management of acute renal failure in children

SympoSium: nephrology

Management of acute renal failure in childrenmohan Shenoy

nick plant

AbstractThe term acute kidney injury (AKi) has replaced acute renal failure,

recognizing that an acute decline in renal function is often secondary to

an injury or insult. The incidence of AKi was 8 per million total popula-

tion in a uK retrospective study. AKi is classified into three groups: pre-

renal, intrinsic renal and obstructive post-renal AKi. haemolytic uraemic

syndrome and acute tubular necrosis (ATn) are the most common causes

in children. This review discusses the clinical evaluation, investigation

and management of AKi and its associated complications. The prognosis

for AKi depends upon the underlying cause. it is good for ATn and inter-

stitial nephritis but AKi following cardiac surgery has the worst outcome.

other poor prognostic factors include multiorgan failure, inotropic sup-

port, ventilation and need for dialysis therapy. AKi due to primary renal

disease is not common but is the cause for the majority of children who

need chronic dialysis therapy. All children with AKi who require renal re-

placement therapy need long-term follow-up to monitor blood pressure,

proteinuria and renal function.

Keywords acute kidney injury; aetiology; children; management;

prognosis; prevention

Introduction

Acute renal failure (ARF) is a common problem characterized by abrupt increase in blood levels of creatinine and nitrogenous waste products like urea with or without reduction in urine out-put. ‘ARF’ has been replaced by the term ‘acute kidney injury (AKI)’, recognizing that an acute decline in renal function is often secondary to an injury or insult that causes functional or structural changes in the kidney.1

Definition

There is no widely agreed definition of AKI and this has been a major constraint in assessing interventions to improve outcome of AKI. To overcome this, a recent conference reached the follow-ing consensus definition: an abrupt (less than 48 h) reduction in

Mohan Shenoy MBBS MRCPCH is Consultant Paediatric Nephrologist at

the Department of Paediatric Nephrology, Royal Manchester Children’s

Hospital, Manchester M27 4HA, UK.

Nick Plant MBBCH MRCP FRCPCH is Consultant Paediatric Nephrologist at

the Department of Paediatric Nephrology, Royal Manchester Children’s

Hospital, Manchester M27 4HA, UK.

pAeDiATriCS AnD ChilD heAlTh 18:8 37

kidney function evidenced by an absolute increase in serum creat-inine concentration by either greater than 0.3 mg/dl (greater than 26.4 μmol/litre) or an increase of greater than or equal to 50% or a reduction in urine output (less than 0.5 ml/kg/h for 6 h).1

Epidemiology

The problems with establishing a definition mean that the inci-dence and prevalence of AKI in children is not known. How-ever, a study reported an overall incidence of 0.8 per 100 000 total population.2 Age-related incidence is highest in the neona-tal period: 6–24% of newborns in some neonatal intensive care units develop AKI. It is particularly common in neonates who have undergone cardiac surgery.3

Aetiology (Table 1)

Haemolytic uraemic syndrome (HUS) and acute tubular necrosis (ATN) of unspecified cause are the commonest causes of AKI requiring renal replacement therapy and are generally associated with a good prognosis.4 Primary renal disease is the cause of only 7% of cases of AKI but has a poor prognosis, accounting for the majority of children who subsequently require chronic renal replacement therapy.2 Many drugs can cause AKI (Table 2) and these should be avoided whenever possible in children with renal impairment.

Pathophysiology

The mechanism of AKI depends on the underlying cause. Pre-renal AKI (following hypotension and hypovolaemia) and intrin-sic AKI due to ischaemia and nephrotoxins are responsible for most causes of AKI. AKI resulting from obstruction to urinary flow (post-renal AKI) is less common. A detailed review of the pathophysiology is beyond the scope of this review and the reader can refer to previously published review articles.5,6 Essentially, however, following ischaemic injury to the kidney, structural and biochemical changes result in vasoconstriction, desquamation of tubular cells, intraluminal tubular obstruction and transtubular back-leakage of the glomerular filtrate.

History

A carefully taken history will often provide clues to the underly-ing cause of the AKI. A history of diarrhoea, vomiting, trauma or surgery point to hypovolaemia and therefore pre-renal AKI.

