Renal Impairment & Renovascular Hypertension Flashcards
What are principles for body fluids and electrolyte regulation in the pediatric patient?
Effective kidney function maintains the normal volume and composition of body fluids.
Although there is wide variation in dietary intake and nonrenal expenditures of water and solute, water and electrolyte balance is maintained by the excretion of urine, with the volume and composition defined by physiologic needs.
Fluid balance is accomplished by glomerular ultrafiltration of plasma coupled with modification of the ultrafiltrate by tubular reabsorption and secretion.
The excreted urine, which is the modified glomerular filtrate, is the small residuum of the large volume of nonselective ultrafiltrate modified by transport processes operating along the nephron.
The glomerular capillaries permit free passage of water and solutes of low molecular weight, while restraining formed elements and macromolecules.
The glomerular capillary wall functions as a barrier to the filtration of macromolecules based on their size, shape, and charge characteristics.
The glomerular filtrate is modified during passage through the tubules by the active and passive transport of certain solutes into and out of the luminal fluid and the permeability characteristics of specific nephron segments.
The transport systems in renal epithelial cells maintain global water, salt, and acidbase homeostasis.
An adequate volume of glomerular filtrate is essential for the kidney to regulate water and solute balance effectively.
Renal blood flow accounts for 20–30% of cardiac output.
Of the total renal plasma flow, 92% passes through the functioning excretory tissue and is known as the effective renal plasma flow.
The glomerular filtration rate (GFR) is usually about one-fifth of the effective renal plasma flow, giving a filtration fraction of about 0.2.
The rate of ultrafiltration across the glomerular capillaries is determined by the same forces that allow the transmural movement of fluid in other capillary networks.
These forces are the transcapillary hydraulic and osmotic pressure gradients and the characteristics of capillary wall permeability.
A renal autoregulatory mechanism enables the kidney to maintain relative constancy of blood flow in the presence of changing systemic arterial and renal perfusion pressures.
This intrinsic renal autoregulatory mechanism appears to be mediated in individual nephrons by tubuloglomerular feedback involving the macula densa (a region in the early distal tubule that juxtaposes the glomerulus) and the magnitude of resistance in the afferent and efferent arterioles.
Under normal conditions, the reabsorption of water and the reabsorption and secretion of solutes during passage of the glomerular filtrate through the nephron are subservient to the maintenance of body fluid, electrolytes, and acid–base homeostasis.
In the healthy, nongrowing individual, the intake and the expenditure of water and solute are equal and the hydrogen ion balance is zero.
Renal function may be impaired by systemic or renal disease and by medications such as vasoactive drugs, nonsteroidal anti-inflammatory drugs, diuretics, and antibiotics.
Hypoxia and renal hypoperfusion appear to be the events most commonly associated with postoperative renal dysfunction.
H&A
How do you evaluate renal function in the pediatric patient?
The evaluation of renal function begins with the patient’s history, physical examination, and laboratory studies.
Persistent oliguria or significant impairment in renal concentrating capacity should be evident from the history.
Examination of the urinary sediment may provide evidence of renal disease if proteinuria and/or cellular elements and casts are present.
Normal serum concentrations of sodium, potassium, chloride, total CO2 , calcium, and phosphorus indicate appropriate renal regulation of the concentration of electrolytes and minerals in body fluids.
The serum creatinine concentration is the usual parameter for estimating GFR.
Important limitations and caveats must be observed when using creatinine to estimate GFR.
Urinary creatinine excretion reflects both filtered and secreted creatinine because creatinine is not only filtered by the glomerular capillaries, but is also secreted by renal tubular cells. As a consequence, creatinine clearance, which is calculated by using serum creatinine concentration and the urinary excretion of creatinine, overestimates true GFR (as measured by using inulin clearance) by 10–40%.
Serum creatinine concentration and the rate of urinary creatinine excretion are also affected by diet. The ingestion of meat, fish, or fowl, which are substances containing preformed creatinine and creatinine precursors, causes an increase in serum creatinine concentration and in urinary creatinine excretion.
The overestimation of GFR by creatinine clearance increases as kidney function deteriorates owing to the relative increase in the tubular component of urine creatinine.
Another caveat should be applied in the case of the patient with an abnormal muscle mass. The smaller the muscle mass, the lower is the release of creatinine into the circulation, resulting in lower blood levels and urine excretion rates of creatinine.
The opposite picture will be seen in a patient with very large muscle mass.
Another indicator of GFR, the serum concentration of cystatin C, a nonglycosylated 13.3-kDa basic protein, has been shown to correlate with GFR as well as or better than serum creatinine.
From about age 12 months and up until age 50 years, normal serum cystatin C concentrations are similar in children and adults (0.70 - 1.38 mg/L).
Currently, the measurement of cystatin C has not yet been incorporated into routine clinical practice.
In contrast, the following is a practical equation to estimate GFR:
eGFR = 0.413 × Height (cm)/Serum creatinine (mg/dL)
This equation has been developed in children with chronic kidney disease (CKD) based on data generated from the measurement of GFR using the plasma disappearance of iohexol.
This bedside formula is most applicable to children whose GFR is in the range of 15–75 mL/ min/1.73 m2.
H&A
How is renal function evaluated using urine volume?
The appropriate urine volume depends on the status of body fluids, fluid intake, extrarenal losses, obligatory renal solute load, and renal concentrating and diluting capacity.
Patients with impaired renal concentrating capacity require a larger urinary volume for excretion of the obligatory renal solute load.
On the other hand, patients with elevated levels of antidiuretic hormone (ADH) retain water out of proportion to solute and are prone to hyponatremia.
Increased levels of ADH may occur because of physiologic factors such as hypertonic body fluids or a decrease in the effective circulatory volume (as encountered with low levels of serum albumin or with generalized vasodilatation as with sepsis).
Some researchers have expressed concern that “usual maintenance fluids” providing 2–3 mEq/L of sodium, potassium, and chloride per 100 calories metabolized may contribute to the development of hyponatremia in children hospitalized with conditions likely to be associated with ADH excess.
The children at risk are those with nonosmotic stimuli for ADH release, such as central nervous system disorders, the postoperative patient, pain, stress, nausea, and emesis.
It has been proposed that in patients prone to developing the syndrome of inappropriate secretion of ADH, isotonic 0.9% normal saline might be a better choice for maintenance fluid therapy.
Approximately 30 mOsm of obligatory renal solute/100 mL of usual maintenance water is taken as the obligatory renal solute load in children 2 months and older.
Urinary concentrating capacity increases rapidly during the first year of life and reaches the adult level of 1200–1400 mOsm/L at around year 2.
