Saudi Journal of Kidney Diseases and Transplantation

ORIGINAL ARTICLE
Year
: 2011  |  Volume : 22  |  Issue : 6  |  Page : 1187--1192

Acute renal failure: Nephrosonographic findings in asphyxiated neonates


Mohd. Ashraf1, Nazir Ahmed2, Javed Chowdhary2, Riyaz U Saif3,  
1 Department of Pediatrics, Shere-i-Kashmir Institute of Medical Sciences (SKIMS) Medical College, Bemina, Srinagar, India
2 Department of Pediatrics, GMC, Srinagar, India
3 Department of Gastroentrology, Shere-i-Kashmir Institute of Medical Sciences, Soura, Srinagar, India

Correspondence Address:
Mohd. Ashraf
Registrar in Pediatrics, Shere-i-Kashmir Institute of Medical Science (SKIMS) Medical College, Srinagar
India

Abstract

To determine the incidence of acute renal failure (ARF) and nephrosonographic findings among asphyxiated neonates, and to correlate this with uric acid levels and the severity of hypoxic encephalopathy, we studied 80 full-term appropriate-for-date singleton neonates with perinatal asphyxia, and 30 healthy full-term neonates as controls from March 2006 to February 2007. A detailed history, thorough clinical examination along with investigations, including urine examination, 24-h urine collection, ultrasonography of abdomen and cranium, serum electrolytes, blood urea nitrogen, serum creatinine, and serum uric acid were obtained. ARF developed in 45% (36/80) of the asphyxiated neonates. Forty-eight (60%) neonates showed significant elevation of blood urea and 41 (51.3%) neonates had significant elevation of serum creatinine than the control group (P < 0.001). Sixty-two (77.5%) neonates developed significant elevation of serum uric acid levels, and nephrosonography revealed hyperechogenicity in all of them, while only two among the healthy neonates showed the raised uric acid levels (P < 0.001). Nonoliguric renal failure was seen 28/36 (77.8%) of the neonates with ARF, whereas eight (22.2%) neonates had oliguric renal failure. Eight (27.8%) patients among ARF patients maintained abnormal biochemical parameters after 2 weeks, and of whom four patients died after variable lengths of time with a mortality rate of 11.11%. Kidneys are the most common organs involved in perinatal asphyxia, and uric acid might be a causative factor for failure in addition to hypoxic insult. Routine use of kidney function test, along with abdominal ultrasonography form an important screening tool to detect any additional morbidity in these patients.



How to cite this article:
Mohd. Ashraf, Ahmed N, Chowdhary J, Saif RU. Acute renal failure: Nephrosonographic findings in asphyxiated neonates.Saudi J Kidney Dis Transpl 2011;22:1187-1192


How to cite this URL:
Mohd. Ashraf, Ahmed N, Chowdhary J, Saif RU. Acute renal failure: Nephrosonographic findings in asphyxiated neonates. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2022 Oct 6 ];22:1187-1192
Available from: https://www.sjkdt.org/text.asp?2011/22/6/1187/87230


Full Text

 Introduction



Perinatal asphyxia refers to a condition of impaired gas exchange that results, if persistent, in fetal hypoxemia and hypercarbia. [1] Perinatal asphyxia is an important cause of mortality and morbidity in the newborn infant and of neurologic disability, mainly cerebral palsy (CP) in later life, accounting for one third of the cases of neurologic deaths. [2],[3] However, only 3%-13% of infants with CP had evidence of actual intra-partum hypoxia. [4]

Renal system is involved in about 50% of the cases of perinatal asphyxia. Conversely, perinatal asphyxia producing ischemia is the commonest cause of neonatal renal failure. [5],[6] All difficult deliveries requiring resuscitation at birth cause an initial episode of shock and renal ischemia, which triggers a transient ischemic state sensitive to oxygen deprivation and within 24 h of the ischemic episode, renal insufficiency occurs, which if prolonged may lead to circulatory cortical or medullary necrosis. [7],[8] Renal vascular resistance is greater while renal blood flow is lesser in newborn compared with adults, and renders the kidneys more susceptible to severe renal failure. [9] The aim of this study is to evaluate in hospitalborn asphyxiated neonates with respect to renal involvement, serum uric acid levels, and nephrosonographic findings.

