RENAL Flashcards
renal system
kidneys, bladder, ureters, urethra
kidneys
mesenchyme; three primitive kidneys:
pronephros (disappears by 4 week GA)
mesonephros (glomeruli, mesonephric tubules and ducts, cloaca, distal portion Wolffian duct)
metanephros (proximal tubule, loop of Henle, distal convoluted tubule, collecting duct
ureters and bladder
cloacal division
urine formation and excretion begins when?
6-10 weeks GA
when is nephrogenesis complete?
full term infant 36GA; FANAROFF: 34GA
GFR
Glomerular Filtration Rate: is measured by creatinine clearance, the most consistent marker of GFR in the fetus and neonate
essential for: body fluid homeostasis, electrolyte homeostasis, elimination of drugs;
adult GFR 110-120 reached by 2 years old
postnatal 15-25
renal vasoregulators
NO, prostaglandins, ANP, sympathetic nervous system, catecholamines, RAAS
buffer system modulation
intracellular: hemoglobin, organic phosphates, bone apatite
extracellular: phosphates, plasma proteins, bicarbonate-carbonic acid system
acid base homeostasis
buffer system modulation
respiratory modulation (alveolar ventilation)
renal modulation
functions of the tubular system
reabsorption( from the lumen to the blood)
secretion (from the blood to the lumen)
transport (solute through the nephron and into the ureters for excretion as urine)
tubular transport
proximal convoluting tubule PCT
loop of Henle LOH
distal tubule DCT
collecting ducts
GENETIC ABNORMALITIES
Autosomal Dominant Polycystic Kidney Disease
Autosomal Recessive Polycystic Kidney Disease
Multicystic Dysplastic Kidney Disease
Wilms Tumor
Bartter Syndrome
maternal health influences RENAL
prematurity and LBW
GDM, smoking, alcohol, malnutrition: vit A;
drugs: ACE inhibitors and angiotensin, NSAIDs;
Acute Kidney Disease
the abrupt deterioration in renal function resulting in the inability to maintain fluid and electrolyte balance
PRERENAL (hemodynamic)
RENAL (intrinsic)
POSTNATAL (obstructive)
S&S: elevated BUN and creatinine, hyperkalemia (peaked T wave); metabolic acidosis
Congenital Hydronephrosis
abnormal accumulation of the urine within the collecting system resulting in renal cavity distention
developmental and positional anomalies RENAL
AGENESIS (absence) DYSPLASIA (errors in renal induction) HYPOPLASIA (abnormally small) HORSESHOE KIDNEY (fusion of lower poles) ureteropelvic junction obstruction posterior urethral valve disease
ureteral and urachal anomalies
renal duplication (renal duplex) patent urachus (urine backflow from bladder out to umbilicus)
total body fluids
extracellular (interstitial and plasma) and intracellular water.
75% at birth
normal weight loss at birth
10% term
15% premie
normal physiological transition process caused by atrial natriuretic peptide
glomerulotubular imbalance
physiologic state that is present when the glomerular filtration rate (GFR) exceeds the reabsorptive capacity of the renal tubules
what controls water balance
ADH antidiuretic hormone
urinary concentrating ability in preterm infant?
diminished preterm and term
urinary diluting ability in preterm infant?
diminished in preterm, normal in term
insensible water loss
GA, environmental temperature, increase body temperature; skin breakdowns, phototherapy
urine formation depends on what?
renal function and the renal solute load
electrolyte requirements
sodium and chloride…start after day 1-2
potassium..start after urinary flow is established
third spacing
including sepsis, hydrops fetalis, hypoalbuminemia, intra-abdominal infections, and after abdominal or cardiac surgery
infants who accumulate fluid and electrolytes in static body fluid compartments
normal urine specific gravity neonate
1.008-1.012
normal urine output
1-3 mL/kg
hypo and hyper natremia
130-150;
treatment for hyperkalemia
potassium above 7
insulin given with glucose; sodium polystyrene sulfonate resin (kayexalate); sodium bicarbonate, if metabolic acidosis is present; and peritoneal dialysis.
if arrhythmeia RX; calcium chloride or calcium gluconate
common diuretics
furosemide: loop diuretic, , causes a marked increase in urinary sodium, potassium, and hydrogen ion excretion, leading to hypokalemic metabolic alkalosis.
