The stressed neonatal kidney: from pathophysiology to clinical management of neonatal vasomotor nephropathy

The healthy term, and particularly the premature infant, is born with a ver y low glomerular filtration rate (GFR), controlled by a delicate balance of intrarenal vasoconstrictor and vasodilator forces. Vasoactive disturbances can easily further reduce the already low GFR. The newborn infant is thus prone to develop vasomotor nephropathy (VMNP) or acute renal failure (ARF). The main causes for ARF at this young age are prerenal mechanisms, and inc lude hypotension, hypovolemia, hypoxemia perinatal asphyxia, and neonatal s epticemia. Other causes include the administration of angiotensin convertin g enzyme inhibitors, indomethacin and tolazoline. The most-important factor s governing the ultimate renal prognosis are the severity of the underlying disorder, the rapidity of an accurate diagnosis, prompt treatment, and avo idance of severe iatrogenic complications. The immediate treatment is of pa rticular importance in VMNP, i.e., prerenal ischemic ARE and consists of co rrecting abnormalities in fluid homeostasis and reduction of the complicati ons of the acute azotemic state (uremia, hyperkalemia, acidosis, and hypert ension). In severe and prolonged (established) ARF, temporary dialysis ther apy may be indicated. Prerenal ARF with oliguria or anuria warrants immedia te volume resuscitation. Special attention should be given to infants with congestive heart failure (CHF). The sick neonate with persistent oliguria a nd CHF should be treated with intravenous dopamine. Furosemide (FM) is the second line of therapy for babies with indomethacin-induced ARE In most oth er conditions, the therapeutic effect of FM is limited to a transient incre ase in urine flow, without improving basic renal function. The special cond itions of the maturing kidney have to be appreciated in order to protect ba bies from undue renal injury. With the increasing knowledge of the mechanis ms governing the development of ARF, progress has been made in the developm ent of new treatment modalities. For example theophylline, calcium antagoni sts, ATP-MgCl2, thyroxine, and a variety of cytokines may in the near futur e be used to prevent or ameliorate VMNP and/or recently established ARE Wit h a combination of time-honored and new therapeutic strategies, there may w ell be a brighter future for neonates with vasomotor, prerenal, ischemic AR F.