Renal Flashcards
Kidney begins functioning at …
9-10 weeks of gestation
nephrogenesis, the process of ___________, is complete by about ______ weeks GA
process of nephron formation, completed by 34-36 weeks
Bladder formation begins at ______ weeks gestation
4-6 weeks
uretheral development is complete by _____ weeks
12-13 weeks
the major determinate of GFR
blood pressure in the peritubular capillary system
Tubular function: proximal tubules
are generally re-absorptive and absorb water, sodium, potassium glucose, amino acids, bicarb, phosphorous, magnesium, chloride, and calcium
secreted: organic acids, hydrogen ions
distal tubular function
secrete potassium and hydrogen ions
reabsorb: water in the presence of arganine vasopressin, variable sodium reabsorption (dependent on presence of aldosterone)
ADH system
regulates renal blood flow through the renin-angiotensis-aldosterone-AHD system
ADH system: in the ascending loop of henle, a drop in sodium chloride will cause a ______ of the afferent arteriole, allowing for _______ blood flow
relaxation —–increased
ADH system: the macula dense cells will stimulate the juxtaglomerular cells to release _______ activating the ADH system.
renin
The goal of the ADH system is to maintain adequate renal perfusion by _______ sodium chloride and water _______ by the peritubular capillaries to increase intravascular volume, increasing cardiac output and blood pressure.
increasing sodium chloride and increasing water reabsorption
Renin
released in response to decreased renal blood flow; converts angiotensinogen from the liver to angiotensin I
angiotensin I
undergoes further conversion to angiotensin II in the lungs and renal endothelium by enzyme angiotensin-converting-enzyme (ACE)
Angiotensin II
a potent vasoconstrictor of peripheral blood vessels and the efferent arteriole that increases tubular sodium, chloride, and water reabsorption
Aldosterone
a mineral corticoid hormone released by the adrenal cortex in response to angiotensin II, adrenocorticotropic hormone, or hyperkalemia.
aldosterone increases intravascular volume through sodium, chloride, and water reabsorption and excretion of potassium and hydrogen ions
Arginine Vasopressin
increases the permeability of the collecting ducts to water, and allows for water reabsorption into the peritubular capillaries, increasing intravascular volume
Atrial natriuretic Protein and B natriuretic protein
reverse the action of the ADH system
Elevated maternal serum or amniotic alpha-fetoprotein levels indicate (renal)
obstructive uropathy, renal agenesis, or congenital nephrotic sydrome
oligohydramnios associated with
renal agenesis, dysplasia, polycystic kidney disease or urinary tract obstruction
polyhydramnios may be associated with (renal)
due to renal tubular dysfunction and decreased ability to concentrate urine
Elevated BUN
may be seen in AKI or hypercatabolic states or with increased protein intake
An increase in serum creatinine
increase >0.2mg/dL per day or creatinine >1.5 indicate renal dysfunction
creatinine at birth reflective of mother but should either remain the same or decrease after that (depending on GA)
BUN / Creatinine ratio
disproportionate rise - prerenal azotemia
proportionate rise - intrinsic AKI
Potassium in AKI
often elevated in AKI due to impaired excretion
Normal urine specific gravity
1.021 to 1.025 in full term infants
glycosuria in infants <34 weeks
common due to decreased tubular reabsorption of glucose
Fractional Excretion of Sodium
amount of urinary sodium excretion is a percentage of the filtered sodium, reflecting the balance between glomerular filtration and tubular reabsorption of sodium
(urine sodium x plasma creatinine) / plasma Na x urine creatinine x 100%
FENa >3% indicative of intrinsic renal injury
FENa <2.5% indicative of pre-renal injury
Pre-renal azotemia causes and incidence
85% of AKI (most common)
State of hypoperfusion
- hypotension
- CHF
- RDS
- Dehydration
- Nephrotoxic meds (ACE inhibitors,NSAIDS, COX2 inhibitors, ARBs, aminoglycosides)
Intrinsic AKI
- renal dysfunction due to direct structural damage
- may result from prolongation of prerenal causes of renal injury,
- congenital defects,
- inflammation / infection due to viral or yeast infections
- vascular ischemia/hypoperfusion such as aortic or artery thrombosis