The maximum urinary concentrating capacity of the term infant from 1 week to 2 months of age is about 800 mOsm/L; from 2 months to 3 years, about 1000 mOsm/L; and beyond that age, about 1200 mOsm/L.
H&A
How is renal function evaluated using GFR?
GFR is the most useful index of renal function because it reflects the volume of plasma ultrafiltrate presented to the renal tubules.
Decline in GFR is the principal functional abnormality in both acute and chronic renal failure.
Assessment of GFR is important not only for evaluating the patient with respect to kidney function, but also for guiding the administration of antibiotics and other drugs.
Inulin clearance, which is the accepted gold standard for measurement of GFR, is too time consuming and inconvenient for use in the clinical evaluation of most patients.
Serum urea nitrogen concentration shows so much variation with dietary intake of nitrogen-containing foods that it is not a satisfactory index of GFR.
As noted previously, serum creatinine concentration and creatinine clearance have become the usual clinical measures for determining the GFR. However, precautions should be taken when creatinine alone is used for estimation of GFR because of the effect of diet as well as common medications on serum creatinine concentration and excretion rate.
Ingestion of a meal containing a large quantity of animal protein increases serum creatinine levels by about 0.25 mg/dL in 2 hours and increases the creatinine excretion rate about 75% over the next 3- to 4-hour period.
Serum creatinine concentrations are also increased by ingestion of commonly used medications such as salicylate and trimethoprim. These agents compete with creatinine for tubular secretion through a base-secreting pathway. They do not alter GFR, but they do elevate the serum creatinine concentration.
Because of the difficulties in timed urine collection, several equations have been developed to estimate GFR. Historically the most commonly used equation has been the one developed by Schwartz and is based on the serum creatinine value (as determined by the Jaffe kinetic method) and the child’s height:
eGFR ( mL/min/1.73m2 ) =
k × Height(cm)/ Serum creatinine (mg/dL)
where k for infants with low birth weight is 0.33; fullterm infants, 0.45; males 2–12 and females 2–21 years, 0.55; and males 13–25 years, 0.70.
More recently, the use of enzymatic methods to determine serum creatinine prompted the development of new GFR estimating equations.
The Flanders Metadata equation has been used to estimate GFR in healthy children between 2 and 15 years of age.
This equation is eGFR (mL/min/1.73 m2 ) = (0.014 × ln(age) + 0.3018) × L/Scr.
In contrast and as noted earlier, the updated Schwartz equation, eGFR = 0.413 × L/Scr, was derived from a study of children with CKD.
Estimating equations that combine serum creatinine and cystatin C result in more precision, but the complex nature of the equations compromises their clinical usage.
Creatinine is formed by the nonenzymatic dehydration of muscle creatine at a rate of 50 mg creatine/kg muscle.
The serum creatine concentration in the neonate reflects the maternal level for the first 3–4 days of life and somewhat longer in the premature infant due to delayed maturation of kidney function.
After this time, the serum creatinine concentration should decrease.
From age 2 weeks to 2 years, the value averages about 0.4 ± 0.04 mg/dL (35 ± 3.5 μM).
The serum creatinine concentration is relatively constant during this period of growth because the increase in endogenous creatinine production, which is directly correlated with muscle mass, is matched by the increase in GFR.
During the first 2 years of life, GFR increases from 35–45 mL/ min/1.73 m 2 to the normal adult range of 90–170 mL/ min/1.73 m2 .
The normal range for serum creatinine concentration increases from 2 years through puberty, although the GFR remains essentially constant when expressed per unit of surface area.
This occurs because growth during childhood is associated with increased muscle mass and therefore increased creatinine production, which is greater than the increased GFR per unit of body weight.
Normative data of serum creatinine may differ from one laboratory to another, depending on the methodology used, although efforts are being made for standardization.
H&A
How is renal function evaluated using fractional excretion of substances?
Fractional excretions (FEs) are indices of renal function that are helpful in evaluating specific clinical conditions.
Conceptually, an FE is the fraction of the filtered substance that is excreted in the urine.
In clinical practice, FE is calculated by obtaining simultaneous blood and urine samples for creatinine and the substance studied.
The formula used to express FE as a percentage is:
FE = Us/Ps × Pcr/Ucr × 100
where Us is urine solute concentration, Ps is plasma solute concentration, Pcr is plasma creatinine concentration, and Ucr is urine creatinine concentration.
Fractional Excretion of Sodium
The FE of sodium (FE Na) is 2–3% in normal newborns and may be higher in premature infants.
In older children it is usually less than 1%, but may be elevated with high salt intake, adaptation to chronic renal failure, and diuretic administration.
When a decrease in renal perfusion occurs, which is common in intravascular volume depletion or congestive heart failure, the normal renal response results in a marked increase in the tubular reabsorption of sodium leading to a decrease in sodium excretion and consequently a FE Na of less than 1%.
The FE Na is usually greater than 2% in ischemic acute kidney injury (AKI; also known as acute tubular necrosis), reflecting the impaired ability of the tubules to reabsorb sodium.
When using FE Na to aid in differentiating prerenal azotemia from AKI, it is important that diuretics have not been recently given, because the FE Na will be artificially high.
However, if they have been given, the FE of urea can be used, being less than 35% in the case of prerenal azotemia.
The FE Na, as well as the other diagnostic indices used to help differentiate prerenal azotemia from ischemic AKI, is not pathognomonic for either disorder.
Furthermore, the FE Na is often less than 1% in cases of AKI due to glomerular disease, especially early in the disease process because tubular function remains intact.
Renal Tubular Acidosis
Renal tubular acidosis (RTA) comprises a group of disorders in which metabolic acidosis occurs as a result of an impairment in the reclamation of filtered HCO3 in the proximal tubule or from a defect in the renal hydrogen ion excretion in the distal tubule, in the absence of a significant reduction in GFR.
RTA is considered in the differential diagnosis of the patient with metabolic acidosis, a normal serum anion gap (hyperchloremic metabolic acidosis), and, in other than a few exceptions, a urinary pH above 6.0.
It is important to remember that an identical biochemical profile is seen in the child with diarrhea, which needs to be excluded before considering the diagnosis of RTA.
In addition to several genetic disorders such as cystinosis, proximal tubular damage is often seen in children receiving chemotherapy.
The diagnosis of a defect in proximal tubular reabsorption of HCO3 is made by showing that the FE of bicarbonate (FE HCO3) is greater than 15% when the plasma HCO3 concentration is normalized with alkali therapy.
Classic distal RTA is caused by a defect in the secretion of H+ by the cells of the distal nephron.
