliferation of interstitial fibroblast and matrix: TGF-B
UA: pyuria, eosinophiluria
cause: penicillin, cephalosporin, NSAIDS; infections, autoimmune, infection
Sx: fever, rash, joint pain, eosinophils, sterile pyuria

74
Q

obstructive uropathy

A

tubular injury and possible RBC

75
Q

mesangial pattern tubular disease

A

UA: hematuria, RBC casts without proteinuria

76
Q

hereditary renal glucosuria

A

AR: PT

mutation of SGLT2

77
Q

Cystinuria

A

AR: PT: amino aciduria
mutation of brush border transporter responsible for reabsorption of cystine, ornithine, lysine, arginine
cystine stones
UA: cystine casts

78
Q

X-linked hypophosphatemia

A

mutation of PHEX gene: increased FGF23
Sx: urinary Pi wasting, elevated serum alkaline phosphatase, normal Ca and calcitriol
presents: rickets in children and osteomalacia in adults

79
Q

autosomal recessive hypophosphatmic Rickets

A

mutation that leads to increased FGF-23

mutation in Na/Pi IIc transporter

80
Q

oncogenic hypophosphatemic osteomalacia

A

aquired

increased production of FGF-23 by tumors (fibromas, angiosarcomas, hemangiopericytomas)

81
Q

Hartnup disease

A

defect in neutral amino acid transporter SLC6A19

Sx: failure to thrive, photosensitivity, intermittent ataxia, nystagmus, tremor

82
Q

vitamin D dependent rickets type 1

A

mutation of 1 alpha hydroxylase

Sx: hypophosphatemia, rickets

83
Q

Faconi syndrome

A

generalized PT dysfunction
Sx: aminoaciduria, glucosuria, hypophophatemia, hyperchloremic metabolic acidosis, hypokalemia, uricosuria
polyuria, polydipsia, volume depletion, arrhythmia, proteinuria, growth retardation, rickets, renal stones
inherited: cysinosis, lots of others
acquired: tenofovir, multiple myeloma, lots of of others

84
Q

glucocorticoid-remediable hyperaldosteronism (GRA)

A

congenital
recombination of 11-B-hydroxysteroid dehydrogenase and aldosterone synthase: promoter that makes cortisol is stuck on gene that produces aldosterone
Sx: low renin HTN, hypokalemia
Tx: glucocorticoids

85
Q

apparent mineralcorticoid excess (AME)

A

mutations in kidney isozyme of 11BHSD: increase cortisol in kidney that activates aldosterone receptor
Sx: low renin HTN, hypokalemia
Tx: glucocorticoids

86
Q

PHA type 1

A

AD: mutation in mineralocorticoid receptor, childhood
AR: loss of function mutation in ENaC
Sx: hyperkalemia, hypernatremia, HYPOTENSION
Tx: Na, fluids, Kayexalate
mirror image of Liddle

87
Q

PHA type II
Gordon syndrome
chloride shunt syndrome

A

mutation: WNK1, WNK4, ser/thr kinase that regulates Na/Cl cotransporter
Sx: hyperkalemia, hyperchloremic metabolic acidosis, HTN, low renin and aldosterone
mirror image of Gitelman
Tx: thiazides

88
Q

renal tubular acidosis (RTA)

A

normal anion gap metabolic acidosis

positive urine anion gap

90
Q

Focal segmental glomerulosclerosis (FSGS)

A 
A.A.
nephrotic: subepithelial immune complex
non-selective proteinuria
EM: podocyte effacement 
H&E: focal, segmental 
immuno: neg
suPAR, apoL1
Sx: may have HTN, half develop ESRD
2: HIV, parvo, heroin, lithium, pamidronate, partial nephrectomy 
mutations: alpha-actinin-4, podocin, TRPC6, apoL1
90
Q

minimal change disease (MCD)

A 
children
nephrotic: podocyte injury
proteinuria: ALBUMIN
EM: foot process EFFACEMENT
H&E: normal
immuno: neg.
2: Hodkin's, NSAID, IFN-alpha
Tx: GLUCOCORTICOIDS
91
Q

rapidly progressive glomerulonephritis

A

nephritic
renal failure over days/weeks
features of vasculitis
ex: ANCA vasculitis, lupus nephritis