Common causes of acute kidney injury in children

haemolytic uraemic syndrome

Acute tubular necrosis

post cardiac surgery

primary renal disease including glomerulonephritis

haematological/oncological and bone marrow transplantation

Sepsis

obstructive uropathy

Table 1

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Bloody diarrhoea, contact with farm animals and eating under-cooked food would suggest HUS is the cause. In all children, any history of recent administration of drugs associated with AKI (Table 2) should be recorded. Haematuria, facial swelling, rash and joint swelling point to nephritis in association with an evolving vasculitis. A history of urinary tract obstruction such as dribbling, poor urinary stream and reduced urine output is significant as this suggests post-renal AKI. It is also important to ask about previous renal disease as in children with pre-exist-ing kidney disorders AKI can lead to rapid deterioration in renal function and progression to chronic renal failure.

Clinical examination

Table 3 lists the common physical signs that can be seen in patients presenting with AKI. The list is not exhaustive and specific conditions require detailed assessment of other sys-tems. For example, ophthalmological assessment is necessary if diagnoses of systemic lupus erythematosus (SLE) (to ascertain whether scleritis, uveitis or retinitis are present) or tubulointer-stitial nephritis and uveitis (TINU) are considered.

Investigations

These are guided by the history and clinical examination. However, all children with AKI should have the following investigations.

Urine • Dipstick for blood, protein and glucose. • Microscopy: To look for (1) red blood cells (RBCs): crenated RBCs suggest glomerulonephritis, absence of RBCs in a child with AKI, haemolytic anaemia and positivity for blood on dip-stick testing suggests haemoglobinuria; (2) white blood cells: eosinophils are seen in ATN and numerous white blood cells would suggest urinary tract infection; and (3) casts: the presence of RBC casts suggests glomerulonephritis, white cell casts may be seen in ATN. • Urine sodium and creatinine: A urine sodium of less than 10 mmol/litre suggests intravascular depletion and pre-renal AKI, whereas in intrinsic AKI a value of greater than 20 mmol/litre is often seen. Measurement of the fractional excretion of sodium, which is the percentage of the filtered sodium that is

Common drugs associated with acute kidney injury

nonsteroidal anti-inflammatory drugs

Angiotensin converting enzyme inhibitors

Aminoglycoside antibiotics

radiocontrast agents

Amphotercin B

Cisplatin

methotrexate

Ciclosporin/tacrolimus

penicillins and cephalosporins

Aciclovir

Table 2


excreted:FeNa% = [(urine Na/serum Na) × (serum creatinine/urine creatinine)] × 100, all values expressed using the same units, is extremely useful to differentiate between pre-renal and intrinsic AKI. A FeNa of less than 1% is suggestive of pre-renal AKI and a FeNa of 2–3% is indicative of intrinsic renal failure. These measurements cannot be interpreted if the child has al-ready received diuretics such as furosemide because they often increase urinary sodium losses.

Blood tests • Sodium: Hyponatraemia (Na less than 135 mmol/litre) is of-ten seen due to fluid overload relating to oligoanuria. • Potassium: Hyperkalaemia (K greater than 6.0 mmol/litre) is common and is exacerbated by acidosis. However, serum potas-sium is often normal in acute HUS due to potassium loss in the diarrhoeal stools and in AKI due to tubulointerstitial disease. • Urea: Plasma urea is almost always elevated in AKI, although there is a disproportionate rise in urea when compared to cre-atinine in pre-renal AKI. However, urea cannot be used as an accurate marker of renal function as high levels can also be seen in the absence of AKI. Such instances include steroid therapy, gas-trointestinal bleeding, high protein intake and catabolic states. • Creatinine: Creatinine is the most reliable and easily avail-able tool for an indirect assessment of glomerular filtration rate (GFR). The modified Schwartz formula:GFR (ml/min/1.73 m2) = [(40 × height (cm)/serum creatinine (μmol/litre))]is often em-ployed. Serum creatinine does have its limitations as it reflects total body supply of creatinine and correlates with muscle mass. Therefore, children with a small muscle mass because of, for example, neuromuscular disorder, will have a lower creatinine