It is characterized by hyperchloremic metabolic acidosis, urine pH greater than 6.0 at normal as well as at low serum HCO3 concentrations, and FE HCO 3 less than 5% when the serum HCO 3 is normal.
Type IV RTA, a form of distal RTA associated with low urinary pH (<6.0) and hyperkalemia, is a result of decreased H + and K + secretion in the distal tubule and is related to a failure to reabsorb sodium.
Type IV RTA is probably the most commonly recognized type of RTA in both adults and children.
The hyperkalemia inhibits ammonia synthesis, resulting in decreased available ammonia to serve as a urinary buffer.
Therefore, a low urinary pH occurs despite decreased H+ secretion (NH3 + H + = NH4 +).
Type IV RTA is physiologically equivalent to aldosterone deficiency, which is one cause of the disorder.
In children, it may reflect true hypoaldosteronism, but it is much more common as a consequence of renal parenchymal damage, especially that due to obstructive uropathy.
In children, the physiologic impairment of type IV RTA resolves in a few weeks to months after relief of an obstructive disorder.
H&A
What is the pathophysiology of acute kidney injury?
AKI is characterized by an abrupt decrease in kidney function.
Because AKI is caused by a decrease in the GFR, the initial clinical manifestations are elevations in serum urea nitrogen and creatinine concentrations and frequently a reduction in urine output.
Among pediatric surgical patients, an impairment in kidney function is most common to those who are undergoing cardiopulmonary procedures.
In recent years, research has focused on the identification of biomarkers that indicate imminent kidney failure, even before a rise in serum creatinine is noted.
The idea is to identify urine and possibly blood proteins and enzymes released from the tubules very early in the development of AKI.
A substantial amount of data has been collected in children undergoing elective heart surgery, using the biomarkers neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), and kidney injury molecule-1 (KIM-1). Biomarkers also have been studied for their ability to distinguish between the various types of AKI and to predict the need for renal replacement therapy.
However, at this point, such markers, which seem to have a better negative predictive value in ruling out impending AKI, have not been incorporated into routine clinical practice.
The most important factor in the pathogenesis of postoperative kidney failure is decreased renal perfusion.
In the early phase, the reduction in renal blood flow results in a decline in GFR.
Intact tubular function results in enhanced reabsorption of sodium and water.
This clinical condition is recognized as prerenal azotemia.
Analysis of the patient’s urine reveals a high urinary osmolality of greater than 350 mOsm/kgH2O, and, as discussed earlier, the FENa is less than 1% in term infants and children and below 2.5% in premature infants.
In most patients with prerenal azotemia, intravascular volume depletion is clinically evident. However, in patients with diminished cardiac output (pump failure), clinical appreciation of reduced renal perfusion can be obscured because body weight and central venous pressure may suggest fluid overload.
Similarly, assessment of volume status is difficult in patients with burns, edema, ascites, anasarca, or hypoalbuminemia.
The reduced effective intra-arterial volume might be evident from the reduced systemic blood pressure, tachycardia, and prolonged capillary refill time.
Prerenal azotemia can be alleviated by improving renal perfusion by either repleting the intravascular fluid volume or improving the cardiac output.
The improved kidney function is recognized by increased urine output and normalization of serum urea nitrogen and creatinine concentrations.
However, if renal hypoperfusion persists for a significant period or if other nephrotoxic factors are present, parenchymal kidney failure can result.
Factors that may predispose the patient to AKI include preexisting congenital urinary anomalies or impaired kidney function, septicemia, hypoxemia, hemolysis, rhabdomyolysis, hyperuricemia, drug toxicity, and the use of radiocontrast agents.
Also, abdominal compartmental syndrome resulting from tense ascites can impair renal perfusion.
In this setting, kidney failure may be alleviated by abdominal decompression.
In an effort to better define AKI and the stages of its severity, in 2004 a group of experts developed the empiric RIFLE (Risk, Injury, Failure, Loss, End-Stage Kidney Disease) criteria. The criteria, later modified to include the pediatric population, are based on the rate of rise in serum creatinine, magnitude of oligoanuria, and severity and length of renal failure. They are currently used primarily for research purposes because the care and prognosis of the individual patient may depend on additional factors such as fluid status, cause of the AKI, and involvement of other systems.
H&A
How is acute kidney injury managed medically in pediatric patients?
The child with postoperative oliguria and an elevated serum creatinine concentration should be assessed for possible prerenal azotemia.
If the child is found to be hypovolemic, an intravenous fluid challenge of 20 mL/ kg of isotonic saline or plasma is commonly given.
In acidotic patients, it may be physiologically advantageous to provide a solution in which bicarbonate accounts for 25–40 mEq/L of the anions in the fluid bolus (0.5 isotonic NaCl in 5% glucose, to which is added 25–40 mEq/L of 1 M NaHCO 3 and additional NaCl or NaHCO 3 to bring the solution to isotonicity).
If no response is observed and the child is still dehydrated, the dose can be repeated.
When the urine output is satisfactory after fluid replenishment, the child should receive appropriate maintenance and replacement fluids.
Body weight, urinary volume, and serum concentrations of urea nitrogen, creatinine, and electrolytes also should be monitored.
As discussed later, if a solution containing alkali is used, the serum ionized calcium level should be closely monitored.
If urinary output is inadequate after the fluid challenge, an intravenous dose of furosemide, 1 mg/kg, may be given.
Patients with renal failure may require higher doses, up to 5 mg/kg.
If no response occurs after the initial dose of furosemide, a second, higher dose can be repeated after 1 hour.
Some patients may require furosemide every 4–8 hours to maintain satisfactory urinary volume.
A protocol with constant furosemide infusion has been successfully used in oliguric children after cardiac surgery.
Furosemide is infused at 0.1 mg/ kg/h, with the dose increased by 0.1 mg after 2 hours if the urinary volume remains less than 1 mL/kg/h.
The maximum dose is 0.4 mg/kg/h.
At times, urine output can be increased by the use of vasoactive agents such as dopamine; however, their efficacy in otherwise altering the course of AKI is not well established.
It is very important to maintain adequate blood pressure and effective renal plasma flow.
Children who fail to respond to furosemide are at risk for fluid overload.
Overzealous fluid administration during anesthesia and surgery and for the management of persistent hypoperfusion, along with decreased urinary output, can result in hypervolemia, hypertension, heart failure, and pulmonary edema.
In extreme cases, fluid administration should be decreased to the minimum necessary to deliver essential medications.
In less severe instances and in euvolemic patients with impaired kidney function, total fluid intake should equal insensible water loss, urine volume, and any significant extrarenal fluid losses.