92
Q

chronic glomerulonephritis

A

HTN, renal insufficiency, proteinuria greater than 3 g/day
SHRUNKEN kidneys
ex: diabetic and HTN nephropathy

93
Q

Alport syndrome (Hereditary nephritis)

A

GBM
X-linked COL4A5: male
Sx: hematuria, progressive proteinuria, ESRD
assoc.: hearing loss, lens abnormalities, platelet defects, esophageal leiomyomas
HE: focal, segmental or global glomerulosclerosis, interstitial fibrosis, foam cells
EM: BASKETWEAVE, focal effacement of podocytes
IF: neg.

94
Q

hemolytic uremic syndrome (HUS)

A

hemolytic anemia, renal dysfunction , thrombocytopenia
ONION SKIN
HE: fibrin and platelets in lumen, fibrin in subintima and media of vessels
E. coli H7:O157 verotoxin

95
Q

thrombocytpenia purpura (TTP)

A

FEVER, NEUROLOGIC, PURPURA
hemolytic anemia, renal dysfunction , thrombocytopenia,
ONION SKIN
HE: fibrin and platelets in lumen, fibrin in subintima and media of vessels
ADAMTS13 or autoimmune disorders

96
Q

membranoproliferative glomeruluonephritis

A

asymptomatic, acute nephritic, nephrotic, crescentic rapidly progressive glomerulonephritis
subendothelial
EM: TRAM TRACKS
HE: hypercellular glomerulus, increased mesangium
immuno: C3, C4, IgG; monoclonal gammopathy (kappa or lambda)
Sx: HTN, decreased GFR
rheumatoid factor, ANA, LOW C3
immune complex mediated: classical pathway
complement mediated: alternative pathway

97
Q

type 1 MPGN

A

most common
HE: mesangial hypercellularity, monocytes
sub endothelial and mesangial
IF: IgG
2: neoplasm, infection, collagen vascular disease
Hep. C; LOW C3 and C4

98
Q

type 2 MPGN

A 
dense deposit disease in capillary wall
deficiency of FACTOR H
C3c present
partial liphodystrophy: loss of fat upper body; macular deposits in eyes
LOW C3
99
Q

type 3 MPGN

A

subedothelial and sub epithelial with GBM disruption and lamina dens layering

100
Q

thin basement membrane

A 
female
heterozygote COL4A5: defects in alpha-3 or 4 type IV
Sx: hematuria
HE: normal
IF: negative
EM: thin GBM
101
Q

polyarteritis nodosa

A

medium vessel: infarcts
ANCA NEG.
assoc.: Hep B (and Hep C and Hairy cell leukemia)
Sx: arthralgia, fatigue weight loss, fever, abdominal pain, near, renal, HTN, skin lesions
HE: SEGMENTAL TRANSMURAL NECROTIZING vasculitis

102
Q

What indicates ANCAs are pathogenic?

A

activate PMN
increase contact and adhesion with endothelial cells and vasculature structures
adhesion: B-2 integrin, Mac-1, Fc gamma
*endothelial cells are the primary target in small cell vasculitis

103
Q

thrombotic microangiopathy (TMA)

A

normal PTT and PT (prolonged in DIC)
HUS, TTP
drugs, SLE, antiphospholipid, complement defects, HIV, cancer

104
Q

class I lupus nephritis

A

minimal measngial

RARE

105
Q

class II lupus nephritis

A

mesangial proliferative

106
Q

class III lupus nephritis

A

focal proliferative

107
Q

class IV lupus nephritis

A

diffuse proliferative

MOST COMMON

108
Q

class V lupus nephritis

A

membranous

nephrotic

109
Q

class VI lupus nephritis

A

advanced sclerosing

110
Q

scleroderma

A

females AA
fibrosis and vascular occlusion
mild renal involvement: dysfunction, proteinuria, HTN
renal crisis: accelerated arterial HTN and/or rapidly progressive oliguria renal failure
Risk factors for renal crisis: early diffuse systemic sclerosis, rapidly progressing, anti RNA polymerase Ab, steroids
HE: intimal and medial proliferation arcuate arteries, fibrinoid necrosis and thrombosis