Physical signs in acute kidney injury

Signs of intravascular depletion

Tachycardia

hypotension

Cold peripheries

Dry mucous membranes

Capillary refill time > 2 s

Signs of fluid overload

oedema

hypertension

gallop rhythm

lung crepitations

hepatomegaly

elevated jugular venous pressure

Signs of underlying disease

Anaemia (chronic renal failure)

palpable purpura (henoch–Schönlein purpura)

malar rash (systemic lupus erythematosus)

enlarged kidneys (renal venous thrombosis, hydronephrosis)

poor growth (chronic renal failure)

Tender kidney (pyelonephritis, rejection in transplanted kidney)

enlarged bladder (obstructive uropathy)

Table 3

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than children with normal muscle mass at any given GFR. Thus, the serum creatinine can underestimate the true GFR in such children. Conversely, in children with chronic renal failure, se-rum creatinine tends to overestimate the GFR as tubular secretion and diffusion into the gut is known to occur as plasma creatinine increases. • Bicarbonate: Acidosis due to reduced renal excretion is seen in AKI due to all causes and can worsen hyperkalaemia. • Calcium: Hyperphosphataemia and inadequate vitamin D pro-duction from the kidneys leads to hypocalcaemia. Measurement of ionized calcium is important as this is the unbound physi-ologically active fraction of calcium. Correction of acidosis can precipitate hypocalcaemic tetany and seizures as alkalization re-duces ionized calcium levels. • Phosphate: Reduced renal excretion leads to hyperphospha-taemia in AKI. • Full blood count and film: Anaemia is commonly seen and is often dilutional due to fluid overload. Microangiopathic anaemia with fragmentation of RBCs and thrombocytopaenia is diagnostic of HUS.

Table 4 lists the other investigations which should be con-sidered depending on the clinical presentation and examination findings.

ImagingUltrasound scan (USS) of the renal tract is essential to exclude urinary tract obstruction. A unilateral hydronephrosis may indi-cate a pelviureteric junction obstruction whereas hydronephrosis with hydroureter are seen in vesicoureteric junction obstruction. Bilateral hydronephrosis and hydroureter with a large bladder with a thickened wall are highly suggestive of posterior urethral valves but a micturating cystourethrogram is often necessary to exclude bladder outlet obstruction. Echogenic kidneys with poor corticomedullary differentiation on USS are suggestive of AKI. Small shrunken kidneys are seen in chronic renal failure.

Investigations in acute kidney injury

Complement levels (C3 and C4): low C3 and normal C4 are

suggestive of post-infective glomerulonephritis, low C3 and low

C4 levels are seen in systemic lupus erythematosus

Autoantibody screen – AnA, DnA, AnCA, anti-gBm: positivity is

suggestive of autoimmune disease

Anti-Dnase and ASo titre: may aid diagnosis of post-infective

glomerulonephritis

lactate dehydrogenase: elevated in haemolytic uraemic

syndrome

uric acid: high in tumour lysis syndrome

Creatine kinase: raised in myoglobinuria

parathyroid hormone: raised in renal osteodystrophy/chronic

renal failure

gentamicin and vancomycin levels: to exclude drug-induced

acute kidney injury

urine osmolality: in pre-renal AKi, concentrated urine with values

> 500 mosmol/kg are seen, whereas in intrinsic AKi they are <

350 mosmol/kg

Table 4


Computerized tomography (CT) or magnetic resonance imag-ing (MRI) are sometimes required for a more detailed study of the anatomy, especially in children where obstruction due to calculi or extrinsic mass is suspected. A MAG 3 scan is useful in con-junction with an USS in diagnosing pelviureteric or vesicoureteric junction obstruction.

Renal biopsyIt is not necessary to perform a biopsy in all children with AKI. A biopsy is not required in those with pre- or post-renal AKI or those with ischaemic or toxin-related AKI. In most other cases of primary renal disease a biopsy is essential to establish the diag-nosis and guide treatment. Renal biopsy is especially useful in the diagnosis and management of transplant rejection, glomeru-lonephritides (other than post-infective glomerulonephritis like post-streptococcal), tubulointerstitial disease and SLE.

