Acute renal failure in the newborn diagnosis & management

Acute renal failure in the newborn ,c/f ,dx & treatment (cont.)
Tej K Mattoo, MD, DCH, FRCP

[size=18]CLINICAL PRESENTATION — ARF is suspected in newborns who have an elevated or rising serum creatinine and/or anuria/oliguria. Oligoanuria is defined as no urine output noted by 48 hours of age or a diminished urine output (urine volume less than 1.0 mL/kg per hour). Although the time of the first void is variable, at least 50 percent of newborns void by eight hours of age and nearly all before 24 hours [33]. However, the presence of urine does not rule out ARF since some infants are nonoliguric [34]. This could reflect volume expansion and/or tubular dysfunction, as seen in obstructive uropathy and other disorders. An elevated or rising serum creatinine (>1.5 mg/dL [133 micromol/L] is an indicator of a reduction in GFR, which is the hallmark of ARF.

ARF also may be associated with a number of other laboratory abnormalities, including hyponatremia, hyperkalemia, hyperphosphatemia, hypocalcemia, and acidosis:

Hyponatremia — Hyponatremia almost always results from the intake of water that cannot be excreted due, for example, to ARF.

Hyperkalemia — Potassium excretion generally remains at near-normal levels in patients with renal disease as long as both aldosterone secretion and distal flow are maintained. Thus, hyperkalemia usually develops in a newborn who is oliguric or who has an additional problem, such as increased tissue breakdown or impaired aldosterone secretion due to congenital adrenal hyperplasia.

Metabolic acidosis — Acid-base balance is normally maintained by renal excretion of the acid load (approximately 1 meq/kg per day), derived mostly from the generation of sulfuric acid during the metabolism of sulfur-containing amino acids. Elimination of this acid load is achieved by the urinary excretion of hydrogen ions. Thus, ARF may lead to hydrogen retention and metabolic acidosis.

Hyperphosphatemia — The kidney also plays a major role in phosphate excretion. Thus, ARF, particularly if moderate to severe, can lead to hyperphosphatemia.

Hypocalcemia — Hypocalcemia is a less common problem that can be caused by hyperphosphatemia and other factors. .

Variable degrees of edema are common in newborns with ARF, who are usually critically ill. This can result from capillary leak, heart failure, or renal failure itself.

DIAGNOSIS — As mentioned in the preceding section, ARF should be suspected in a newborn with no urine output noted by 48 hours of age, a diminished urine output (less than 1.0 mL/kg per hour), or an elevated serum creatinine concentration (>1.5 mg/dL [133 micromol/L]). The next step is to determine the cause of ARF, which is made on the basis of a careful history and physical examination and laboratory and imaging studies.

History — The history should include prenatal conditions such as oligohydramnios, polyhydramnios, renal abnormality detected on antenatal ultrasound examination, and antenatal medications. Neonatal conditions that may be associated with ARF include prematurity, perinatal asphyxia, respiratory distress syndrome, sepsis, umbilical artery catheterization, drug administration at or soon after birth, volume depletion, delayed first urine output, and an abnormal urine stream in males. Family history should be obtained for conditions including congenital nephrotic syndrome, polycystic kidney disease, diabetes insipidus (which can cause marked hypovolemia and hypernatremia if the urinary losses are not replaced), or any other renal disease. These disorders are discussed in the appropriate topic reviews.

Physical examination — Findings on the physical examination that may be associated with ARF include edema, elevated or diminished blood pressure, enlarged or absent kidneys, and a distended bladder. Dysmorphic features should also be noted, including meningomyelocoele, anal atresia, prune belly syndrome, or facial and limb deformities associated with oligohydramnios resulting from decreased fetal urine production.

Serum creatinine — Estimation of the GFR, usually by measurement of the serum creatinine concentration, is used clinically to assess the extent of renal impairment and to follow the course of the disease. It is important to recognize that estimation of the GFR has no diagnostic utility; as described below, the urinalysis is an important initial diagnostic tool.