111
Q

acute kidney injury (AKI or ARF)

A

less than 1 month
Cr: greater than 0.5 mg/dl
usually asymptomatic

112
Q

pre-renal ARF

A 
decrease renal blood flow
BUN: Cr ratio: greater than 20
urine mOsm: greater than 500
urine Na: less than 25
FeNa less than 1
causes: volume depletion, CHF, shock, hepatorenal syndrome, renal artery stenosis and ACEI/ARB, NSAIDS
113
Q

intrinsic renal ARF

A

glomerular: nephrotic and nephritic
tubular: ATN AIN
vasculitis
BUN: Cr ratio: less than 15
urine mOsm: less than 250
urine Na: greater than 20
muddy brown casts

114
Q

post-renal ARF

A

obstruction of flow: voiding complaints
Dx: ultrasound
causes: prostate, cancer, neurogenic bladder,

115
Q

hepatorenal syndrome

A

pre-renal AKI
cirrhosis: portal HTN leading to vasodilation and therefore decreased ECV and activation of renin
decrease BP with increased ECFV
UA and kidneys: normal; urine Na less than 10
Tx: liver transplant

116
Q

chronic kidney disease

A

Sx: voiding complaints, HTN, edema, flank mass
SERIAL labs needed
SMALL kidneys, WAXY cast, PERIPHERAL NEUROPATHY
usually ASYMPTOMATIC, BONE change with hyperparathyroidism
high risk of CVD
Effects:
nervous system: asterixis, intellectual function, encephalopathy
hypoglycemia (decreased insulin degradation and decreased gluconeogenesis)
anemia
anorexia
drug metabolism effects
decreased Vit D: hypocalcemia, increase PTH
hyperphosphatemia
HYPERKALEMIA
metabolic ACIDOSIS NON ANION GAP

117
Q

K over 7mmol/L

A

MEDICAL EMERGENCY

Tx: IV calcium gluconate, IV insulin + glucose

118
Q

autosomal dominant polycystic kidney disease

A

ADULT
slow growing cysts compress normal tissue and cause ischemic atrophy
HUGE kidneys
polycystin-1 or 2
ciliopathy, defective mechanosensigin of urine flow, dysregulation of cell adhesion
two hit genetics

119
Q

autosomal recessive polycystic kidney disease

A

CHILDREN
cysts replace normal tissue in fetus
mutation: fibrocystin
pulmonary hypoplasia and death

120
Q

nephronophthisis

A

medullary cystic disease
SMALL kidneys with numerous small cysts at corticomedullary junction and chronic tubulointerstitial nephritis and fibrosis
mutation: cilia components
most common genetic cause of ESRD in CHILDREN

121
Q

kidney stones

A 
males
dysuria, hematuria, restless, writhing in distress, N/V, flank pain
CT: sensitive
UA, ultrasound, xray
Tx: fluids
122
Q

calcium stones

A

most: Ca oxalate; Ca Pi next
calcium oxalate crystals
cause: hypercalcemia, reduced citrate, excess Na
Tx: do NOT restrict dietary Ca, thiazide diuretics, Na restriction,, K citrate

123
Q

Magnesium ammonium phosphate (Struvite) stone
or
triple phosphate

A

UTI with urease producing organism (Proteus, Klebsiella)
urine pH greater than 7 (ammonium produced by bacteria)
coffin lid crystal
Tx: infection

124
Q

uric acid stones

A 
cause: hyperuricemia
urine pH less than 5.5
diamond cyrstals
RADIOLUCENT 
Tx: restrict protein, K citrate, allopurinol
125
Q

cystine stones

A

decreased PT reabsorption
Tx: penicillamine, K citrate, alkalinize urine
hexagon crystals
CHILDREN

