Quick look at Renal Diseases Flashcards

1
Q

Minimal Change Disease

A

Nephrotic syndrome (mostly kids)
Foot process effacement on EM–> Albuminuria
Steroids

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2
Q

FSGS

A

Nephrotic syndrome
Black adults
IgM and C3 IF
Steroids, not all respond

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3
Q

Membranous Glomerulopathy

A

Nephrotic syndrome (white adults most common nephrosis)
RVT and PE!
silver stain spikes
Antiphospholipase A2 receptor = antigen

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4
Q

Diabetic Glomerulosclerosis

A

Nephrotic Syndrome (most common kidney dz cause)
Diffuse, KW nodules, membrane thickening
BP reduction w/ ACE I

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5
Q

Amyloidosis

A

Nephrotic Syndrome
Rheum arthritis, gamma light chain stain w/ CONGO RED
2 cause: AL amyloid (primary) AA amyloid (SAA)
treat inflamed state, symptom tx

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6
Q

Nephrotic syndrome

A

U/A protein >3.5 g/day
Oval fat bodies/maltese cross
Low albumin, edema, hyperlipidemia

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7
Q

ATN

A

Tubulointerstitial disease
Ischemic or nephrotoxic kidney failure
muddy brown casts, high FeNa
Don’t biopsy

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8
Q

AIN

A

Tubulointerstitial disease
Mostly drug induced (beta lactams, NSAIDS, PPI)
Rash/hematuria, eosinophils

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9
Q

Acute pyelonephritis

A

Tubulointerstitial, unilateral; no biopsy
CVA T, fever, pyruia
Hematogenous vs ascending (more common)
85% gram neg (e coli)

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10
Q

Chronic pyelonephritis

A

Tubulointerstitial dz
Slow onset RF, scarring and inflammation, U scars
Usually from VUR (reflux/obstruction)
Relieve reflux

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11
Q

Papillary necrosis

A

Tubulointerstitial dz
Analgesis/NSAID abuse, flank pain
SODA: Sickle cell, obstructive pyelo, DM, analgesic abuse,

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12
Q

Post Strep (or infectious) GN

A

Nephritic syndrome (Glomerulonephritis)
Mostly kids, 10-14 day onset. Sub epithelial.
LOW COMPLEMENT, high ASLO titer
IF shows IgG/C3, humps/bumps

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13
Q

Nephritic Syndrome

A
Hematuria (RBC Casts or deformed/crenated, acanthocytes)
Low GFR
Oliguria
Edema
HTN
Variable proteinuria
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14
Q

IgA Nephropathy

A
Nephritic syndrome (GN)
IgA and C3 deposits in mesangium
Due to defective glycosylation of hinge region of IgA
Normal complement; biopsy
Treat w/ ACE I, steroids
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15
Q

Henoch Schonlein Purpura

A

Systemic version of IgA nephropathy

Abd pain, LE purpura, arthralgias

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16
Q

Lupus Nephritis

A

Nephritic Syndrome (GN)
“Full house staining” of IgA, IgG, IgM, C3, C1Q
LOW COMPLEMENT
ANA and anti dsDNA positive
Only treat Class III/IV focal and diff w/ steroids, most resolve, rituximab

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17
Q

Granulomatosis w/ polyangiitis

A
Nephritic Syndrome (GN)
Aka "ANCA" and "Wegener's"; test for ANCA
RPGN, crescentic! Pauci-immune 
Cavitary lesion in lungs, post URI
Rituximab, steroids, plasmapheresis
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18
Q

Angi-GBM aka Goodpasture’s

A
Nephritic Syndrome (GN)
RPGN, rare
Onset s/p URI or viral infx 
Linear IgG on IF
Steroids, plasmapheresis
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19
Q

Shiga Toxin HUS

A

TMA (Renal Vascular Disease)
D+, Mostly kids (hamburgers, petting zoo)
Gastroenteritis from E Coli
Acute TMA (fibrin deposition, RBC congestion)
Supportive care (dialysis, transfusion)

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20
Q

TMA

A
Vascular = Thrombotic microangiopathy
Anemia (elevated LDH, low haptoglobin)
Schistocytes
Systemic organ damage from ischemia
Thrombocytopenia
Caused from endothelial injury and clot formation
FIBRIN on imaging
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21
Q