Management

PrinciplesThe initial management focuses on correcting the fluid balance and electrolyte abnormalities, which can be life-threatening. Pre-vention of further injury to the kidney by maintaining adequate blood pressure and avoiding nephrotoxic drugs is extremely important to ensure quick recovery and avoid permanent damage to the renal function.

Fluid managementClinical assessment of the fluid status (hypovolaemia, euvolae-mia or fluid overload) of the child dictates fluid therapy. Physical signs (see Table 3), recent weight changes and laboratory param-eters like urine sodium, FeNa and urine osmolality are useful tools to assess the volume status. If there is uncertainty, it is best to administer a fluid challenge of an appropriate fluid, such as normal saline, 10–20 ml/kg over 30–60 min, and then to reassess. If the child is dehydrated, an improvement can be anticipated in the urine output (urethral catheterisation may be required) and renal function in the next 4–6 h. Sometimes more fluid boluses are required and this can be administered provided the urine output improves and the child is monitored carefully for signs of fluid overload. If the child requires greater than 40 ml/kg of fluid resuscitation, septicaemia and surgical abdominal pathology should be considered and appropriate help should be sought.

If, following the initial fluid bolus, there is no improvement in the urine output and the child is clinically felt to be volume replete, intravenous furosemide can be administered. The ratio-nale for this therapy is that converting oliguric AKI to nonoliguric AKI facilitates fluid and electrolyte management and avoids the need for dialysis. Nonoliguric AKI also has a better prognosis. However, a recent meta-analysis of studies in adults did not con-firm this finding and it has been suggested that patients who show a diuretic response to furosemide may have less severe AKI in the first place.7 We would recommend a single, intravenous 2 mg/kg dose of furosemide after fluid resuscitation in children with oliguric AKI. In the absence of a response to this there is no role for further doses as they are unlikely to be of any benefit and high-dose furosemide is associated with an increased risk of ototoxicity. There is also no role for low-dose dopamine in AKI.8



In children with established oliguric AKI, appropriate fluid management can prevent fluid overload and hence delay the need for dialysis therapy. The most practical method is millilitre per millilitre replacement of the urine output along with insensible losses (estimated at 400 ml/m2 or 15 ml/kg) and any other fluid deficit (such as from diarrhoea, a nasogastric tube or a stoma). Careful documentation of the input and output along with daily weight measurement is mandatory.

HyponatraemiaThis is often a consequence of fluid overload and/or inappropri-ate hypotonic fluid administration. Hyponatraemia can necessi-tate the need for urgent dialysis therapy which could potentially have been avoided. However, more often than not, the hypo-natraemia is mild and restriction of free water leads to gradual increase in serum sodium values. Hyponatraemia causing neu-rological symptoms such as seizures, usually when the plasma sodium is less than 120 mmol/litre, should be urgently corrected with 3% sodium chloride (approximately 1 mmol Na/ml) using the formula:

Na (mmol) = [125−Plasma Na (mmol/litre)] × [weight (kg)] × 0.6.

HyperkalaemiaThe kidney is responsible for excretion of approximately 90% of the dietary potassium intake and therefore, hyperkalaemia is common in AKI. The accompanying metabolic acidosis contrib-utes to the problem by causing potassium shifts from the intracel-lular to the extracellular compartment. Hypocalcaemia, which is common in AKI, exacerbates the cardiac side effects of hyperka-laemia. The first manifestation of cardiac toxicity of hyperkalae-mia is tall and peaked T waves. This is followed by prolongation of the PR interval, flattening of the P waves and widening of the QRS complexes. Severe hyperkalaemia eventually leads to ventricular tachycardia and fibrillation.

Treatment of hyperkalaemia is indicated if the plasma potas-sium is greater than 6.0 mmol/litre or if there is a cardiac conduc-tion abnormality. Table 5 summarizes the emergency treatment of hyperkalaemia. The first step is to reduce dietary potassium intake (seek dietetic advice) and also eliminate all potassium in the intravenous fluids. Calcium gluconate increases the threshold

Emergency treatment of hyperkalaemia

1. in the event of eCg changes associated with hyperkalaemia,

administer 10% calcium gluconate 0.5 ml/kg (max 20 ml of 10%

calcium gluconate or 4.5 mmol)

