The answer of case 2 renal failure

 1. Studies have shown that almost 100% of newborns have 

the first void within 24 hours after birth and nearly half of 

them void 8 hours after birth (Clark, 1977). Although very 

few infants of less than 32 weeks’ gestation were documented in these studies and the time of the first void varies considerably, failing to pass urine beyond 24 hours 

should prompt the physician to evaluate and intervene for 

newborns of any gestational age.

2. She required resuscitation at birth and has a persistently 

low blood pressure that may be limiting perfusion of vital 

organs, including the heart and kidneys. Prolonged hypotension could serve as a prerenal etiology for acute ischemic and hypoxic injury to the kidney and should be 

corrected immediately. A normal saline infusion at 10 mL/kg (over 30 minutes) can be given at this time, and a re-

peated dose with the same volume could be considered if 

there is no significant improvement in the blood pressure. 

A renal ultrasound is also recommended. She needs fre-

quent monitoring of respiratory, cardiac, and fluid status. 

Placement of a Foley catheter is recommended to drain 

the urine from the bladder and for subsequent monitoring 

of urine output. If the blood pressure remains low despite 

the fluid boluses, consideration should be given to use of 

a pressor such as dopamine.

3. Aminoglycosides are frequently used to treat infants with 

the possibility of sepsis due to their fast bactericidal effect, 

synergy with b-lactam antibiotics, and low cost. However, 

they can accumulate in tissues such as the kidney and the 

ear, causing nephrotoxicity and ototoxicity. Gentamicin is 

one of the most nephrotoxic and best-studied aminoglycosides (Lopez-Novoa et al, 2011). The kidney excretes gentamicin, which can be toxic to all compartments of the 

kidney. The incidence of gentamicin nephrotoxicity ranges 

from 10% to 25%. Risk factors contributing to its toxicityinclude reduced renal mass, intravascular volume deple tion, long duration and high dose of treatment, and  

concomitant use of other nephrotoxic medications. Gentamicin causes apoptosis and necrosis of renal tubular cells,  

especially epithelial cells of the proximal tubules, by complex mechanisms including phospholipidosis, reduced ATP  

production in the mitochondria, and increased oxidative

stress. Death of tubular cells results in tubular obstruction

and increased hydrostatic pressure in the tubular lumen

and the Bowman capsule, leading to a reduced filtration

pressure gradient and a low glomerular filtration rate

(GFR). Cell death is accompanied by interstitial inflammation. Injury to epithelial cells interferes with ion transport  

and may result in nonoliguric or polyuric renal failure.

Excessive delivery of water and solutes to the distal nephron triggers tubuloglomerular feedback (tubuloglomerular  

feedback is one of several mechanisms the kidney uses to

regulate glomerular filtration rate) further reducing GFR.

In addition, gentamicin can cause direct functional alterations in the glomerulus and increase resistance of renal  

vasculature, thus reducing renal blood flow. Because its

toxicity is usually related to blood concentration and duration of treatment, close monitoring of drug levels is required before subsequent administration, especially when  

renal compromise is suspected. In this case the patient has

an increased risk for gentamicin toxicity because of low

nephron numbers from prematurity, possible higher drug levels from decreased blood flow to the kidneys, and renal  

hypoperfusion secondary to the low blood pressure. Improving her systemic circulation with fluid and inotropic  

agents, if indicated, may help reduce renal injury