Atypical HUS

A

TMA (Renal Vascular Disease)
ESRD at young age, D-
Genetic or auto-immune against complement regulating Factor H, I or MCP
LOW COMPLEMENT, high recurrence in transplant
tx: eculizumab

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22
Q

TTP

A

TMA (Renal Vascular Disease) not always renal involvement
Low platelets, bruising, anemia, normal PT/aPTT
Neurologic symptoms (AMS)
Caused from genetic or acquired ADAMTS13 deficiency
Tx: Daily plasmapheresis, rituximab

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23
Q

APS (Anti phospholipid Ab syndrome)

A

TMA (Renal Vascular Disease)
Recurrent clots in multiple organs (e.g., placenta–> miscarriages)
Arthralgia/fever/malaise, SLE or lupus like
ANA pos, false VDRL, RBC casts
Fibrin thrombi

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24
Q

Renal Atheroembolic Disease

A

Renal Vascular Disease
Worsening HTN, usually following invasive arterial procedures (CABG)
Acute renal failure
Cholesterol emboli due to loosened plaque (needle shaped inclusions on biopsy)

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25
Q

Pre-Renal Azotemia

A

Volume depletion, poor perfusion 2/2 sepsis or antihypertensives, heart failure.
Low FeNa (kidneys working still) increased BUN:Cr
Concentrated urine

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26
Q

Intrarenal causes (ATN specifically)

A
2/2 ischemia or nephrotoxins
Muddy brown casts
Due to nephrotoxic drugs or pigments (Hgb, Mgb)
Can see hyperK, oliguria, low GFR
high FeNa, Normal BUN:Cr
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27
Q

Post-renal failure

A

Obstructive from stones, tumors, BPH

Anuria (

28
Q

ADPKD

A

Cystic Kidney Disease
Hetero AD mutation in PDK1 or PDK2, “2nd hit” causes disease (polycystins in cilia)
Adult onset HTN (high RAAS) & gross hematuria
Massively enlarged kidneys, bilateral
Extrarenal: aneurysm, hepatic cysts (80%)
Cardiac PFO or MV prolapse
tx: Nephrectomy

29
Q

MCKD

A

Cystic Kidney Disease
AD mutation in MUC1 or UMOD
Altered proteins trapped in ER –> damage and fibrosis
Adult onset, polyuria, renal insufficiency
Biopsy: chronic tubular interstitial nephritis, BM disruption
Hyperuricemia and gout (due to low uric acid excretion)

30
Q

NPHP

A

Cystic Kidney Disease
AR Pleiotropic mutations in NPHP1-15
Most frequent genetic cause of ESRD in kids
Retinitis pigmentosa, cerebellar vermis aplasia, liver fibrosis
BLINDNESS

31
Q

AR PKD

A

Cystic Kidney Disease
AR mutation in PKHD1 (fibrocystin in biliary/renal cilia)
very rare, echo genetic in utero
Neonates w/ Potter’s sequence, survivors have HTN, RF and liver disease.
Potters: Lung hypoplasia, IUGR, characteristic face
Liver fibrosis, portal HTN

32
Q

Bartter’s syndrome

A

Hypotension. Genetic disease resembling chronic furosemide use

  • chronic volume depletion, high renin/aldo
  • hypokalemia, met alkalosis
  • mutations in either: NKCC, ROMK (these ones won’t have hypokalemia), CLC-Kb
33
Q

Gittleman’s syndrome

A

Hypotentsion. Genetic disease resembling thiazide abuse. Mutation in NaCl transporter in DCT, mild volume depletion, hypocalciuria, hypomagnesiuria

34
Q

2 subepithelial diseases

A

Membranous

Post-infectious

35
Q

3 Mesangial diseases

A

IgA, amyloidosis, lupus nephritis (LN can be pretty much anywhere)

36
Q

4 diseases w/ low complement

A

LN, MPGN, Cryo, post-infx

37
Q

Diabetes insipitus

A

ADH not made –> dilute urine

38
Q

Nephrogenic Diabetes insipitus

A

ADH not sensed at kidney –> dilute urine.

