What is causing fetal hydronephrosis if it is: 1. Obstructive + unilat 2. Non-ob + unilat 3. Bilateral in a boy

1. Kink in ureto-pelvic jxn - makes sense since the junction is the last part of the system to become hollow 2. Incomplete CLOSURE of the vesicouretral jxn 3. Posterior urethral valves -> may also cause Potter sequence

Many causes defective PCT 1. Metabolic acidosis - can't reabsorb bicarb 2. ↑U AA, glucose, bicarb, P

CHAPTER: Renal Flashcards by Logan Kolakowski

The kidney develops in 3 nephros parts - name each part and its role

1st = PRO-nephros - degenerates by wk 4
2nd = MESO-nephros - 1st trimester kidney
3rd = META-nephros - permanent kidney that has 2 parts: uretric bud (from bottom of meso duct) + metanephric mesenchyme

How well did you know this?

Not at all

Perfectly

What adult structures arise from the :
Meso-nephros
Uretric bud
Metanephric mesenchyme

Meso = male vas deferans
Metanephric mesenchyme = glomerulus -> DCT
Uretric bud = (everything else) ureter, renal pelvis + calyces, CDs

How well did you know this?

Not at all

Perfectly

What is causing fetal hydronephrosis if it is:

Obstructive + unilat
Non-ob + unilat
Bilateral in a boy

Kink in ureto-pelvic jxn - makes sense since the junction is the last part of the system to become hollow
Incomplete CLOSURE of the vesicouretral jxn
Posterior urethral valves -> may also cause Potter sequence

How well did you know this?

Not at all

Perfectly

No uretric bud means….

No kidney = agenesis aka the primordial tissue was never even there

How well did you know this?

Not at all

Perfectly

What are you thinking if a baby has unilat vs bilat cystic kidney on US

Unilat = multicystic dysplastic kidney (NOT inherited)
Ureteral bud is there - kidney exists
But doesn’t cause metanephric mesenchyme to differentiate - no glom -> DCT
Kidney is not fxnal - mass of cystic CT
Bilat = AR PCKD (can cause Potter’s)

How well did you know this?

Not at all

Perfectly

If a kid presents with recurrent UTIs due to asynchronous muscle contractions + vesicoureteral reflux - what deformation are you thinking?

Duplex collecting system
2 pelvises -> 2 ureters -> 2 diff insertions into bladder
There was an early separation of the ureteric bud

How well did you know this?

Not at all

Perfectly

Which kidney do you use for transplant and why?

L kidney b/c longer renal vein (has to cross over aorta)

How well did you know this?

Not at all

Perfectly

Walk through renal BF from renal art -> afferent art

Lobe - arch - LOB
Renal art
Segmental art
Interlobar art
Arcuate art
Interlobular art
Afferent art

How well did you know this?

Not at all

Perfectly

SAD PUCKER for retroperitoneal organs

Supra-renal (adrenals)
Aorta + IVC
Duodenum pts 2-4
Pancreas except top 1/3
Ureters (water under bridge)
Colon - ascending + descending 
Kidneys
Esophagus - lower 2/3
Rectum

How well did you know this?

Not at all

Perfectly

The ureter has 3 sources of blood supply - name them. What dermatomes does kidney pain localize to?

Top 1/3 = renal art
Middle 1/3 = middle iliac + gonadal art
Lower 1/3 = int iliac
T10/11 dermatomes = CVA tenderness (T10 = belly button)

How well did you know this?

Not at all

Perfectly

2 things you can measure with inulin

GFR - 100% filtered, no secretion or absorption

ECF (also mannitol) = 1/3 of TBW

How well did you know this?

Not at all

Perfectly

Where do NSAIDs affect the kidney

PGs dilate the AFFERENT arteriole, so NSAIDs cause constriction
PGs secreted from kidney, work paracrine
X PGs -> ↓RPF -> ↓GFR
No change to FF = GFR/RPF

How well did you know this?

Not at all

Perfectly

Fanconi syndrome

Many causes defective PCT

Metabolic acidosis - can’t reabsorb bicarb
↑U AA, glucose, bicarb, P

How well did you know this?

Not at all

Perfectly

Bartter syndrome

X Na/K/2Cl - AR
Looks like chronic loop diuretic use:
1. Metabolic alkalosis
2. HypoK (duh) 
3. ↑U Ca (duh)

How well did you know this?

Not at all

Perfectly

Gitelman syndrome

X NaCl @ DCT - AR
Looks like chronic thiazide use (metabolic alkalosis)
↓U Ca (duh)

How well did you know this?