- nephrotoxic administration of meds in utero or postnatal
- ATN may be due to perinatal asphyxia
Postrenal AKI
primarily due to obstruction of urine flow
- posterior uretheral valves
- bilateral ureteropelvic junction obstruction
- bilateral ureterovesical junction obstruction
- neurogenic bladder
- obstructive nephrolithiasis
AKI management
fluid challenge for prerenal AKI
renal ultrasound to assess for presence of urine in bladder
low of low-dose dopamine may be used to increase renal blood flow
treat underlying condition
lasix for fluid overload
fluid management for AKI
fluid restriction for low output injury
fluid replacement for high-output injury
bilateral renal agensis
the failure of renal development or the complete absence of the kidneys
associated w/ potter sequence
management of bilateral renal agenesis
oligohydramnios leads to compression of the fetus leading to pulmonary hypoplasia
comfort measures, dialysis if pulmonary hypoplasia is not severe
almost always 100% mortality
Polycystic Kidney Disease
autosomal recessive cystic kidney disorder; will have a palpable flank mass bilaterally with oliguria or decreased UOP
usually occurs bilaterally
multicystic dysplastic kidney disease
nongenetic, developmental renal disorder which usually occurs in only one kidney; the cysts are described as “grape-like” cysts
usually presents with unilateral abdominal mass
one of the most common causes of abdominal masses in neonates
Hydronephrosis
damage to the kidney from a congenital obstruction of the flow of urine which causes urine to backup into the kidneys which dilates the renal pelvis and calyces
Ureteropelvic Junction Obstruction
UPJO is one of the most common causes of hydronephrosis; more common in males; obstruction at kidney and ureter junction
Posterior urethral valves
most common lower urinary tract obstruction in males;
obstruction via membrane blocking the exit from the bladder into the urethra
Vesicoureteral Reflux
condition that results in urine backflowing out of the bladder into the ureters
Renal Vein Thrombosis
usually unilateral thrombosis, usually on left side;
- abdominal flank mass
- possible abdominal distention
- significant hematuria
- thrombocytopenia
high HCT at birth may contribute
If clots occur with UVCs, often occur in the IVC
Renal Artery Thrombosis
clot in the renal artery, blocks blood flow to the kidney (Frequent w/ UAC)
- asymptomatic OR
- systemic HTN
- hematuria
- thrombocytopenia
- oliguria or anuria
Urinary Tract Infection most common organism
E. Coli (Klebsiella common)
UTI Diagnostic
positive urine culture obtained via sterile bladder tap or a gram stain with high colony count
Prune Belly Syndrome or Eagle-Barrett
a) lack of abdominal wall muscles. b) hydronephrosis with a dilated bladder c) bilateral cryptorchidism
Patent urachus
appearance of clear fluid / urine from the umbilicus at birth; at risk of developing UTI or excoriation of skin; supportive care and surgical closure after 1 year of age
chordee
abnormal ventral curvature of the penis
Cryptorchidism associated with syndromes
Down, klinefelter, noonan, prader-willi, fetal hydantoin syndrome
Renal Tubular Acidosis
Normal kidneys excrete hydrogen ions and reabsorb bicarb to compensate for acidosis. RTA is a failure to to respond or attempt to compensate for acidosis
RTA Types
Type 1 - distal RTA - inability to secrete hydrogen
type 2 - proximal RTA - defect in the ability to reabsorb bicarb
Type 3 - a combination of types 1 and 2
type 4 - hyperkalemic tubular type is due to a problem with aldosterone (deficiency or resistence) that results in high levels of potassium
RTA presentation
polyuria, weight loss despite adequate caloric intake; Normal anion gap
RTA Treatment
sodium bicarb or bicitra; type 4 may require sodium supplementation and potassium restriction
Type 2 - associated with Fanconi anemia - investigate
Creatinine levels
>1.5 indicative of renal impairment, or increase of >0.3-0.5 rise per day worrisome
Fluid challenge
give 10-20ml/kg of NS over 1-2 hours, UOP <2ml/kg/hr worrisome
Hypertension
Term: 100/70 Preterm: 90/60 ; most common cause is acute renal damage, or fluid overload; ARF is most common cause, tx w/ Hydralazine
Metabolic acidosis requiring treatment
pH <7.2 or CO2 <14, if treating, monitor ionized calcium