Chlorothiazide: less potent thiazide diuretic that acts at the distal tubule, also causes a hypokalemic metabolic alkalosis. In contrast to loop diuretics, thiazides decrease urinary calcium excretion.
spironolactone: potassium-sparing aldosterone inhibitor, may be associated with hyperkalemia
nephron
functional unit of the kidney: consist:
Renal Corpuscle - a Glomerulus & a Glomerular Capsule (Bowmans Capsule)
Renal Tubule - proximal, loop of Henle, ascending, distal convoluted tubule & collecting duct
maintenance of acid-base balance
- short: acute compensation, which is accomplished by rapid acid or base buffering by intracellular and extracellular buffers in response to acute decreases or increases in serum pH
- long: long-term compensation, which is accomplished by renal excretion of acid or base, including an obligate daily acid load of approximately 1-2 mEq/kg per day
acute compensation
intracellular buffers: hemoglobin, organic phosphates, bone hydroxyapatite
kidneys role in acid-base homeostasis
- Reabsorption of filtered bicarbonate and excretion of excessive bicarbonate in response to metabolic alkalosis
- Excretion of the obligate daily acid load and any additional acid load from pathogenic processes, such as lactic acidosis related to sepsis or bicarbonate loss from diarrhea
- Compensation for changes in serum pH that result from primary respiratory disorders
acid base maintenance processes in kidneys
bicarbonate reabsorption
ammoniagenesis (in liver glutamine converted to ammonium)
production of titratable acids
metabolic acidosis
excess acid production or increased loss of base
1. increased anion gap:
-lactic acidosis (hypoxemia, shock, sepsis)
-ketoacidosis
2. normal anion gap
-diarrhea
-renal tubular acidosis
RX: correction of underlying cause: bicarbonate (adverse effects)
metabolic alkalosis
loss of acid (hydrochloric) with vomiting, diuretics, chloride deficiency
ingestion of base
contraction of the extracellular volume, with loss fo fluid containing more chloride than bicarbonate
GOES together with: volume depletion: hyperaldosteronism, low potassium, low chloride, respiratory acidosis
RX: dont use ammonium hydrochloride,
ok to use: acetzolamide (CHD), repletion of potassium and chloride
respiratory acidosis and alkalosis
respiratory distress syndrome, meconium aspiration syndrome, pulmonary infections, or congenital diaphragmatic hernia
RX with alkali to correct is not appropriate
Renal Tubular Acidosis
disorder characterized by a normal anion gap metabolic acidosis and is the sequela of either impaired reabsorption of bicarbonate or impaired urinary acidification/H+ ion excretion. TYPES: DISTAL PROXIMAL HYPERKALEMIC
function of prenatal kidneys
formation and excretion of urine to maintain an adequate amount of amniotic fluid
Urine concentration
limited capacity max urinary osmolality 800mOsm/kg
urine dilution
full ability term: 50mOsm/kg; preterm 70mOsm/kg
antenatal drug exposure
ACE and ARBs: oligo, renal failure, limb deformities, pulomonary hypoplasia
NSAIDS, epileptic, chemo
hypertension caused by ?
polycystic kidney disease, acute kidney injury (AKI), renovascular or aortic thrombosis, or obstructive uropathy
hypotension caused by ?
volume depletion, hemorrhage, sepsis
edema caused by ?
AKI, hydrops fetalis, congenital nephrotic syndrome
ascites caused by ?
urinary tract obstruction, congenital nephrotic syndrome, volume overload
most common cause of abnormal renal mass?
hydronephrosis
urinalysis
examination of freshly voided urine:
inspection,
urinary dipstick assessment (heme-containing compounds, protein, and glucose)
microscopic analysis (red blood cells, white blood cells, bacteria, casts, or crystals)
best way for urine culture?
bladder catheterization or suprapubic bladder aspiration
when should neonate first void
by 48 hours
best lab indicator for neonatal kidney function?