Urine output must be monitored hourly, and fluid management should be reevaluated every 4–12 hours, as clinically indicated.
Valuable information about the patient’s overall fluid status can be obtained by carefully monitoring blood pressure, pulse, and body weight. The preoperative values of these parameters serve as a baseline for postoperative evaluation.
Ideally, the patient’s hemodynamic status should be assessed continuously by central venous pressure monitoring.
Fluid overload can lead to hyponatremia. In most cases, because total body sodium remains normal or high, the best way to normalize serum sodium concentration is by restriction of fluid intake and enhancement of urinary volume.
In patients with acute symptomatic hyponatremia, careful infusion of NaCl 3% solution (512 mEq Na/L or 0.5 mEq/ mL) may be given to correct
hyponatremia.
Rapid correction at a rate of 1–2 mEq/h over a 2- to 3-hour period, with an increase in the serum sodium level by 4–6 mEq/L, is usually well tolerated and adequate.
Infusion of 6 mL/kg of 3% NaCl increases serum sodium concentration by about 5 mEq/L.
Hyponatremia present for more than 24–48 hours should not be corrected at a rate more rapid than 0.5 mEq/L/h.
In children with AKI, hyperkalemia often develops. The early sign of potassium cardiotoxicity is peaked T waves on the electrocardiogram.
Higher levels of serum potassium can cause ventricular fibrillation and cardiac asystole.
The treatment of hyperkalemia is shown in Box 4.1.
Emergency treatment of hyperkalemia is indicated when the serum potassium concentration reaches 7.0 mEq/L or when electrocardiographic changes are noted.
In children with AKI, metabolic acidosis rapidly develops. Owing to decreased kidney function, fewer hydrogen ions are excreted.
Organic acids accumulate in the body, causing a reduction in the serum HCO 3 concentration.
Although a child with uncompromised ventilatory capacity is able to hyperventilate and achieve partial compensation, a child with compromised pulmonary function or a hypercatabolic state is at risk for profound acidosis.
Metabolic acidosis is usually treated by administering NaHCO3 . However, attention should be directed toward the excess sodium load associated with this mode of therapy.
Because hypocalcemia develops in many patients with AKI, treatment with alkali should be done cautiously to protect them from hypocalcemic tetany due to a shift of ionized calcium from free to albumin-bound.
It is not necessary to correct the metabolic acidosis completely to prevent the untoward effects of acidemia.
Increasing the serum HCO 3 concentration to 15 mEq/L is usually satisfactory.
H&A
What are the indications for dialysis in pediatric patients?
Dialysis
The inability to control the fluid and electrolyte or acidbase disorders caused by renal failure necessitates the initiation of dialysis.
The indications for urgent dialysis are persistent oligoanuria, hyperkalemia, metabolic acidosis, fluid overload, severe electrolyte and mineral disturbances, and uremic syndrome.
The most common indication for postoperative dialysis in a child is hypervolemia caused by repeated attempts at fluid resuscitation, administration of medications, and total parenteral nutrition.
Repeated intravenous catheter flushes and endotracheal tube lavages can add a significant amount of water and solute to the total intake.
Fluid overload in the postoperative patient can cause pulmonary edema and hypertension and may have a significant negative impact on patient recovery.
H&A
What are the methods of dialysis for pediatric patients?
Dialysis Methods
The three modes of dialysis therapy consist of hemodialysis (HD), peritoneal dialysis (PD), and continuous renal replacement therapy (CRRT).
Although PD has historically been used most often in children, there has been an increased use of CRRT in centers in which the expertise and resources are available.
Recognition of the needs of the patient, the resources of the treating facility, and the advantages and disadvantages of each dialytic technique dictate which modality is best.
The intrinsic factors that affect the efficacy of PD include peritoneal blood flow, peritoneal vascular permeability, and peritoneal surface area.
Although removal of up to 50% of the peritoneal surface area does not seem to interfere with dialysis efficacy, hypoperfusion of the peritoneal membrane vasculature renders PD ineffective.
PD is feasible in the postoperative patient, even in the presence of peritonitis or immediately after major abdominal operations.
It also remains the most common renal replacement therapy modality for the treatment of AKI in developing countries because of its efficacy, coupled with the requirement for minimal resources.
The International Society for Peritoneal Dialysis (ISPD) has recently published guidelines on the use of PD for treatment of AKI to help standardize clinical practice.
Increased intra-abdominal pressure caused by the dialysis fluid can cause respiratory embarrassment and can contribute to leakage from the incisions and the exit site of the PD catheter.
If leakage persists, the smallest effective dialysis fluid volume (10–20 mL/kg) can be tried.
Common additional complications associated with PD are peritonitis, exit site infection, catheter obstruction from omentum or fibrin, and abdominal wall hernia.
The provision of antibiotics at the time of catheter placement is recommended and may decrease the risk for peritonitis.
Also, the use of fibrin glue at the site of catheter entry into the peritoneum has been associated with a decreased incidence of dialysate leakage during the immediate postoperative period and may be particularly beneficial when PD is initiated soon after catheter placement.
A study in 2000 showed placement of a Tenckhoff catheter to be superior to the Cook catheter (Cook Medical, Bloomington, IN) in terms of complication-free survival, and this catheter remains the catheter of choice when initiating acute PD in children. However, there is evidence for equivalent outcomes with the Cook Multipurpose Drainage catheter, a flexible catheter that is placed at the bedside, in contrast to the Tenckhoff catheter, which typically requires operative insertion.
PD is performed with dialysis solutions that contain a 1.5%, 2.5%, or 4.25% dextrose concentration.
Dialysate with a 1.5% dextrose concentration has an osmolality of 346 mOsm/kg H2O, which is moderately hypertonic to normal plasma (280–295 mOsm/kg H2 O).
Other factors being equal, the higher the tonicity of the dialysate and the greater the osmotic gradient between blood and dialysate, the greater is the ultrafiltrate (fluid removed from the body).
Owing to the rapid movement of water and glucose across the peritoneal membrane, the effect of PD on fluid removal is maximal when short dialysis cycles of 20–30 minutes are used.
However, rapid cycling with hypertonic dialysis solutions can result in enhanced free water clearance and the development of hypernatremia, which mandates close monitoring of the patient’s electrolyte status.
Close monitoring of the patient’s serum glucose concentration is also necessary when dialysis solutions containing dextrose concentrations higher than 1.5% are used.
If hyperglycemia develops with a blood glucose concentration greater than 200 mg/dL, it can be controlled by the addition of insulin to the dialysate solution or by intravenous insulin drip.