2. nebulized salbutamol 5–10 mg

3. in the presence of acidosis (serum bicarbonate < 20 mmol/

litre), administer 8.4% sodium bicarbonate 1 mmol/kg over 30

min (needs dilution and extravasation can cause severe tissue

damage)

4. glucose 0.5 g/kg and insulin 0.1 u/kg iV over 30 min

(hypoglycaemia can occur and glucose monitoring is essential)

5. Sodium polystyrene sulphonate 125–250 mg/kg po or pr,

can be repeated 6–8 hourly

Table 5


potential of the excitable myocardial cells and counteracts the depolarizing effect of hyperkalaemia. Nebulized salbutamol is eas-ily available on most paediatric wards and this treatment should be commenced without delay while unfamiliar and infrequently used intravenous medications are checked and prepared. Steps 2–4 are temporary measures which stimulate cellular uptake of potassium and do not eliminate potassium from the body. Poly-styrene sulphonate resins (125–250 mg/kg every 6–8 h), which can be administered orally or by rectum, exchanges sodium for potassium but has been associated with side effects such as sodium retention and intestinal necrosis. Persisting hyperkalae-mia despite correction of the metabolic derangements in AKI is frequently an indication to initiate dialysis therapy.

AcidosisThis can be corrected by oral or intravenous administration of sodium bicarbonate (1–2 mmol/kg/day in two to three divided doses), but this usually leads to temporary improvement and can increase sodium load. Correction of acidosis can precipitate hypocalcaemia and tetany.

Calcium and phosphateHypocalcaemia should preferably be treated by the oral route (0.2–0.25 mmol/kg four times a day). In severe hypocalcaemia or if bicarbonate therapy is necessary for hyperkalaemia, 10% calcium gluconate 0.5 ml/kg (maximum 20 ml) can be given over 30–60 min through a secure intravenous line as severe extravasation injury can occur.

Hyperphosphataemia is managed by reducing dietary phos-phate and by administering oral phosphate-binding agents such as calcium carbonate.

HypertensionHypertension (defined as blood pressure [BP] greater than 95th centile for age, sex and height percentile) is usually a conse-quence of fluid overload but is also seen in all forms of glomer-ulonephritides. Salt and water restriction alone is sufficient in controlling the BP in a majority of patients. Persisting hyperten-sion can be treated with calcium channel blockers (nifedipine 200–300 μg/kg three times a day, max 3 mg/kg/day or 100 mg daily, or amlodipine 100–400 μg/kg once daily) or a beta-blocker (atenolol 1–2 mg/kg once daily, max 100 mg daily).

Cases of hypertensive emergency (defined as BP greater than 99th centile for age, sex and height percentile and presenting with end-organ damage such as encephalopathy and congestive cardiac failure) should be admitted to a high-dependency unit or paediatric intensive care unit (PICU) and advice should be sought from a paediatric nephrologist at an early stage. The aim of treatment is a 25% reduction in systolic BP during the first hour after presentation with a hypertensive emergency and not achieving BP below the 95th centile until 48 h following presenta-tion. We would recommend using labetalol continuous infusion (0.5–3 mg/kg/h) in this situation. Sodium nitroprusside (500 ng–8 μg/kg/min) is another option but caution should be exer-cised in renal impairment as accumulation of cyanide is well rec-ognized, especially with prolonged use. Blood pressure should be closely monitored as wide fluctuations can occur, ideally by using invasive arterial continuous readings or every 15–30 min recorded using a sphygmomanometer or automated machines.

8 © 2008 elsevier ltd. All rights reserved.


DrugsIdeally, nephrotoxic drugs should be avoided in AKI to prevent further injury to the kidneys. However, if potentially nephrotoxic drugs are considered necessary, there should be appropriate adjustment in dosage after considering the mechanism of drug elimination and GFR of the patient, and careful monitoring of the drug levels and potential adverse effects.

NutritionThe aim is to provide proper nutrition and adequate calories to prevent a catabolic state which can exacerbate uraemia. Tight fluid restriction and a ‘renal diet’ (dietary restriction of potas-sium, sodium, phosphate and protein) makes this challenging and sometimes impossible. Dialysis therapy should be considered in this situation. Early input from a renal dietician is extremely useful.