serum creatinine level
term at birth 0/6-1mg/dL then decrease to 0.4
radiologic evaluation of kidneys
US: anatomy
voiding cystourethrography: use of contrast
tests for vesicoureteral reflux and posterior urethral valves
radioisotopic renal scanning: identified obstruction or scarring
CT: tumor, abscesses
Hematuria
microscopic
macroscopic
Proteinuria
urinary dipstick value of at least 1+ (30 mg/dL), with a specific gravity of 1.015 or less, or a urinary dipstick value of at least 2+ (100 mg/ dL), with a specific gravity of more than 1.015
persistent heavy proteinuria, edema and hypoalbuminemia, DX?
congenital nephrotic syndrome
glycosuria
presence of glucose on a urinary dipstick
caused by: sepsis or TPN
Acute Kidney Injury
AKI: sudden decline in kidney function over hours to days, resulting in derangements in fluid, electrolyte, and acid–base balance
3 stages
S&S: oliguria, systemic hypertension, cardiac arrhythmia, evidence of fluid overload or volume depletion, decreased activity, seizure, vomiting, and anorexia.
LABS: elevated serum creatinine and blood urea nitrogen, hyperkalemia, metabolic acidosis, hypocalcemia, hyperphosphatemia, and a prolonged half-life for medications excreted by the kidney
causes of AKI
prerenal: low volume, hypotension, hemorrhage, sepsis, NEC, CHD, meds
renal: acute tubular necrosis, renal dysplasia
postrenal: obstructive
RX for AKI
catheter (exclude postrenal obstruction)
fluid challenge: 10-20ml/kg (exclude prerenal
daily weights
renal replacement therapy purpose?
ultrafiltration (removal of water)
dialysis (removal of solutes)
hypertension
common in chronic lung disease, renal disease, or a history of umbilical arterial catheterization., coarctation of the Aorta (check BP in 4 extremities), IVH, ECMO, withdrawals
measure BP in the upper arm
BP in 95th% term MAP 72-75
nephrocalcinosis SG
calcium salt deposition in the renal interstitium
risk factor: hypercalciuria, subcutaneous fat necrosis, hypocitraturia
renal vascular thrombosis
classic clinical triad: a flank mass, macroscopic hematuria, and thrombocytopenia
LABSL CBC, prothrombin time, activated partial thromboplastin time (aPTT), and fibrinogen concentration
renal agenesis
the ureteric bud fails to induce proper differentiation of the metanephric blastema,
VACTERL
vertebral abnormalities, anal atresia, cardiac abnormalities, tracheoesophageal fistula or esophageal atresia, renal agenesis and dysplasia, and limb defects
renal dysplasia
abnormal renal development in the fetus, leading to replacement of the renal parenchyma by cartilage and disorganized epithelial structures.
Multicystic Dysplastic Kidney
(MCDK) represents the most severe form of renal dysplasia and is characterized by a nonfunctioning kidney that is devoid of normal renal architecture and composed of multiple large cysts that resemble a cluster of grapes
Hydronephrosis SG
significant dilation of the upper urinary tract, is one of the most common congenital conditions detected by prenatal ultrasonography
hydronephrosis differental DX
physiologic hydronephrosis (50%-70% of cases), ureteropelvic junction obstruction (10%-30%), vesicoureteral reflux (10%-40%),
ureterovesical junction obstruction (5%-15%),
multicystic dysplastic kidney (2%-5%),
posterior urethral valves (1%-5%),
ureterocele (1%-3%),
Eagle-Barrett syndrome (<1%)
Inherited renal disorders
Congenital Nephrotic Syndrome
Polycystic Kidney Disease (enlarged, echogenic kidneys, hypertension)
Neonatal Bartter Syndrome
Renal Tubular Acidosis (defect in reabsorption in bicarb)
tumors of the kidneys
congenital mesoblastic nephroma, multilocular cystic nephroma, and Wilms tumor (nephroblastoma
polycystic kidney disease SG
autosomal recassive or dominant; enlarged and echogenic kidneys, oligohydraminios, HPT; hyponatremia
exstrophy of the bladder SG
mild: epispadias
severe: cloacal exstrophy: omphalocele, bladder exstrophy, imperforated anus, spinal defect
potter syndrome SG