The volume of fluid removed by dialysis in a 24-hour period generally should be limited to 500 mL in the neonate, 500–1000 mL in infants, and 1000–1500 mL in young children.
The effect of dialysis on the removal of solutes depends mainly on the length of the dwell time of the dialysate within the peritoneal cavity, the dialysis fill volume, and the molecular weight of the solute.
The following are the relative rates of removal of common substances: urea > potassium > sodium > creatinine > phosphate > uric acid > calcium > magnesium. Standard dialysate solutions do not contain potassium.
Therefore, hyperkalemia can be controlled with a few hours of effective PD.
HD has the advantage of more rapid ultrafiltration and solute removal than either PD or CRRT.
Adequate vascular access is the most important requirement, and a variety of temporary pediatric catheters are available.
Insertion of the dialysis catheter in the right internal jugular vein is preferred, followed by the femoral vein and the left internal jugular vein.
Placement in the subclavian vein should be discouraged because of the potential development of subclavian stenosis and the subsequent inability to create a dialysis fistula in the ipsilateral arm of patients who go on to develop end-stage renal disease.
Fluid removal can be problematic in the patient who is hypotensive and receiving HD because of poor patient tolerance and is better accomplished by either PD or CRRT in this clinical setting.
The types of CRRT consist of continuous venovenous HD (CVVHD), continuous venovenous hemofiltration (CVVH), and continuous venovenous hemodiafiltration (CVVHDF).
CRRT is now widely practiced in many tertiary pediatric centers because of the safety and efficacy of the technique in even the sickest patients.
The choice of one method of CRRT over another depends on whether one chooses to make use of the diffusive (CVVHD) or convective (CVVH) method or a combination of the two (CVVHDF) properties of the technique.
As in HD, a wellfunctioning vascular access catheter is crucial for CRRT.
Data suggest that the optimal access is the one with the largest diameter preferably located within the right internal jugular vein. Likewise, large extracorporeal blood volumes are necessary for the CRRT (and HD) circuit and require blood products in the small patient in whom the circuit volume exceeds 10% of the patient’s blood volume.
Particular attention must be paid to the possible development of hemofilter-related reactions that might occur with the initiation of therapy.
The predictability and efficiency of ultrafiltration and solute removal make CRRT an ideal dialytic technique for hemodynamically unstable patients.
In children at risk for hemorrhage, a protocol using citrate instead of heparin as the anticoagulant has been developed.
Finally, new information has provided direction regarding the preferred timing of dialysis initiation.
Fluid overload itself appears to be a significant risk factor for mortality, and its early and aggressive management with dialysis before a fluid overload threshold of 10–20% is reached may prove particularly beneficial.
One analysis found a 30% mortality with less than 10% fluid overload, 40% with 10–20% fluid overland, and 66% with more than 20% fluid overload.
H&A
What are the major causes of acute renal failure in the neonate?
AKI occurs in as many as 25% of all patients admitted to the neonatal intensive care unit (NICU).
The definition of AKI in a term neonate has historically been considered to be a serum creatinine level above 1.5 mg/dL for more than 24 hours in the setting of normal maternal renal function.
On occasion, it may be diagnosed in the term infant with a serum creatinine value less than 1.5 mg/dL when it fails to decrease in a normal manner over the initial day to weeks of life.
It also has been defined by an age-independent increase in serum creatinine to 1.5 times or greater compared to the lowest prior value, which is known to have been drawn within the past 7 days, or a urine volume less than 0.5 mL/kg/h for 6 hours.
A recent proposed neonatal-specific classification has characterized stage 1 AKI as an increase in serum creatinine of 0.3 mg/dL within 48 hours, an increase in the serum creatinine to 1.5–2 times the previous value, or urine output less than 1 mL/kg/h over 24 hours.
A pediatric modification (pRIFLE) of an adult AKI classification system also has been developed.
The limited availability of cystatin C data from the neonatal population currently precludes its routine use to define AKI.
AKI is of the oliguric variety when the elevated serum creatinine concentration is accompanied by a urine output below 1 mL/kg/h after the initial 24 hours of life and when urine output fails to improve in response to a fluid challenge.
In contrast, solute retention develops in some neonates, as evidenced by an elevated serum creatinine level, with a normal (>1.0 mL/kg/h) urine flow rate. These neonates are diagnosed as having nonoliguric AKI.
The nonoliguric form is particularly common in neonates with AKI secondary to perinatal asphyxia and appears to be associated with a better prognosis than does the oliguric form.
The diagnosis of nonoliguric AKI can be missed if patients at risk for developing renal insufficiency are monitored solely by the evaluation of urine output without repeated assessments of the serum creatinine concentration.
The causes of AKI in newborns traditionally have been divided into three categories: prerenal, intrinsic, and postrenal (Box 4.2).
This division, based on the site of the problem, has important implications because the evaluation, treatment, and prognosis of the three groups can be quite different.
H&A
What are the causes of prerenal AKI in the neonate?
Impairment of renal perfusion is the cause of 85% of AKI during the neonatal period.
Prerenal AKI can occur in any patient with hypoperfusion of an otherwise normal kidney.
This may occur secondary to excessive gastrointestinal losses, decreased intravascular volume as a result of placental blood loss around delivery, and increased insensible losses.
Although prompt correction of the low perfusion state usually reverses this impairment, delay in fluid resuscitation can result in renal parenchymal damage.
H&A
What are the causes of intrinsic AKI in the neonate?
AKI as a result of intrinsic injury of the renal parenchyma accounts for 11% of cases of AKI in neonates.
Intrinsic AKI usually falls into one of the following categories:
ischemic (acute tubular necrosis),
nephrotoxic (aminoglycoside antibiotics, indomethacin),
congenital renal anomalies (autosomal recessive polycystic kidney disease), and
vascular lesions (renal artery or vein thrombosis), especially with a solitary kidney.
H&A
What are the causes of postrenal AKI in the neonate?
Postrenal AKI, which accounts for 3% of cases in neonates, results from obstruction of urine flow from both kidneys or from a solitary kidney.
The most common causes of postrenal AKI in neonates are posterior urethral valves (PUV), bilateral ureteropelvic junction (UPJ) obstruction, and bilateral ureterovesical junction (UVJ) obstruction.
Although these types of obstructions are characteristically reversible, neonates with long-standing intrauterine obstruction have varying degrees of permanent impairment of kidney function.
This impairment may be due not only to the presence of renal dysplasia, but also to cellular damage secondary to AKI.
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What is the clinical presentation of neonates with AKI?
The clinical presentation of the neonate with AKI often reflects the condition that has precipitated development of the renal insufficiency.