The serum creatinine concentration at birth is similar to that in the mother (usually less than 1.0 mg/dL [88 micromol/L]). It declines to normal values (serum creatinine 0.3 to 0.5 mg/dL [27 to 44 micromol/L]) in approximately one week in term infants and two to three weeks in preterm infants. However, the serum creatinine concentration may increase after birth, especially in very preterm infants [35]. This effect appears to be mediated by tubular reabsorption of creatinine [35], a finding not seen in older children and adults in whom creatinine excretion is determined solely by the GFR and tubular creatinine secretion, not reabsorption.

This was illustrated in a retrospective study of preterm infants with birth weights 1500 g from a single center [36]. Infants were excluded if they were anuric/oliguric, treated with indomethacin, amphotericin, inotropes (eg, epinephrine, dobutamine, dopamine), diuretics, or high ventilator settings, had major anomalies, or received a five-minute Apgar score below five. The following findings were noted in 138 infants who met inclusion criteria: Serum creatinine decreased steadily from day two (0.75 ± 0.22 mg/dL [66.3 ±19.4 micromol/L]) to day six (0.67 ± 0.22 mg/dL [59.2 ± 19.4 micromol/L]. In a subset analysis, infants with birth weights <1000 g, had an initial increase in serum creatinine and serum creatinine values did not differ between days 2 and 6 of life. In this study, 89 percent of patients received gentamicin, 48 percent xanthines, and 21 percent received respiratory support (eg, mechanical ventilation of continuous positive airway pressure [CPAP]).

ARF is diagnosed if the creatinine concentration is >1.5 mg/dL (133 micromol/L) or increasing by at least 0.2 to 0.3 mg/dL (17 to 27 micromol/L) per day. A BUN >50 mg/dL (17.9 mmol/L) is also consistent with ARF but can result from increased urea production due, for example, to increased tissue breakdown.

Urinalysis — The urinalysis is the most important noninvasive test in the diagnostic evaluation, since characteristic findings on microscopic examination of the urine sediment suggest certain diagnoses. (See "Urinalysis in the diagnosis of renal disease" and see "Diagnosis of acute tubular necrosis and prerenal disease"). The urinalysis is relatively normal in prerenal disease, most cases of urinary tract obstruction, and some cases of ATN. The presence of muddy brown granular casts and epithelial cell casts is highly suggestive of ATN (show sediment 1A-1C). However, the absence of these urinary findings does not exclude the diagnosis. The presence of red blood cells, tubular cells, and proteinuria indicates intrinsic renal disease. However, microscopic hematuria should be interpreted cautiously, as it commonly occurs in urine samples obtained by bladder catheterization.

Complete blood count — A complete blood count should be performed to identify hematologic abnormalities. Infants with ARF due to thrombotic complications such as bilateral renal vein thrombosis may have polycythemia or thrombocytopenia.

Urine sodium excretion — Measurement of the urine sodium concentration is helpful in distinguishing prerenal from intrinsic renal disease. The gold standard in the studies that evaluated the diagnostic accuracy of the urine sodium concentration was the response to volume repletion. Recovery of renal function within 48 hours was considered diagnostic of prerenal disease, while persistent renal failure was considered to represent intrinsic renal disease.

The urine sodium concentration usually is less than 20 to 30 meq/L in prerenal disease. Since the kidney is sensing underperfusion and tubular function is intact, the kidney is responding appropriately by limiting sodium excretion and preventing further volume loss. In contrast, the urine sodium concentration is typically above 30 to 40 meq/L with intrinsic renal disease. This can occur because tubular function is impaired, as in ATN. It also represents the normal value in infants who are not volume depleted and therefore not sodium avid, as in those with renal and urinary tract abnormalities.

However, there is substantial overlap in the urine sodium concentration, due in part to variations in the urine volume. As an example, a child with diabetes insipidus will have a low urine sodium concentration even though sodium excretion may not be reduced.

The urine sodium concentration also may be misleading if measured after the administration of volume expanders or inotropic agents, which can restore renal perfusion in an infant with prerenal disease, or after the administration of diuretics, which directly impair sodium reabsorption.