DialysisIndications for dialysis are listed in Table 6. It is important that close liaison is maintained with the tertiary nephrology centre to ensure early transfer and prompt intervention prior to the devel-opment of any of the severe complications of AKI.

The three commonly used modes of dialysis are: (1) perito-neal dialysis (PD); (2) haemodialysis (HD); and (3) continuous renal replacement therapy (CRRT). Although PD is the most commonly preferred mode of dialysis in the paediatric popula-tion as it is well tolerated and is not associated with rapid fluid shifts, the choice of therapy is guided by the clinical condition of the child and the access available. In a critically ill child on PICU, CRRT is the treatment of choice. Haemodialysis is preferred if there is an urgent need for solute clearance in a short period of time. Sometimes a change in modality is necessary following loss of vascular access in a patient on HD or development of perito-nitis in a child on PD.

Prevention

Early identification of children at risk of developing pre-renal AKI (such as following cardiac surgery) and close monitoring with aggressive fluid and blood pressure management can prevent renal hypoperfusion and injury. Nephrotoxic drugs such as non-steroidal anti-inflammatory drugs and aminoglycosides should be used with extreme caution in children with renal impair-ment, especially in a dehydrated state as rapid deterioration in renal function can occur. Caution should also be exercised in administrating intravascular contrast medium in these children. N-acetylcysteine along with hydration has been shown in adult

Indications for dialysis in acute kidney injury

Severe or persisting hyperkalaemia

Fluid overload with hypertension, congestive cardiac failure or

pulmonary oedema

uraemia with CnS symptoms, nausea, pericarditis

persistent severe acidosis despite bicarbonate therapy

Severe hypo- or hyper-natraemia

Table 6


studies to be beneficial in reducing the rise in serum creatinine following administration of intravascular contrast medium.9 Recently there have been reports of acute deterioration in renal function in patients with chronic renal failure following MRI using gadolinium-based contrast agents and hence serum creatinine should be measured prior to the administration of these agents.10

Prognosis

The prognosis and outcome is highly dependent on the underly-ing cause of AKI. Children with ATN and interstitial nephritis usually make a quick recovery and are low risk for long-term problems. Although the majority of children with HUS have good recovery of renal function, long-term monitoring is essential as they are at increased risk of developing proteinuria, hypertension and impaired renal function due to a substantial loss of nephron mass.11 Factors associated with poor outcome are multiorgan fail-ure, inotropic support, mechanical ventilation and need for dialy-sis therapy.12 There is wide variation in the outcome data from different countries and centres depending upon the population studied. A single-centre study from the UK reported an overall mortality rate of 25% (56 of 227).2 Children and especially neo-nates with AKI following cardiac surgery had the worst outcome, accounting for 64% (36 of 56) of the deaths.2 Children have a much better outcome when compared to adults and prognosis is excellent as long as the precipitating cause of AKI is treatable. Children with primary renal disease account for the majority of patients who progress to need chronic dialysis therapy.

Follow-up

All children who need renal replacement therapy should have secondary or tertiary care follow-up to monitor renal function. The frequency of review depends on the degree of renal function, with children having normal values needing only 6–12-monthly visits. They can be discharged from regular review after 5 years provided there is no proteinuria (early morning urine albumin:creatinine ratio less than 20 mg/mmol) and they have normal blood pressure and serum creatinine for age and sex. ◆

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1 mehta rl, Kellum JA, Shah SV, et al. Acute Kidney injury network:

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8 prins i, plotz FB, uiterwaal CS, et al. low-dose dopamine in

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radiographic-contrast-agent-induced reduction in renal function by

acetylcysteine. N Engl J Med 2000; 20: 180–184.

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Practice points

• AKi is nearly always a secondary event due to hypoxic or

toxic insult to the kidney

• haemolytic uraemic syndrome and acute tubular necrosis are

the commonest causes of AKi

• The need for dialysis can be avoided/delayed by appropriate

fluid and electrolyte management

• prevention of further injury to the kidney by maintaining

renal perfusion and avoiding nephrotoxic drugs is essential

to ensure quick recovery and avoid permanent damage to the

renal function


management of acute renal failure in children

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