Accordingly, sepsis, shock, dehydration, severe respiratory distress syndrome, and other related conditions may be present.
Nonspecific symptoms related to anemia, such as poor feeding, lethargy, emesis, seizures, hypertension, and anemia, are also often found.
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How is AKI in the neonate evaluated?
Evaluation of the neonate with AKI should include a thorough patient and family history and a physical examination.
Suspected prerenal causes of acute oliguria are usually addressed diagnostically and therapeutically by volume expansion, with or without furosemide.
If this approach does not result in increased urine output, a more extensive evaluation of renal function is indicated.
Laboratory studies are an important component of this evaluation and include complete blood count and determination of serum concentrations of urea nitrogen, creatinine, electrolytes, uric acid, calcium, glucose, and phosphorus.
The serum creatinine value during the first several days of life is a reflection of the maternal value.
In term infants, a value of 0.4–0.5 mg/dL is expected after the first week of life.
In contrast, the expected value in preterm infants is related to their gestational age, with an initial increase followed by a gradual decrease.
In all cases, a urinalysis should be obtained to check for the presence of red blood cells, protein, and casts suggestive of intrinsic renal disease.
Urine indices can help distinguish intrinsic renal failure from prerenal azotemia in the oliguric newborn.
As mentioned previously, the index usually found to be most useful is the FE Na.
This factor is based on the assumption that the renal tubules of the poorly perfused kidney reabsorb sodium avidly, whereas the kidney with intrinsic renal disease and tubular damage is unable to do so.
Accordingly, in most cases of neonatal oliguric renal failure secondary to intrinsic disease, the FE Na is >2.5–3.0%, a value that is different from that of the older child.
The FE Na should be measured before administering diuretic therapy. In addition, the results should be interpreted with caution in the very premature infant who normally has an even higher (i.e., >5%) FE Na.
Ultrasonography commonly is the initial imaging study. The urinary tract should be evaluated for the presence of one or two kidneys and for their size, shape, and location.
In addition, a voiding cystourethrogram (VCUG) may be necessary, specifically when the diagnosis of PUV or vesicoureteral reflux (VUR) is entertained.
In this setting, a VCUG is deemed preferable to radionuclide cystography because of its superior ability to provide reliable anatomic information about the grading of VUR and the appearance of the urethra.
Antegrade pyelography or diuretic renography with either 99m Tc-dimercaptosuccinic acid (DMSA) or 99m Tc-dimercaptoacetyltriglycine (MAG3) may be needed to evaluate for ureteral obstruction.
Finally, assessment of the differential kidney function can be performed with radioisotope scanning as well.
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How is AKI in the neonate managed?
The treatment of neonatal AKI should proceed simultaneously with the diagnostic workup.
Bladder catheter placement is a good immediate therapy for PUV, whereas proximal surgical drainage may be needed for other obstructive lesions in the neonate.
Insensible water losses through the transepidermal and respiratory routes can be substantial, and a fluid challenge consisting of 20 mL/kg of an isotonic solution containing 25 mEq/L of NaHCO3 infused over a 1- to 2-hour period should be considered.
In the absence of a prompt diuresis of 2 mL or more of urine per kilogram over 1–2 hours, intravenous furosemide at 1–3 mg/kg may be helpful.
As noted previously, the potential role of low-dose (0.5–3.0 μg/kg/min) dopamine continues to be debated, but recent guidelines recommend against its use to prevent or treat AKI.
The failure to achieve increased urinary output after volume expansion in the neonate with an adequate cardiac output and an unobstructed urinary tract indicates the presence of intrinsic kidney disease and the need to manage oliguric or anuric kidney failure appropriately.
Maintenance of normal fluid balance is of primary concern in the management of the patient with AKI.
Daily fluid intake should equal insensible water loss, urine output, and fluid losses from nonrenal sources.
In term infants, insensible water losses amount to 15–25 mL/kg/day (180–310 mL/m2 /day) and as much as 50–100 mL/kg/day in premature infants.
A frequent assessment of the neonate’s body weight is essential for fluid management.
The electrolyte content of the fluids administered should be guided by recent laboratory studies.
Insensible water losses are electrolyte free and should be replaced using 5% dextrose in water.
Important systemic disturbances that may arise secondary to AKI include hyperkalemia, hyponatremia, hypertension, hypocalcemia, hyperphosphatemia, and metabolic acidosis.
All exogenous sources of potassium should be discontinued in patients with AKI.
Despite this restriction, elevated serum potassium levels develop in many neonates and must be treated aggressively due to the potential for cardiac toxicity.
Treatment should be initiated by correction of metabolic acidosis with NaHCO3. A dose of 1–2 mEq/ kg should be given intravenously over a 10- to 20-minute period, provided that salt and water balance is not problematic.
The quantity of NaHCO3 that is needed also can be calculated in the following manner:
(0.3 × Body weight [kg] × Base deficit [mM]).
Associated hypocalcemia should be treated with the intravenous administration of 10% calcium gluconate at a dose of 0.5–1 mL/kg injected slowly over a 5- to 15-minute period with continuous monitoring of the heart rate.
If a progressive increase in the serum potassium concentration is noted, additional treatment measures may include the use of a sodium–potassium exchange resin (sodium polystyrene sulfonate in 20–30% sorbitol, 1 g/kg by enema), with recognition of its frequent ineffectiveness and/or associated complications (e.g., necrotizing enterocolitis) when used in infants with low birth weight.
The use of glucose (0.5–1 g/kg) followed by insulin (0.1–0.2 unit regular insulin per gram glucose over a 1-hour period) may be the preferred approach.
Either intravenous salbutamol or inhaled albuterol is an additional therapeutic option that shifts potassium into the intracellular compartment.
Dialysis should be considered if these measures prove unsuccessful.
Hyponatremia and systemic hypertension are most often related to overhydration in the infant with oliguria. These problems should be treated initially with fluid restriction or water removal with dialysis, if necessary.
The addition of high-dose intravenous furosemide (5 mg/kg) may be helpful.
Serum sodium levels below 125 mEq/L can be associated with seizures, and levels below 120 mEq/L should be corrected rapidly to at least 125 mEq/L by calculating the amount of sodium required in the following manner:
Na + (mEq) = ([Na+] Desired − [Na+] Actual) × Weight (kg) × 0.8
When serum sodium levels are less than 120 mEq/L and are associated with symptoms (e.g., seizures), prompt treatment with hypertonic (3%) saline is indicated.
The provision of 10–12 mL/kg of 3% saline is generally therapeutic.
