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Flashcards in Renal Deck (31):

Fetus w/ oligohydramnios (can't pee)
=> consecuences, causes

= "Potter Sequence"
Causes: ARPKD, posterior urethral valves, bilat. renal agenesis
Consequences: Limb and facial deformities, pulmonary hypOplasia (= cause of death)


Pronephros vs. Mesonephros vs. Metanephros

1st: Pronephros = to wk 4, then degenerates
2nd : Mesonephros = 1st trimester. => adult Male genital system
*"ureteric bud" (caudal end) => ureters, pelvises, calices, collecting ducts
3rd: Metanephros = permanent, => adult kidney


#1 site of obstruction of urinary tract in fetus

= Ureteropelvic junction,
* Last to canalize => failure -> hydronephrosis


Renin-Ang-Aldosterone signal molecs & actions

1. Renin (from JG cells in kidney) -> Angiotensinogen to Angiotensin I
2. Ang I --> Ang II via ACE (Angiotensin Converting Enzyme)
3. Ang II => systemic effects:
a) vasoconstrict (AT1 Rs), b) constrict eff. arterioles
c) stimulate aldosterone & ADH, d) increase Na/K exchange in PCT
e) stimulate thirst @ hypothalamus


signal molecs that respond to low blood volume:

1. Angiotensin II
2. ADH (=> insert aquaporins in renal collecting duct to retain H2O)
3. Aldosterone (=> insert more Na+ channels in principle cell to retain Na & H2O, & increase K+ excretion "BK" channels)
*ANP responds to HIGH volume in heart atria => regulates RAAS*


components of Juxtaglomerular Apparatus

- JG cells: modified sm. muscle on aff. arteriole => secrete renin
(when low NaCl delivery to DCT, low renal BP, or B1 stim.)
- Macula Densa: on distal conv. tubule, sense low NaCl


Effect of ANP on kidney

(secreted from atria of heart when HIGH pressure/volume)
increase GFR & Na filtration @ distal tubule
=> Na+ & volume loss
(opposes Renin/Ang/Aldosterone)


Effect of PTH on kidney

secreted when:
low plasma [Ca2+], high plasma [PO4---], or low 1,25-(OH)2 VitD

=> decrease PO4 resorption (PCT), increase Ca resorption at DCT, and increase 1,25-OH2 vitD activation


Angiotensin II vs. ANP

BOTH increase GFR, but
ANP: no compensatory Na resorption => net volume loss
Ang II: w/ compensatory Na resorption => net maintenance of renal BF (& NO volume loss)


Electrolyte changes associated with Aldosterone activity

bc aldosterone increases Na resorption at collecting duct,
=> increased K+ and H+ excretion
(may become hypoKalemic or alkalotic)


Causes of K+ shift OUT of CELL

1. Digitalis ==> hypERkalemia
2. hyperOsmolarity
3. Insulin deficiency
4. Lysis of cells
5. Acidosis
6. Beta-adrenergic antagonist


Causes of K+ shift INto CELL

==> hypOkalemia
1. hypO-osmolarity
2. Insulin presence (increases Na/K ATPase)
3. Alkalosis
4. Beta-adrenergic AGonist (also increases Na/K ATPase)


Signs/symptoms of Na+ imbalance (High or Low)

Both: stupor/coma
High Na+: irritability
Low Na+: nausea, malaise


Signs/Symptoms of K+ imbalance (High or Low)

Both: arrhythmias, mm weakness
High K+: Wide QRS complex & peaked T waves
Low K+: U waves on ECG & flattened T waves


Signs/Symptoms of Ca2+ imbalance (High or Low)

High Ca2+: "stones, bones (pain), groans (abdom. pain), & psychiatric overtones" (anxiety, altered mental status)

Low Ca2+: tetany, seizures


Signs/Symptoms of Mg2+ imbalance (High or Low)

High Mg2+: decreased deep tendon reflexes, lethargy, bradycardia, hypotension, cardiac arrest, hypoCa2+

Low: tetany, arrhythmias


Signs/Symptoms of PO4(3-) imbalance (High or Low)

High: kidney stones, metastatic calcifications, hypoCa2+

Low: bone loss, osteomalacia


Calculation for Anion Gap

Anion gap = Na+ - (Cl- + HCO3-)

* normal = 8-12


Calculation for respiratory compensation in metabolic acidosis

PaCO2 = 1.5([HCO3-]) + 8 +/-2

* if PCO2 is:
a) MORE than predicted, = COMBINED met. acidosis & resp. acidosis
b) LESS than predicted, = MIXED met. acidosis & resp. ALKalosis


3 types of RTA (Renal Tubular Acidosis 1, 2, & 4)

(normal anion gap metabolic acidosis)
Type 1: "distal" = can't excrete H+ => urine pH >5.5, hypoK+
Type 2: "proximal" = can't reabsorb HCO3- => urine pH poor NH3 synth => poor buffer ability, very acidic urine.


Type 1 RTA

"Distal" = can't excrete H+
=> urine pH >5.5, hypoK+
*Assoc. w/ Sjogrens & Amphotericin B


Type 2 RTA

"Proximal" = can't reabsorb HCO3-
=> urine pH s anemia, mult. myeloma, carb.anhydrase Is


Type 4 RTA

"HyperK+" = hypoAldo or no response to aldosterone
=> poor NH3 synth. = poor buffer ability, very acidic urine.
*assoc. w/ Diabetes, adrenal insuff., ACE Is


Kidney stones that occur in ACIDIC environment:
(vs. alkaline)

LOW pH (acidic)
#1: Calcium oxalate, 2. uric acid, 3. cysteine (hexagonal)

Basic (high pH):
Ca-phosphate, Struvite (NH3-Mg-PO4, *from urease+ bacteria)


RadioLUCENT kidney stones

= Uric acid stones => need CT or ultrasound to visualize (NOT xray)
in acidic environment w/ hyperuricemia


Acute vs. Chronic Pyelonephritis

Acute: WBC casts in urine, neutrophilic infiltration into renal cortex

Chronic: from recurrent acute episodes, => eosinophilic casts, corticomedullary scarring/fibrosis & blunted calyces.


Drugs that can induce interstitial nephritis (5 total)

(drugs act as haptens, induce hypersensitivity)
1-2 weeks after taking: diuretics, penicillins, sulfonamides, or rifampin
1 mo. after taking NSAIDs


Common nephrotoxins (known to induce Acute Tubular Necrosis)

1. Antibiotics (Aminoglycosides & amphotericin B)
2. radiocontrast (*decrease risk if taken w/ prednisone)
3. acetaminophen overdose
4. cisplatin
5. heme (ie: myoglobin, hemoglobin)


Stages of Acute Tubular Necrosis ("ATN")

* #1 cause of INtrinsic renal failure!
1. inciting event (renal ischemia)
2. maintenance phase: oliguria, 1-3 wks. *risk hyperK
3. recovery phase: polyuria => decrease creatinine & BUN, risk hypOK!


Pathogenesis of oliguria in Acute Tubular Necrosis

ATN = necrosis/apoptosis AND sublethal injury to TUBULAR epithelial cells.
because of damage, low Na+ delivery to macula densa
=> retain Na & H2O ==> low urine output (despite normotension)


Sign of acute renal failure & 3 types of causes

increasing Creatinine AND BUN (also often oliguria, 20!
- intrinsic renal failure (ATN, AIN, or RPGN) *BUN/Creatinine ratio <15
- post-renal (outflow obstruction) *exclude w/ ultrasound