 Patients and Methods



The study included 110 term neonates (gestation 37-42 weeks), from March 1, 2006 to February 28, 2007 (80 asphyxiated and 30 healthy controls), born in our hospital, and those referred from adjoining LD Hospital, Associated Hospitals of Government Medical College (GMC), Srinagar, and admitted in the neonatal section of Department of pediatrics G. B. Pant General Hospital, Srinagar.

An Apgar score (A/S) of ≤7 at 5 min of life was taken as a criterion for inclusion in the study as a case of perinatal asphyxia. However, preterm and low birth weight neonates were excluded from the study as A/S may be low in them even without asphyxia, [10] and also because of immature renal functions in preterm neonates. Similarly, such neonates who had any problems, such as jaundice at birth, septicemia, heart disease, hepatosplenomegaly, congenital abnormality of kidneys and urinary tract, perinatal exposure to medicine that might change renal hemodynamics, polycythemia, pharmacologic depression, and twining were excluded from the study as these could have acted as confounding factors. [11]

Clinical data obtained from each neonate, was recorded by pediatric residents attending the deliveries. Based on clinical examination at 5 min of life, neonates who had Apgar scoring ≤ 7 were included in the study. Similarly, neonates were classified as per the degree of hypoxic insult to central nervous system, referred as hypoxia ischemic encephalopathy (HIE). Neonates who had hypoxic insult but no central nervous system (CNS) involvement were considered as HIE stage-0. Other neonates who had CNS insult were grouped using Fenichel HIE staging [12] system, a modified version of Sarnat and Sarnat HIE staging system, as HIE stage-0, HIE Stage-I, HIE Stage-II, and HIE Stage-III. All the cases were subjected to sampling instantaneously and at 24-72 h of age by drawing 5 mL of blood with aseptic precautions and a disposable syringe from any large peripheral vein for various tests.

Renal function tests (blood urea and serum creatinine levels) were repeated, in case they were found abnormal in the first instance. Simultaneously retained serum was sent for uric acid estimation. Twenty-hour urine output collection was measured using self-adhesive plastic urine collecting bags and sent for routine and 24-h urine examination.

For blood urea, diacetyl monoxime [13] (DAM) Method; serum creatinine: Jaff's reaction [13] (picric acid reaction); serum uric acid: phototungsten method [13] ; urine protein [14] : Albustix (plastic strip with the indicator), bromophenol blue and a citrate buffer; and Serum electrolytes (S·Na + S·K + ), electronic analyzer (Biolyte 2000 EC-REP, Nova Biochemical, UK), were used. Routine examination of urine, [15] both macroscopic and microscopic methods, abdominal ultrasound, and cranial ultrasonography were done in every case. Statistical analysis was done by using Chi-square test.

 Results



The demographic details and laboratory findings of the 80 asphyxiated neonates and the 30 controls are shown in [Table 1] and [Table 2], respectively. The asphyxiated group revealed significantly higher levels of blood urea, serum creatinine, and serum uric acid levels than the control group (P < 0.001). Similarly, abnormal urine examination and decreased urine output were encountered more in the asphyxiated neonates than in the controls. Renal ultrasonography done on day one, three and seven, revealed hyperechogenicity of kidneys in 59/80 (73.8%), well correlated with the severity of the hypoxic encephalopathy and elevated serum uric acid levels. Overall, we observed an incidence of 45% (36/80) of acute renal failure (ARF), more so in the severely asphyxiated neonates (P < 0.001; all of them had hyperechogenicity on nephrosonography, and raised serum uric acid levels in 77.5% (62/80), while none among the healthy controls developed the ARF; however, two among them were having raised levels of uric acid levels. Nonoliguric renal failure was seen in 77.77% (28/36) of the ARF patients, while 22.22% (8/36) developed oliguric renal failure.{Table 1}{Table 2}

Elevated uric acid levels, deteriorated renal function, and abnormal urinalysis were observed in 62 patients; the majority was from HIE stages II and III. The majority of the asphyxiated neonates showed improvement in renal function and sonographic findings over a period of two weeks. However, eight neonates among the asphyxiated group having blood urea levels ≥ 50 mg/dL and serum creatinine levels > 1.6 mg/dL, showed persistently abnormal renal functions, serum uric acid levels, and sonographic findings. They were followed-up for a variable length of time; and four among them died.