The treatment of persistent hypertension may include parenterally administered hydralazine (0.1–0.4 mg/kg/ dose) or labetalol (0.2–1 mg/kg/dose or 0.25–3.0 mg/kg/h infusion).
Orally administered amlodipine (0.1–0.6 mg/ kg/dose) can be prescribed for the patient who is without symptoms.
Treatment of the patient with marked or refractory hypertension can include intravenous sodium nitroprusside (0.5–10 μg/kg/min infusion), nicardipine (0.5–4 μg/kg/min infusion), or labetalol.
Caution should be exercised when initiating therapy with captopril (initial oral dose, 0.01–0.05 mg/kg/dose), owing to the profound hypotension that can occur in neonates in association with higher doses.
In the infant in whom AKI does not fully resolve and progresses to CKD, the development of hyperphosphatemia (serum phosphorus level >7 mg/dL) necessitates the use of a low-phosphorus infant formula and possibly calcium carbonate (50–100 mg/kg/day) as a phosphate binder.
The use of aluminum hydroxide as a binder is contraindicated, owing to its association with aluminum toxicity in infants and children with renal insufficiency.
No experience has been published about the use of noncalcium-containing phosphate-binding agents, such as sevelamer, in the neonatal population.
Hypocalcemia, as reflected by a low total serum calcium level, often occurs in AKI in association with hypoalbuminemia.
Less commonly, the ionized calcium level is low and the patient is symptomatic.
In these cases, intravenous 10% calcium gluconate, 1–2 mL/kg, over a 5–10-minute period with cardiac monitoring, should be given until the ionized calcium level is restored to the normal range.
Metabolic acidosis can arise as a result of retention of hydrogen ions and may require NaHCO3 for correction. The dose of NaHCO3 to be given can be calculated as follows:
NaHCO 3 (mEq) = (Desired bicarbonate - observed bicarbonate) x weight (kg) x 0.5
This dose can be given orally or added to parenteral fluids and infused over several hours.
Adequate nutrition should be provided, with the goal of 100–120 calories and 1–2 g of protein/kg/day, provided intravenously or orally.
Additional protein may be needed to account for dialysis-related losses in patients receiving PD and CRRT.
For neonates who can tolerate oral fluids, a formula containing low levels of phosphorus and aluminum, such as Similac PM 60/40 (Abbott Labs, Abbott Park, IL) or Renastart (Vitaflo, Alexandria, VA) is recommended.
An aggressive approach to nutrition may well contribute to kidney recovery by providing necessary energy at the cellular level.
Although most neonates with AKI can be managed conservatively, occasional patients require PD or CRRT for the treatment of the metabolic complications and fluid overload.
The mortality rate in this group of patients can be exceedingly high in the setting of AKI after cardiac surgery.
Apart from the need for pressor support, in one report, CRRT was well tolerated in 85 children weighing less than 10 kg, with survival rates of 25% and 41% for those weighing less than 3 kg and 3–10 kg, respectively.
A recent retrospective study of PD treatment of AKI after cardiac surgery in 146 neonates and infants revealed that the mortality rate was decreased by more than 40% in those patients who received “early PD” (day of surgery or postoperative day 1) versus “delayed PD” (postoperative day 2 or later).
Another retrospective study of 435 neonates who underwent cardiac surgery emphasized the importance of fluid management because fluid overload of more than 16% was an independent risk factor for a poor outcome.
Finally, when AKI occurred in neonates receiving extracorporeal membrane oxygenation, the mortality rate was 3.2 times higher than in those without AKI.
Moreover, patients who required renal replacement therapy had a 1.9 higher odds of death than those who did not receive this treatment.
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What are the physiologic implications of obstructive uropathy in the neonate?
Obstructive uropathy in the neonate is the most common renal abnormality diagnosed prenatally and is most often the result of UPJ obstruction, UVJ obstruction, or PUV.
Obstruction also represents a significant cause of endstage renal disease in children, accounting for 13% of all cases.
Accordingly, early recognition and treatment of these lesions is desirable because of the adverse effects that obstruction can have on kidney function.
Regardless, after surgical intervention and relief of obstruction, alterations of GFR, renal blood flow, and renal tubular function can still occur.
Specifically, injury to the renal tubules can result in an impaired capacity to reabsorb sodium, to concentrate urine, and to secrete potassium and hydrogen, all of which can have profound clinical implications.
The resorption of other solutes, such as magnesium, calcium, and phosphorus, also may be affected.
The ability of the renal tubule to reabsorb salt and water after relief of obstruction typically depends on whether the obstruction is unilateral or bilateral.
In unilateral obstruction, the proximal tubules of the juxtamedullary nephrons are unable to reabsorb salt and water maximally, whereas the fractional reabsorption of salt and water is increased in the superficial nephrons.
However, the amount of sodium excreted by the previously obstructed kidney is not different from that of the contralateral kidney because tubuloglomerular balance is maintained.
In contrast, relief of bilateral obstruction or, on occasion, unilateral obstruction in neonates results in a postobstructive diuresis characterized by a marked elevation in the absolute amount of sodium and water lost.
In part, these changes are a result of an osmotic diuresis secondary to retained solutes, such as urea.
Some contribution also can occur from atrial natriuretic factor, the plasma level of which is elevated during obstruction, as well as from enhanced synthesis of prostaglandins.
Decreased renal medullary tonicity and decreased hydraulic water permeability of the collecting duct in response to ADH, the latter a result of reduced aquaporin channels, contribute to the impaired concentrating ability of the kidney.
The clinical conditions associated with prolonged salt wasting are severe volume contraction and circulatory impairment.
Conditions associated with the concentrating abnormalities are secondary nephrogenic diabetes insipidus and hyponatremic dehydration.
Accordingly, management must ensure the provision of adequate amounts of fluid and salt. Sodium intake should be monitored by serum and urine electrolyte determinations. Fluid intake should equal insensible losses, urine output, and nonrenal losses and should be guided by frequent assessments of body weight.
Ureteral obstruction also can result in the impairment of hydrogen and potassium secretion, and the syndrome of hyperkalemic, hyperchloremic metabolic acidosis, or type IV RTA.
This clinical situation appears to be the result of the impaired turnover of the sodium–potassium pump or a decreased responsiveness of the distal renal tubule to the actions of aldosterone.
In a portion of patients with this presentation, the FE Na is normal and the FE κ is inappropriately low, relative to the elevated serum level.
Treatment is directed toward correcting the underlying obstructive abnormality as well as providing NaHCO3 to alleviate the metabolic acidosis and hyperkalemia.
Finally, the outcome of obstructive uropathy in the neonate in terms of preservation of GFR is, in part, related to how promptly relief of obstruction occurs.