FENa — The potentially confounding effect of the urine volume on the urine sodium concentration can be removed by calculating the fractional excretion of sodium (FENa). The FENa, which represents the fraction of the filtered sodium load that is excreted, is calculated from the following equation:

UNa x PCr

FENa, percent = ————————— x 100

PNa x UCr

where UCr and PCr are the urine and plasma creatinine concentrations, respectively, and UNa and PNa are the urine and plasma sodium concentrations, respectively. Note that the urine volume is not part of the equation.

A related formula called the renal failure index (RFI) is similar to the FENa except that the plasma sodium concentration is not included. This formula is similar to and as useful as the FENa but will not be discussed further here.

The FENa is a more accurate screening test than the urine sodium concentration alone to differentiate between prerenal and intrinsic ARF. However, values of FENa overlap in newborns with and without ARF, which limits its clinical usefulness compared to older children and adults [2,37]. In general, a value below 2 percent suggests prerenal disease, since the reabsorption of almost all of the filtered sodium represents an appropriate response to decreased renal perfusion. FENa values in prerenal newborns are higher than those in older children (less than 2 percent versus less than 1 percent) because of their decreased ability to reabsorb sodium. A value above 2.5 to 3 percent usually indicates intrinsic disease in the absence of diuretic therapy [31,38].

The FENa appears to be less useful in preterm infants, although data are limited. One report evaluated 72 oliguric infants 25 to >37 weeks gestation [39]. The following findings were noted: FENa >3 percent differentiated intrinsic from prerenal ARF in infants >31 weeks gestational age FENa >6 percent was consistent with intrinsic ARF in infants 29 to 30 weeks gestational age Because of overlap, the FENa was not useful in infants <28 weeks gestation

Urine osmolality — Term infants are able to concentrate the urine to more than 400 mosmol/kg. Hypovolemia is a potent stimulus to the release of antidiuretic hormone; as a result, prerenal disease is typically associated with a urine osmolality above 400 mosmol/kg. Such a concentrated urine suggests prerenal disease, while lower values in a hypovolemic newborn are consistent with intrinsic renal disease, which impairs concentrating ability (as may occur with ATN, dysplastic kidneys, or obstructive uropathy), but do not exclude prerenal disease [6].

Urine specific gravity is too variable to be used as a diagnostic tool. This is because proteins and glucose alter the correlation between osmolality and specific gravity, and their regulation is not as stable in newborns as in older children.

Renal imaging — Renal ultrasound examination is the initial imaging study to evaluate newborns with ARF. Depending upon the clinical circumstances, voiding cystourethrography and radionuclide scintigraphy may be useful.

Renal ultrasound — Renal ultrasound examination is used to document the presence of one or two kidneys, delineate renal size and shape, help evaluate the renal parenchyma for the presence of echogenicity or cysts, and to help detect urinary tract obstruction. The absence of hydronephrosis and hydroureter and a normal size bladder with normal emptying rules out urinary tract obstruction. Simultaneous Doppler examination allows assessment of renal blood flow and can help diagnose occlusion of the major renal vessels.

Voiding cystourethrogram — A voiding cystourethrogram (VCUG) should be performed to rule out vesicoureteral reflux in newborns with renal anomalies detected on ultrasound. In infants with urinary tract obstruction, a VCUG is also used to identify associated reflux and to evaluate the anatomy of the ureters and bladder.

Radionuclide scintigraphy — Radionuclide scintigraphy can be used to demonstrate renal structure and function. Renal function and blood flow can be assessed using isotopes such as DTPA or MAG 3 that are handled by glomerular filtration. The renal cortex can be evaluated using isotopes such as technetium-99m-dimercaptosuccinic acid (DMSA) that bind to renal tubules.
Although these studies are difficult to accomplish in sick infants, they are essential in newborns with prolonged anuria to evaluate ischemic renal damage (cortical necrosis) or urinary tract obstruction.

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» Acute renal failure in the newborn ,management(cont.)
» Acute renal failure in the newborn etiology & pathophysiology
» Prevention of acute renal failure in children
» الفشل الكلوي الحاد Acute Renal Failure
» Renal Biopsy