Not at all

Perfectly

Liddle syndrome - present, inheritance, treat

Presents as HTN w/ ↓aldo - weird!
GOF of ENAC - AD
+ Amiloride

How well did you know this?

Not at all

Perfectly

Syndrome of apparent mineralcorticoid excess - inheritance + treat

X 11 beta OH deH
Can’t inactivate cortisol -> will cross react to bind aldo R (looks like excess aldo @ CD but really ↑cortisol)
Presents as HTN w/ ↓Pk + metabolic acidosis (excess aldo)
+ CS - exog CS ↓prod of endog CS

How well did you know this?

Not at all

Perfectly

What food can cause acquired SAME (↑cortisol)

BLACK licorice

How well did you know this?

Not at all

Perfectly

What type of RTA causes basic urine w/ hypoK? Name drug that can cause this?

T1 RTA (normal gap metabolic acidosis)
Alpha int cells @ CD won't secrete H+
Means you hold H, waste K (hypoK)
↑Risk Ca stones (basic urine) + ↑bone turnover
AMPHO B

How well did you know this?

Not at all

Perfectly

What type of RTA causes acid urine w/ hypoK? 1 disease cause vs 1 drug cause

T2 RTA (normal gap metabolic acidosis)
X HCO3 reabsorbed @ PCT 
But urine gets acidified by alpha int cells @ CD
Idk why hypoK
1. Fanconi = defective PCT
2. CA Is

How well did you know this?

Not at all

Perfectly

What type of RTA causes acidic urine w/ hyperK?

T3 RTA (normal gap metabolic acidosis)
Hypoaldo 
Waste Na, hold K -> hyperK ↓NH3 syn @ PCT -> ↓NH4 excretion = acid urine

How well did you know this?

Not at all

Perfectly

MUDPILES = gap metabolic acidosis (K+Na - Cl+HCO3)

Methanol
Uremia
DKA
Propylene glycol 
Iron tab or INH
Lactic acidosis
Ethylene glycol --> oxalic acid
Salicylates

How well did you know this?

Not at all

Perfectly

HARD ASS = non-gap metabolic acidosis

Hyperalimentation = feeding tube
Addison disease
RTA
Diarrhea
Acetazolamide (T2 RTA)
Spironolactone
Saline infusion

How well did you know this?

Not at all

Perfectly

Signs of hyper vs hypo Mg

Hypo: torsades, tetany (no just hypoCa), hypoK
Hyper: ↓DTR, ↓HR + BP, ↓Ca, cardiac arrest

How well did you know this?

Not at all

Perfectly

Why might chronic NSAID use cause renal pap necrosis?

X PGs -> constrict afferent arteriole | Chronically ↓renal BF states = ischemia = renal pap necrosis

Where in the kidney is dopamine made - what is its effects at high vs low doses?

PCT - goal = naturesis ↓dose = dilates interLOBULAR, afferent + efferent = ↑RBF ↑dose = vasoconstrict

Where does PTH ↑Ca reabsorb vs ↑P excrete

DCT reabsorb Ca | Trash P at PCT

How does ANP/BNP cause natriuresis

↑cGMP -> relax SM -> dilate A art + constrict E art ↑GFR = ↑Na filtered w/o ↑Na reabsorption This is how diuretics are limited in effectiveness

What is the JGA - what 2 cells make it up?

JG cells = SM @ afferent art Macular densa = Cl sensor @ DCT Apparatus secretes renin

Casts seen in ESRD

Waxy

Nephritic syndromes are characterized by immune complexes. What cell mediated the damage to the glomerulus in these diseases?