126
Q

urinary tract obstruction

A

mechanical: intraluminal, intramural, extrinsic
functional: neurogenic
common locations: ureter crosses iliac vessels, enters bladder, ureterovesical junction
proximal to bladder: one kidney, normal Cr
distal: both kidneys, increased Cr

127
Q

retroperitoneal fibrosis

A

can cause urinary tract infection

128
Q

chronic bilateral partial urinary tract obstruction

A

polyuria, azotemia, nonunion gap metabolic acidosis, hyperkalemia, RTA

129
Q

clear cell carcinoma

A

MOST COMMON
malignant
chromosome 3p: VHL
gross: solitary, yellow, cysts, necrosis, hemorrhage
HE: clear or eosinophilic cytoplasm, vascular
sporadic: translocation or deletion chromosome 3
hereditary: inactivated mutated VHL, hyper-methylation of VHL
risk: dialysis related renal cystic disease
grade indicates survival rate

130
Q

oncocytoma

A 
benign 
renal epithelial neoplasm
large cells with lots of mitochondria 
MAHOGANY BROWN with central STELLATE scar
may be multiple
131
Q

renal carcinoma

A

male, smoker, older, HTN, obesity
tubule epithelial cells
encapsulated, necrosis, hemorrhage (rupture invaded vein, abnormal new vessels)
metastasis: perinephric fat, VENOUS, LUNG, BONE; next: lymph, liver, adrenal, brain
Sx: dull flank pain, hematuria, abdominal mass

132
Q

papillary carcinoma

A

malignant
renal parenchymal tumor
bilateral, multifocal
sporadic: trisomy 7, 16, 17, loss Y
activated MET, translocation 1: PRCC oncogenes
hereditary: trisomy 7, activated MET
risk: dialysis related renal cystic disease

133
Q

chromophobe carcinoma

A

large pale cells with prominent cell membranes
lower mortality
Hale’s colloidal iron stain

134
Q

renal pelvis carcinoma

A

urothelial: transitional cell carcinoma; can get squamous
CENTRAL location
smoker: get in bladder and can get higher in collecting system

135
Q

Wilm’s tumor (nephroblastoma)

A

KIDS: 2-5 yrs
embryonal kidney tumor
HE: mixture of cell types: blastemal, stromal, epithelial
ABDOMINAL MASS

136
Q

WAGR

A

no iris, genital abnormalities, mental retardation
Wilm’s tumor
deletion of WT1 gene

137
Q

Denys-Drash

A

gonadal dysgenesis
Wilm’s tumor
inactivating mutation WT1 gene

138
Q

Beckwith-Wiedemann

A

Wilm’s tumor
one sided organomegaly
genetic imprinting doesn’t silence maternal allele that controls IGF2

139
Q

light chain disease

A

nephrotic: glomerular capillary wall deposition
MONOCLONAL
precipitation of Ig chains without elongation
MULTIPLE MYELOMA
Sx: proteinuria, renal failure, tubuolinterstitial syndrome, cardiomegaly, hepatomegaly, sicca syndrome, peripheral neuropathy, GI, pulmonary nodules, arthopathy

140
Q

sickle cell nephropathy

A

val for glutamate: 6th aa beta global chain
polymerize with low O2 and sickle
early: glomerular hypertrophy, HEMOSIDERIN, focal hemorrhage or necrosis
late: interstitial inflammation, edema, fibrosis, tubular atrophy papillary infarcts
end: FSGS
vaso-occlusive
Sx: pain crises, hemolysis, reticulocytosis, hyperbilirubinemia, elevated lactate dehydrogenase, low haptoglobin
SICKLE cell, Howell- Jolly

141
Q

amyloidosis

A

deposition of proteinaceous material in vessels then interstitium
BETA-PLEATED SHEETS
nonproliferative, noninflammatory glomeruopathy
vascular; tubular atrophy and interstitial fibrosis
APPLE GREEN BIREFRINGENCE
CONGO RED

