Renal, Water/Electrolytes and GU Flashcards
Clinical triad in renal vein thrombosis
Hematuria
Flank mass
Thrombocytopenia
Can propagate from origin in small renal veins to IVC
Mechanism of hypertension in renal artery thrombosis
Release of renin as a response to renal hypoperfusion from the clot
Initial trigger for renin release
Decreased renal perfusion pressure
Renin ultimately stimulates ___ in the lungs to make more ____
- ACE— throughout body, but highest in vascular endothelium of lungs.
- Angiotensin II—potent vasoconstrictor
Effects of angiotensin II (immediate and if sustained)
Vasoconstriction
Vascular hyperplasia and hypertrophy
(Reason ACEI can help with preventing long term sequelae if vascular injury/hypertension is prolonged)
Two downstream proteins after Angiotensin II and their effects
Angiotensin III—aldosterone secretion, increases sodium retention and therefore blood volume/fluid overload
Angiotensin IV—increases blood viscosity
ACEI mechanisms
- Decreases ACE activity (lungs)—less angiotensin II that causes vasoconstriction
- Less angiotensin II/III: less aldosterone and decreased vasoconstriction
- Less bradykinin/kallidin activity (vasoactive peptides)
- Long-term, prevents vascular remodeling
Beta blocker mechanisms
- Decreased HR
- Decreased stroke volume
- Decreases renin secretion
Spironolactone mechanism
Blocks aldosterone receptor
Location of:
- Angiotensinogen synthesis
- Conversion to Angiotensin I
- Conversion to Angiotensin II
- Liver
- Kidneys (in response to renin)
- Lung (high concentration of ACE in pulmonary vascular endothelium)
Most common abdominal mass in female neonates
Simple ovarian cyst
“Simple” can have >1 THIN-walled septated region
Thick walls or heterogenous echogenecity means it’s complex (potential torsion/necrosis)
Potter’s sequence findings
Oligohydramnios, arthrogryposis, pulmonary hypoplasia, face with beaked nose, wide-set eyes, low-set ears
Triad of Eagle-Barrett Syndrome
I.e. prune belly syndrome
Absent/hypoplastic abdominal musculature
Cryptorchidism
Renal dysplasia with megaureter and poorly contractile, distended bladder
Ultrasound findings in posterior urethral valve
Megaureters with a thickened, trabeculated bladder (because it’s been pushing against the dysfunctional urethral valve)
Which of the congenital cystic kidney disorders carries the worst prognosis?
Autosomal recessive polycystic kidney disease (ARPKD)
70% survival in neonatal period
50% develop renal failure in childhood
Findings in renal artery thrombosis
Hypertension (if mild/moderate)
Conjugated hyperbilirubinemia
Thrombocytopenia
Hematuria
Which has a higher morbidity/mortality, renal artery or vein thrombosis?
Renal artery thrombosis–10-20% mortality if involves aorta, hypertension common
Treatment for renal artery vs. renal vein thromboses
RAT–systemic heparinization (when moderate/severe)
RVT–supportive care (electrolyte corrections, avoidance of further injury)
(RAT treatment is intensive because outcomes if persists are worse)
Definition of stage 3 AKI (acute kidney injury)
Serum creatinine >3x baseline and/or urine output (UOP) = 0.3ml/kg/h
FeNa and types of renal injury
FeNa (fraction excreted Na)= (uNa x sCr) / (sNa x uCr)
Prerenal: FeNa <1% (because kidneys can still concentrate and hold onto Na)
Acute tubular necrosis (ATN): >2%
uNa goes on top because it’s the fraction in your urine that you’ve peed out
Location and mechanism of action of furosemide
Thick ascending loop of Henle (Na-K-2Cl symporter)
Causes decreased Na, K, Cl (Mg and Ca) reabsorption
Less hypertonic medulla, more water excretion
Location and mechanism of action of thiazides
Distal convoluted tubule (the Na-Cl cotransporter)
Causes decreased Na, K and Cl reabsorption but INCREASED Ca++
Leads to smaller osmotic gradient so don’t reabsorb water
Most common palpable abdominal mass in neonates
Hydronephrosis
Studies to consider in multicystic dysplastic kidney (MCKD/MKD)
- Postnatal ultrasound (30-50% have contralateral renal anomaly)–should be done at 48-72h to decrease false negatives
- DMSA (dimercaptosuccinic acid/radionuclide scan) if other kidney’s also abnormal
- Annual renal ultrasound
Similar to autosomal recessive polycystic kidney disease (ARPKD), posterior urethral valves often results in end-stage renal disease by ____
10 years
ARPKD is the most severe of the cystic kidney diseases
PUV is the most severe of the obstructive uropathies
Frequent concomitant finding with posterior urethral valves (PUV)
Vesicoureteral reflux (VUR) from malpositioned/ectopic ureteral insertion
Non-renal finding associated with autosomal recessive polycystic kidney disease (ARPKD)