epicanthal folds, hypertelorism, low-set ears, a crease below lower lip, and a receding chin; oligohydramnios sequence
Posterior Urethral Valves SG
the most common cause of lower urinary tract obstruction
postnatal RX: securing adequate drainage of the urinary tract
Eagle-Barrett Syndrome SG
triad of genitourinary abnormalities (markedly enlarged bladder with poor contractility without urethral obstruction, megaureters, and renal dysplasia), deficiency of abdominal wall musculature, and cryptorchidism
Bartter Syndrome SG
autosomal recessive; hypokalemic tubulopathy; s&s: salt wasting, polyuria, hypokalemia, hypercalciuria
patent urachus SG
opening between the bladder and the belly button (navel); the urachus is a tube between bladder and belly button present before birth
patent urachus SG
opening between the bladder and the belly button (navel); the urachus is a tube between bladder and belly button present before birth
Fanconi Syndrome SG
Renal Tubular Acidosis, Type II/Proximal
renal failure lab values SG
infant under 120 days of age as an increase in serum Cr more or equal to 0.3mg/dL or 50% or more from the previous lowest value and/or urine output less than 0.5ml/kg/hr
kidneys US SG
when? abnormal antenatal; abdominal mass, AKI, HPT, hematuria, congenital and UT anatomy
DX: hydronephrosis, cystic kidney disease, size an positon, nephrocalcinosis
kidneys VCOG SG
voiding cystourethtography
why? evaluate urethea and bladder for vesicoureteral reflux and posterior urethral valves
significant hydronephrosis, hydroureter, documanted UTI
how? contrast via urinary cath;
HYPOnatremia SG
etiology: decreased GFR caused by AKI
increased proximal tubular fluid and Na re-absorption associated with volume depletion
RX: Na+ volume depletion= increase fluide
Na+oliguria= fluid restriction
Bartter syndrome, Congenital Adrenal Hyperplasia, Pseudohyopaldesteronism (ALDOSTERONE)
ALDOSTERONE
promotes hydrogen secretion
resposnible for Na and K homeostasis
Fractional Excretion of Na
FE Na normal less than 1%; renal sodium loss is proportional to GA; younger the age more negative sodium balance and decreased Na
ADH
Antidiuretic Hormone:
controls water balance
controls water absorption in the collecting duct
where? hypothalmus, baroreceptors of carotic sinus and Left Artium
increased osmolarity= increased ADH
Non-excretory kidney
functions
Produces Renin Produces erythropoietin Metabolizes vitamin D Degrades insulin Produces prostaglandins
Excretory functions kidneys
maintain plasma osmolarity
Maintain electrolyte balance
Maintain water balance
Excretes nitrogenous end products
Renin Angiotensin Aldosterone
System (RAAS)
Stimulation leads to: – Systemic vasoconstriction – Sodium retention – Expansion of ECF Renin – Juxtaglomerular cells – Walls of afferent arteriole
LASIX
Loop diuretic – Blocks reabsorption of Cl- – Increases RBF – Impairs Ca++ & Mg++ reabsorption – Onset of action & duration differs in neonates
Thiazides
Acts on distal tubule
Augment K+ wasting
Stimulate Ca++ resorption
K+ sparing
competitive inhibition of aldosterone
Potassium retained
Theophylline
Mild diuretic effect
Inhibits Na+ reabsorption
Dopamine
Dilation of renal arteries
Inhibits Angiotension II
Inhibits ADH release
Indocin
Inhibits cyclooxygenase pathway Decreases GFR Increases ADH secretion SIADH reabsorption of H20 & decreased UOP
Creatinine
Best clinical measure of GFR
– Five days to reflect neonatal values
– Levels above 130 mmol/l (1.5mg/dl) considered
indicative of renal impairment in the newborn
Levels influenced by gestation and postnatal age
Gestation –and-age based reference charts should be
used in interpretation of creatinine values in the VLBW
0.3-0.5 mg/day abnormal
Urinalysis
reflects structure of tubules – Protein – Blood – Pyuria – Microscopic exam Epithelial cells Casts
fluid challenge
10 ml to 20 ml/kg NS IV over 1-2 hours
Lasix 1 Lasix 1-2 mg/kg should oliguria persist 2 mg/kg should oliguria persist
Response is defined as UOP > 2 ml/kg/hr