If you give ADH and problem doesn’t correct, it’s this one

39
Q

Glucocorticoid remedial aldosteronism (GRA)

A

AD mutation of chimeric aldo synthase w/ regulatory elements of 11beta-hydroxylase gene –> stimulation of aldo by ACTH instead of AT II –> loss off feedback
- low renin, high aldo. Treat w/ corticosteroids

40
Q

Apparent mineralcorticoid excess syndrome (AME)

A

Enzyme that converts cortisol to cortisone doesn’t work –> elevated cortisol, stimulates aldo receptor –> elevated Aldo
Mimicked by licorice!

41
Q

Adrenal adenoma

A

Cushings –> cortisol secreting tumor –> same effect as AME

Also Conn syndrome (hyperaldo)

42
Q

Congenital bilateral adrenal hyperplasia

A

Presents like Conn syndrome (hyperaldo) but congenital AR mutation. Treat w/ mineral corticoid antag.

43
Q

Conn’s syndrome

A

Primary hyperaldo from acquired somatic KCNJ5 mutation in K+ channel

44
Q

Fibromuscular dysplasia

A

Multiple stenoses in renal arteries; young women usually, stenotic kidney w/ “bead” appearance

45
Q

Pheochromocytoma

A

Adrenal medulla tumor secreting Epi and norepi + metabolites, SNS overdrive. . Will see increased urine catecholamine metabolites (metanephrine); remove surgically

46
Q

Liddle’s syndrome

A

Constitutively active ENaC in CD –> Na reabs independent of aldo stimulus
Use amiloride to block enac channel

47
Q

Renal agenesis

A

Unilateral – decreased urine, in utero w/ potter sequence and resp insufficiency at birth
Bilateral – perinatal lethal due to lung hypoplasia

48
Q

Primary VUR

A

intravesical ureter shortening–> reflux into kidney.

M>F, renal hypoplasia from scarring, can be prenatal (Hydronephrosis) or postnatal (post febrile illness or UTI)

49
Q

Secondary VUR

A

Abnormal increase in bladder pressure 2/2 post urethral valves, neurogenic bladder, or functional bladder obstruction.

50
Q

Renal-Coloboma Syndrome

A

AD Pax2 mutation –> renal hypoplasia renal sx, holes of optic nerve w/ visual impairment

51
Q

Wilms’ Tumor

A

Mutations in WT genes, embryonic cancer of developing kidney in children.
Aka nephroblastoma

52
Q

Nephrophthisis (NPH)

A

AR mutations in ciliary function and planar cell polarity, abnormal renal tubules, fibrosis –> ESRD, blindness, liver probs

53
Q

Ascent abnormalities

A

Failure of unilateral ascent –> unilateral pelvic kidney (below IMA)
Bloth stuck –> lower pole fusion, horseshoe kidney

54
Q

Ureteropelvic junction obstruction (UPJ)

A

Often congenital aperistaltic segment or aberrant impinging crossing vessels

55
Q

Ca Oxalate stones

A

70%, dietery oxalate absorbed in colon and bound by Ca2+. Urinalysis: folded envelope appearance
Weird tidbit: low calcium diet actually increases stone risk.

56
Q

Ca2+ phosphate stones

A

10-15%, risk: alkaline urine, hypercalciuria. Coffin lid appearance

57
Q

Uric acid stones

A

10-15%. Risk factors: acidic urine, gout, metabolic syndrome, malignancy. Diamond shape.

58
Q

Struvite stones

A

10-15%. Urease producing bacteria! UTI/chronic UTI. Staghorn stones
Proteus, klebsiella, haemophilus

59
Q

Cystine Stones

A

Less than 1%

Genetic defect plus acidic urine. Microhexagonal crystals

60
Q

Medication caused stones

A
61
Q

Stone inhibitors in urine

A

Mg2+, citrate, tartrate, etc.

62
Q

Stone likely to pass if what size?

A
63
Q

CDK-MBD

A

CKD caused low bit D and phosphate retention. Elevated serum P –> FGF23–> decreased P reabsorption and D production. Complications are calcification of arteries, stomach, anywhere alkaline cells exist. Hyperparathyroidism, ectopic calcification, fractures.

64
Q

RTA I

A

Inability to secrete H+ in distal nephron

65
Q

RTAII

A

Proximal tubular acidosis: Capacity to reabsorb bicarb is impaired.

66
Q

RTA IV

A

Impaired ammoniagenesis, usually have hyperkalemia (hyporenin-hypoaldo)