142
Q

HIV associated nephropathy

A 
progressive azotemia, proteinuria
COLLAPSING FSGS with microcystitic tubular dilation, interstitial inflammation, fibrosis
Nef and Vpr viral genes
ApoL1
Tx: HAART, ACEI/ARB
most still develop ESRD
143
Q

cryoglobulinemia

A

HEP. C
immune complexes: RF, IgG, HCV RNA, complement of endothelial surfaces
precipitate at 4 degrees
MEMBRANOPROLIFERATIVE
Sx: palpable purpura, arthralgia, MPGN, lymphoma, peripheral neuropathy
MELTZER’s TRIAD
lymphocyte infection leads to IgM secreting clones

144
Q

AL amyloid

A 
primary
older
MOST COMMON
MONOCLONAL LIGHT chains
urine: BENCE-JONES proteins
assoc. MULTIPLE MYELOMA; PLASMA CELL DYSCRASIS
Sx: weak, weight loss, NEPHROTIC, peripheral neuropathy, large kidneys and insufficiency, GI, heart
Tx: melphalan, dexamethosone
145
Q

AA amyloid

A 
reactive systemic 
secondary to CHRONIC INFLAMMATION: RA, IBS, ankylosing spondylitis
IL-1 and IL-6
Sx: kidney and GI
Tx: eprodisate
146
Q

Abeta2m amyloid

A

long term hemodialysis

Sx: synovium, joints and tendon sheaths

147
Q

ATTR amyloid

A

senile or familial (AA)
transthyretin
HEART and pulmonary blood vessels
Sx: heart failure or arrhythmia

148
Q

Abeta amyloid

A

Alzheimer’s

149
Q

stage 1 diabetic nephropathy

A

hyperfiltration, increase GFR

increase kidney size

150
Q

stage 2 diabetic nephropathy

A

glomeruli show damage and microalbuminuria

151
Q

stage 3 diabetic nephropathy

A

albumin excretion rate exceeds 200 mg/min
increase serum BUN and Cr
increase BP in some

152
Q

stage 4 diabetic nephropathy

A 
GFR decreases less than 75 ml/min
proteinuria
high BP
further increase BUN and Cr
17 years to develop
153
Q

stage 5 diabetic nephropathy

A

kidney failure or ESRD
GFR less than 10 ml/min
23 years to develop

154
Q

diffuse glomerular diabetic nephropathy

A

early, less sever
MOST COMMON
identical to HTN and aging glomerulopathy
capillary BM thickening and increased mesangial matrix: begins in stalk of glomerular tuft

155
Q

nodular glomerular diabetic nephropathy

A

after 10 years DM
superimposed on glomerulopathy
KIMMELSTIEL WILSON nodules and HYALINE sclerosis of efferent and afferent arterioles

156
Q

papillary diabetic nephropathy

A

pyelonephritis

papillary necrosis

157
Q

tubulo-interstitial diabetic nephropathy

A

tubular basement membrane thickening

interstitial fibrosis

158
Q

pyelonephritis

A

infection of kidney: infected tubules

UA: pyuria and bacteruria

159
Q

acute urethral syndrome

A

does NOT have significant bacteriuria
cause: chlamydia, bacterial lower UTI
Sx: dysuria

160
Q

UTI

A

females (opp. in infants)
intercourse, SPERMICIDE + diaphragm, OBSTRUCTION, trauma, VESICULO-URTERAL REFLUX, intrumentation
pregnancy: progression more likely, higher bacteriuria; need to check for pyelonephritis
ASCENDING infection, hematogenous much less likely
pathogenesis: adhesion (type 1 and P-fimbriae), colonization, invasion, phase variation
complication: sepsis, abscess, chronic renal insufficiency, struvite renal calculi, recurrent infections

161
Q

What causes increase in UTI with age?

A

bacteriuria

male: BPH
female: decrease estrogen and vaginal acidity

162
Q

lower UTI

A

freq. of urination, dysuria, turbid urine, suprapubic discomfort, hematuria, asymptomatic cystitis
Tx: female 1-3 days, males 1 week

163
Q

upper UTI

A

fever, chills, CVAT, asymptomatic pyelonephritis

Tx: 1-6 weeks

164
Q

asymptomatic bacteriuria

A

DO NOT TREAT in elderly or others

SS- Renal (11 decks)

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