 Discussion



The striking result in our study was the high incidence of nonoliguric renal failure 77.77% (28/36) in asphyxiated neonates. This reflects a mild injury to the kidneys in the majority of them. [16] However, kidneys are very sensitive to oxygen deprivation and injury may result in permanent renal impairment in up to 40% of survivors. [17] Hence, renal function should be closely monitored in all asphyxiated neonates, as renal dysfunction is the most common involvement perinatal asphyxia. [18]

We observed an incidence of ARF in 45% of the asphyxiated neonates and none among the controls developed the ARF. We labeled a neonate of having ARF if three of the following criteria were persistently present: (a) elevated of blood urea; (b) elevated serum creatinine; (c) oliguria; (d) or hematuria and proteinuria. Accordingly, the incidence of ARF was similar to earlier studies. [17],[19],[20] However, Dauber et al [21] studied seven infants born with a 1 min A/S of ≤5 for renal parameters and observed that 57% developed ARF.

The difference between theirs and the present study could be because they studied only a group of neonates with moderate to severe asphyxia (A/S ≤5). Furthermore, Mohan et al [22] reported an incidence of 72% in asphyxiated neonates with an overall mortality of 36%, which could be because of employing highly sensitive tests, such as measurements of β2 M, functional excretion of sodium, renal failure index along with urine/plasma ratio of creatinine.

The present study revealed a higher level of uric acid in asphyxiated neonates, which is comparable to earlier studies. [23],[24],[25],[26] Newborns generally have a transient elevation of serum uric acid concentration. The association between increased uric acid production and perinatal asphyxia is well recognized. [26] It seems possible that the increased uric acid production associated with perinatal asphyxia leads to deposition of uric acid in the renal tubules, producing tubular obstruction and subsequent renal dysfunction that can also be due to the nephrotoxic nature of the uric acid. As the renal uric acid load is excreted, normal kidney function is restored. Therefore, uric acid may account for the increased echogenicity of the renal medullary pyramids, and the transient reduced kidney function also supports the hypothesis that serial renal ultrasonographic examinations of patients with Lesch-Nyhan syndrome, a syndrome characterized by hyperuricemia, have revealed hyperechoic renal medullary pyramids. [27] Although there seems to be a positive correlation between the elevated uric acid levels abnormal renal functions, this cannot be considered as a cause and effect relationship due to the presence of other confounding factors.

Ultrasonography of kidney showed diffuse hyperechogenicity in 73.75% (59/80), and it returned to normal over a period of two weeks, except in those who disclosed persistently very high levels of blood urea, serum creatinine, and uric acid for more than two weeks accounting for 10% (8/80) in our study and is comparable to earlier studies. [28] Similar findings may be seen in renal vein thrombosis, hydronephrosis, polycystic kidneys, in addition to a rare and important entity of neonatal transient renal failure with renal medullary hyperechogenicity, and they should be in the differential diagnosis of ARF in the asphyxiated neonates. [29]

The normal sonographic appearance of the neonatal kidney differs greatly from that of older children. The renal medullary pyramids are hypoechoic when compared with the renal cortex, where echogenicity is comparable with the liver and spleen. [30] Increased echogenicity of the renal pyramids during the neonatal period has been associated with serious renal disease, including renal vein thrombosis, nephrocalcinosis, congenital nephrotic syndrome, and cystic kidney disease. [31],[32] The figures in our study do not represent the absolute incidence of ARF, because the number presented here include only hospital born infants, and exclude those who die before reaching the hospital or who are born in far-flung areas and do not reach hospitals due to various reasons.

Out of 80 asphyxiated neonates 36 (45%) developed ARF, and 8 (27.8%) persisted with abnormal renal functions and 4 among them succumbed to renal insult producing a mortality rate of 11.11% among the ARF patients, which is similar to study done by Gupta et al, [17] but contrary to the studies done by Saili et al [19] and Dauber et al, [21] which can be explained on the basis of less number of patients and severity of birth asphyxia they have considered.

In conclusion, ARF represent a significant problem among asphyxiated neonates. All of the hyperechogenic kidney patients were also hyperuricemic, which supports the possible association between both features. In addition, uric acid itself might be the causative factor for failure in addition to hypoxic and ischemic insult. We recommend kidney functions, and abdominal ultrasonography to be done routinely in asphyxiated neonates to evaluate the possibility of acute kidney injury in them.

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