Hepatic fibrosis
Non-renal findings associated with autosomal dominant polycystic kidney disease (ADPKD)
Cysts in other organs (e.g. spleen and pancreas)
Synonym for arginine vasopressin and its location of synthesis
Antidiuretic hormone (ADH)
Posterior pituitary (precursor made in hypothalamus)
Acts mainly on collecting duct and increases aquaporins
Primary hormonal determinant of water excretion
ADH (ie. vasopressin)
Synthesized in hypothalamus but stored in posterior pituitary
Acts mainly on collecting duct (also DCT) and increases aquaporins
Two locations of the V2 receptors
- DCT
- Collecting ducts (CD)
V2R is predominantly in kidneys, V1R is throughout (vascular smooth muscle, liver, etc)
V2R is robust in neonates, even preemies
Reason for neonatal poor response to ADH
Immaturity of renal ADH-specific adenylate cyclase [in both DCT and collecting ducts]
Neonates (even preemies) have many ADH (aka V2) receptors, just can’t respond
(ADH and AVP are synonyms)
Mechanism of action of ADH at the DCT and collecting duct
Stimulates adenylate cyclase–increased cAMP–increased translocation of aquaporins–more water reabsorptive capacity
Mechanism of action of ADH at Loop of Henle
Stimulates adenylate cyclase–increased cAMP–active transport of Na into renal medulla–increased osmotic gradient drives water reabsorption
Bladder extrophy is more common in ____ and usually associated with ____
Males Inguinal hernia
Primary location of sodium reabsorption in the kidney
Proximal tubule (70%)
(Followed by 25% in thick ascending limb of loop of Henle, only 5-10% is in DCT and collecting ducts)
Primary reason for decreased sodium reabsorption in preemies
Decreased number of Na-K-ATPase and ion-specific transporters (everywhere)
Even if aldosterone has a normal concentration (which normally is), preemie kidneys have limited transporters to respond (would normally upregulate number as well as activate them)
Renin is made in the ___
Angiotensinogen is made in the ___
Angiotensinogen is converted to Angiotension I in the ___
Angiotensin II is made in the ____
Aldosterone is made in the ___ and acts at the _____
Kidneys
Liver
Plasma
Lung vasculature (by ACE)
Adrenals
Cortical collecting ducts (CCD) and DCT
Hormonal reason for late (2-6 weeks of age) hyponatremia in preemies
- Poor response to aldosterone (decreased number but normal function of Na-K-ATPase and other transporters) so increase urine loss
Classic laboratory urine findings in premature infants with hyponatremia
High urine sodium and FeNa Kidney can’t hold onto Na (and that’s aldosterone’s job)
Primary role of aldosterone
Upregulates and activates sodium transporters in distal tubule (DCT) and collecting duct (CCD)
(Important even though PCT and Loop of Henle both are more responsible for Na reabsorption than DCT and CCD)
Aldosterone is made in the ____, primarily acts at the ____ by upregulating and activating ____
- Adrenals
- Cortical collecting ducts (CCDs) and distal convoluted tubules (DCTs)
- Na-K-ATPase (pumps) and ENaC channels (cause Na reabsorption)
Hormonal reason for early hypernatremia in preemies
Poor response to ADH (adenylate-cyclases in kidneys are present but immature) so lose too much water
Which RTA causes a non-anion gap acidosis and a normal (acidic) urine pH
RTA Type II: decreased bicarbonate reabsorption in the proximal tubule
You _P_ee 2 much HCO3
What is the issue in RTA I
Cannot secrete H+ in DCT (distal)
(Since you can’t secrete acid, your urine is alkaline)
Type IV RTA is caused by _______ deficiecy
Aldosterone deficiency
Think of CAH–salt wasting, hyperkalemia, acidosis
Draw the nephron, which parts do what, and key associations
FeNa indicative of intrinsic renal injury
FeNa >2-2.5% (depends on source)
Because point of kidney is reabsorption, so if injured can’t pull Na+ back in
If you are highly suspicious of posterior urethral valves, what is the first step in management postnatally
Placement of a foley catheter to relieve the obstruction
(Would be suggested by bilateral hydronephrosis, hydroureters, and a thickened/trabeculated bladder)
What sodium transporters/channels does aldosterone effect?
DCT: Na-Cl transporter (apical AKA urine side)
CCD: ENaC (apical)
Both DCT and CCD: Na/K ATPase (bloode side)
What is the AT2 receptor most important for?
Found in fetal/preemie kidneys, promotes nephrogenesis (via angiotensin II)
The class of antihypertensives to be avoided in preterm infants (and those with acute renal failure)
Angiotensin-converting enzyme inhibitors (ACEI)
Nephrogenesis occurs until ____ (GA or PMA)
36 weeks