C5a attracts neutrophils

Lumpy bump IF + subEPI humps

Post strep GN

SLE presentation of nephritic vs nephrotic

``` Phritic = diffuse prolif GN ask IC deposit Phrotic = mebranous ```

Wire looping capillaries LM + sub-endo IC on EM + granular IM

Diffuse proliferative GN

Basket weave EM w/ splitting of the BM

Alport - X dominant

Hep B/C infection w/ tram track LM, granular IF, GBM splitting

Type 1 membranoprolif GN - sub-endo | Tram track - membranous

Excess C3 nephritic factor stabilizes C3 convertase and causes what GN

Type 2 membranoprolif GN - intramembranous deposits, overall tram track on LM (membranous

Frothy urine means what casts

Fat - think nephrotic

What type of cancer might cause MCD

Hodgkins - RS secreting cytokines effaces foot processes

HIV + sickle cell pts presenting with nephrotic syndrome - which one

FSGS

LM tram track, granular IF, spike + dome EM

Membranous nephropathy | Spike + dome is sub-epi

2 non-enzymatic glycosylation changes to the glomerulus in diabetes // why give ACE Is to diabetic patients

@ GBM @ diffuse thickening @ efferent art -> narrow lumen -> ↑GFR -> mesangial expansion Give ACE to counteract AGT 2 constrict at efferent ↓GFR and minimize mesang prolif

Describe why nephrotic syndromes are a hyper-coag with ↑infection risk

Hypercoag - lost AT3 in urine | Lose Ig in urine = ↑infections

Which 3 stones form in acid urine - what does each look like

Ca oxalate - envelope or dumbell Uric acid - (duh basic would neutralize) diamond or rosette Cystine - cystinuria AR - hexagonal Defective reabsorb COLA - cyteine, orthinine, lysine, arginine

Hydronephrosis if untreated causes atrophy of what 2 parts of the kidney

cortex + medulla

``` RCC Originates from what cells Histo of cells Color of tumor RF Mets via and to Treat ```

``` From PCT Clear cell RCC = filled with fat Therefore gold/yellow color SMOKING + obesity Carcinoma that mes via blood - renal vein -> lung + bone, impt to know b/c commonly see the met 1st Aldesleukin = IL 2 to ↑NK RESISTANT to chemo + radiation ```

Renal oncocytoma - histo, cell arise from, gross

From CD Eosinophilic cells Central scar on gross

3 ways a Wilm's tumor can present depending on WT1 vs WT 2 mutation

WT1: WAGR = Wilms, no iris, GU malform, mental retard WT1: Wilms, male pseudohermaphroditism WT2: Wilms, big tongue, organomeg, hemihypertrophy

4 RF for urothelial/transitional cell bladder cancer + 2 types

Smoking, analine dyes, cyclophosphamide (+mensa) Flat = early p53 mut, starts high grade Papillary = low -> high grade Ex of field effect tumor - multifocal + likely to recur

Detursor muscle instability leads to

Urgency incontinence = any vol in bladder causes urge to void immediately + leak + AntiM = oxybutynin Vs detrusor underactivity = overflow incontinence

3 causes of bladder adenocarcinoma

1. @dome due to urachal remnant 2. Cystitis grandularis = chronic inflam (cystitis) causes columnar metaplasia (glandularis) 3. Extrophy = congenital malformation a tthe bottom of the ant ab + bladder walls (born with bladder outside belly)

Sterile pyuria indicates what cause of UTI (- culture, + WBC)

Neisseria or chlamydia - treat for both!

Imaging of acute pyelo

@ cortex - striated parenchymal enhancement | Aka light up the outside of kidney

Where does the kidney normally scar with chronic vesicouretral reflux?

Upper + lower poles

2 changes to the kidney with chronic pyelo

Cortico/med scarring + blunted calyx | "Thyroidization of kidney" - eos casts

2 major causes of diffuse cortical necrosis

DIC + vasospasm

2 major imaging findings for renal osteodystrophy

Subperiosteal thinning | Tissue calcifications

Why is BUN/Cr ration ↑ w/ pre-renal azotemia/AKI

Pre-renal means kidney think being under-perfused ↓GFR -> RAAS -> ↑Na reabsorb -> H2O follows -> BUN follows Goal = reabsorb to gain vol

Ethylene glycol poisoning cause what 2 things

Gap metabolic acidosis + Ca oxalate crystals

Ps that cause acute interstitial nephritis

Drugs that produce haptans -> eosinophils in urine is pathoneumo Pee = diuretics Pain free - NSAIDs Penicillin + cephalosporins (vs aminoG cause ATN) PPIs RifamPin

3 stages of ATN

Inciting event Maintenance = ↓urine - metabolic acidosis + ↑K + uremia Recovery = tons of urine, risk of hypoK

4 causes of renal pap necrosis

Sick cell Acute pyelo NSAIDs Diabetes

Heart problem in AD PCKD - what parts of the kidney does AR vs AD PCKD affect

Mitral valve prolapse AD - cortex + medulla AR = babies = CD Both HUGE cystic kidneys

If you have cysts in the medulla only of the kidney how will the kidney as a whole look?

Shrunken - medullary cystic kidney disease

Simple vs complex renal cysts on US

Simple: filled with fluid | Complex - septated, enhanced, solid components, bad b/c ↑RCC risk