In these patients, the serum creatinine obtained at age 12 months has been shown to be predictive of long-term kidney function.
Attempts to preserve renal function with fetal surgery in the patient with obstructive uropathy have not proven to be successful.
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What are the causes of renovascular hypertension in children?
Hypertension in children and adolescents is defined as a blood pressure >95th percentile of normative blood pressures based on a 2017 clinical practice guideline published by the American Academy of Pediatrics.
It would be expected, therefore, that the prevalence of hypertension in the pediatric population would be approximately 5%, although epidemiologic studies have demonstrated a prevalence of approximately 3.2–3.4%.
With the rising rates of childhood obesity, it is expected that the prevalence of hypertension in children will increase.
The incidence of secondary causes of hypertension in children is inversely proportional to age. However, approximately 40–50% of adolescents aged 13–19 years will have a secondary cause of hypertension.
Table 4.4 lists some of the potential causes of secondary hypertension in children by organ system.
Among the correctable causes of hypertension is renovascular hypertension. Its reported frequency is variable, because prior publications have estimated a frequency ranging from 5–10% in children with hypertension (more common in younger children), although this percentage is likely decreasing with the rising incidence of obesity related hypertension.
PATHOPHYSIOLOGY AND ETIOLOGY
Delineation of the pathophysiologic mechanisms behind renovascular hypertension began in the late 1890s with identification that renal extracts could induce a rise in blood pressure. However, it was not until the work of Henry Goldblatt that it became clear that renal artery stenosis was directly related to the development of hypertension. Despite these early breakthroughs, it was not until the late 1950s–1960s that a greater understanding of the reninangiotensin pathway revealed the pathophysiologic mechanisms behind renal artery stenosis and the development of hypertension.
Fig. 4.2 demonstrates the basic sequence of events arising from renal artery stenosis that leads to the development of hypertension.
The most common cause of renovascular hypertension in children is fibromuscular dysplasia (FMD), accounting for up to 60% of cases.
Other causes include vasculitis such as Takayasu arteritis, mid-aortic syndrome, and, less commonly, trauma, thrombosis, umbilical artery catheterization in neonates, Kawasaki disease, arterial hypoplasia/aplasia, tumors associated with neurofibromatosis type 1 and tuberous sclerosis, and Williams syndrome.
FMD is a nonatherosclerotic, noninflammatory disease that affects small to medium-sized arteries. Its precise pathophysiologic mechanisms are unknown, but there are clear genetic components to the disease given its tendency to run in families and its increased prevalence in Caucasians.
Whereas FMD is most commonly seen in the renal vascular bed, it can also involve the extracranial carotid arteries, external iliac arteries, and the mesenteric vasculature.
The pathologic classification scheme for FMD is based on the layer of the vessel wall predominantly affected, with the most common presentation being medial fibroplasia. This is characterized by the classic “string of pearls” appearance seen on arteriography.
The other classifications, intimal and adventitial hyperplasia, are much less commonly seen.
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How are patients with renovascular hypertension diagnosed?
There are no evidence-based guidelines to identify children with hypertension who may be more likely to have renovascular disease.
The diagnosis of renovascular hypertension cannot be made by any specific historical or physical examination finding.
Similarly, no specific laboratory study can lead to the diagnosis.
Serum renin and aldosterone levels can be elevated in renovascular hypertension, but are rarely diagnostic. Inflammatory markers, such as erythrocyte sedimentation rate (ESR) and C-reactive peptide (CRP) can indicate potential arteritis but are not diagnostic.
The definitive diagnosis of renovascular hypertension, in turn, depends on the findings of imaging studies.
Ideally, the evaluation in children should occur in a tertiary care center with pediatric radiology expertise whenever possible.
Table 4.5 summarizes the sensitivity and specificity of available imaging modalities.
Doppler ultrasound (US) has been a popular screening test in pediatrics due to its noninvasive nature and the lack of radiation exposure.
However, studies have demonstrated that Doppler US has a sensitivity of only 73–85% in adults for the diagnosis of renovascular disease, rendering this study unacceptable for diagnosis.
Computed tomography angiography (CTA) (Fig. 4.4) and magnetic resonance angiography (MRA) have been growing in popularity as diagnostic tools for renovascular disease due to the clear images of the major abdominal vessels.
CTA, however, is limited by the radiation exposure, and studies in adults have demonstrated a variable sensitivity of 64–94% for diagnosis of renovascular disease.
Similarly, MRA is limited by the need for sedation in young children, and contrast exposure is contraindicated in patients with severe CKD.
MRA in studies in adults has performed comparably with CTA and with near identical sensitivity (6493%) for renovascular disease.
Nuclear medicine studies such as captopril renal scintigraphy or technetium-labeled pentetic acid (DTPA) radionucleotide fractional-flow studies have been used to make the diagnosis of unilateral disease.
Unfortunately, bilateral disease can occur in >50% of patients, making these studies of limited utility due to the lack of internal nondiseased control imaging.
In one study evaluating pediatric patients with renovascular disease diagnosed by angiography, captopril scintigraphy was found to have a sensitivity of only 47%.
Due to the inherent limitations of these imaging studies, conventional arteriography remains the gold standard for the diagnosis of renovascular disease.
Other diagnostic techniques, such as differential renal vein renin sampling, can be performed during the intervention.
Arteriography often can be coordinated to be a part of a joint diagnostic and therapeutic intervention, as discussed in the following section.
Therefore, most children with hypertension and significant concern for renovascular disease should undergo arteriography.
H&A
A healthy term baby is born weighing 3.5 kg after having antenatal diagnosis of bilateral hydroureteronephrosis.
He had a micturating cystourethrogram, as shown in Figure 54.1.
Which of the following is the most likely diagnosis?
A bilateral pelviureteric junction obstruction
B bilateral vesicoureteric reflux
C bilateral vesicoureteric junction obstruction
D posterior urethral valves
E ureterocele
D
This micturating cystourethrogram shows a dilated posterior urethra with trabeculated bladder consistent with posterior urethral valves.
SPSE 1
A healthy term baby is born weighing 3.5 kg after having antenatal diagnosis of bilateral hydroureteronephrosis.
He had a micturating cystourethrogram, as shown in Figure 54.1
What treatment option should be considered?
A deflux procedure
B intravenous antibiotics
C oral prophylactic antibiotics
D re-implantation of ureters
E watchful expectancy
C
He requires insertion of urinary catheter, commencing on prophylactic antibiotics, and paediatric surgical/urological referral.
If there is significant renal impairment due to bilateral renal dysplasia, then referral to a paediatric nephrourological unit is required.
SPSE 1
