acute kidney injury: clinical update€¦ · acute kidney injury: clinical update, vol (1), issue...

Acute Kidney Injury: Clinical Update, Vol (1), Issue (1), 2019

Acute Kidney Injury Kundan M. 2019

Journal of Pediatric Medicine

Open Access Original Article

ACUTE KIDNEY INJURY: CLINICAL UPDATE

Kundan Mittal1, H K Aggarwal2 1. Senior Professor in Pediatrics and Incharge PICU, Respiratory Clinic, Pt B D Sharma, PGIMS Rohtak 2. Senior Professor in Medicine and Nephrology, Pt B D Sharma, PGIMS Rohtak ABSTRACT Introduction: Kidney is silent organ and injury has little clinical evidence and functional renal dysfunction. Kidney injury is pandemic (pan-metabolic, pan-organ, pan endocrinal). Outcome is of clinical importance in acute kidney injury. Even sub-clinical damage not classified (non-creatinine acute kidney injury and creatinine acute kidney injury) is also important cause of morbidity and mortality in acute kidney injury.

Name & Address of Corresponding Author Kundan Mittal, Department of Pediatric Senior Professor in Pediatrics and Incharge PICU, Respiratory Clinic, Pt B D Sharma, PGIMS Rohtak Email Id:- [email protected]

INTRODUCTION Glomerular function, tubular reabsorption and secretion, and urine excretion maintain the fluid and electrolytes in human body. Acute kidney injury (AKI) previously known as acute renal failure (ARF) is the disruption of normal renal function resulting in accumulation of nitrogenous waste products with fluid and electrolytes disturbances. AKI is potentially reversible and ARF indicates sustained renal injury (renal failure is defined as renal function inadequate to clear the waste products of metabolism despite the absence of or correction of hemodynamic or mechanical causes). Presently AKI is defined on the basis of serum creatinine and urine output but AKI also results in disturbances in water, electrolytes and acid-base homeostasis, and endocrine abnormalities. AKI can also occur in patient with chronic kidney disease (CKD). Incidence of AKI varies from 1-31% and mortality 10-60% in various studies. Incidence of AKI depends on whether occurs in the community (0.9%) or hospital (5-7%) settings. Hospital acquired AKI is important cause of morbidity and mortality compare to community acquired AKI. AKI is multisystem disease affecting kidney, liver, brain, lung, metabolic and immune functions and independent predictors of mortality. AKI can be oliguric, non-oliguric, anuric, and polyuric. Oliguria is defined as urine output <0.5 mL/kg/hr (<200-300 mL/m2/d). Non-oliguric AKI is characterised by rising blood urea nitrogen and creatinine in presence of continued urine output greater than 1 mL/kg/hr or 300 mL/m2/d. Kidney receives 25% of cardiac output to maintain GFR and oxygen delivery. Preterm birth is associated with more renal insufficiency and failure as

nephrogenesis starts at 5th week of conception and rapidly progress at 20weeks onward and complete by 34-38weeks of gestational age. AKI is classified as prerenal [30-60% (decrease perfusion either due to reduced intravascular volume or decrease in effective circulating volume)], intrinsic renal disease [40% (glomerular, tubular, interstitial, and vascular)], and postrenal [10% (obstructive)] origin. Renal hypoperfusion leads to activation of renin-angiotensin-aldosterone (RAA) axis (reabsorption of salt and water), sympathetic nervous system (systemic vasoconstriction), prostaglandins, and antidiuretic hormone (retention of water by collecting tubule). Prolonged hypoperfusion can lead to acute tubular necrosis (loss of cell polarity, tubular cell death and cast formation). Risk factors for AKI in intensive care include conditions predisposing to renal hypoperfusion, direct renal injury, severity of illness and drugs (aminoglycosides, cephalosporin’s, penicillin, amphotericin B, acyclovir, acetaminophen, non-steroidal anti-inflammatory drugs, vasopressors, contrast media, myoglobin, haemoglobin, and uric acid). AKI is most commonly associated with sepsis and lead to multiorgan failure. There is great risk of developing chronic kidney disease in children following AKI. AKI can be differentiated from CKD by evaluating old records, renal ultrasonography (decreased renal length and cortical thinning suggest CKD), measuring parathyroid level, and anaemia in association with other factors. Newborn have different criteria to define AKI as various factors can alter the findings of serum creatinine at birth. In established AKI there is parenchymal damage while in function AKI there is no parenchymal damage.

Clinical classification of AKI based on aetiology

Prerenal (30-60%): Intravascular volume depletion, decreased cardiac output, systemic vasodilatation, and renal vasoconstriction Intrinsic (≠40%): Vascular, glomerular, tubular, and

8



interstitial Postrenal (10%): Tubular obstruction, ureteral obstruction, extrinsic ureteral/pelvic obstruction, lower urinary tract obstruction, and urethral obstruction Evaluation of AKI Definition Acute kidney injury (AKI) is a syndrome which results in disruption of normal renal function resulting in accumulation of nitrogenous waste products, fall in glomerular filtration rate, and decrease in urine output.

ADQI-RIFLE criteria for diagnosis of acute kidney injury:

Grades of Severity Damage Status

GFR Criteria Urine output criteria

Risk Increased creatinine x 1.5 or eCCl decrease >25%

UO < 0.5 mL/kg/h x 6 hr

Injury Increased creatinine x 2 or eCCl decrease > 50%

UO < 0.5 mL/kg/h x 12 hr

Failure Increased creatinine x 3 or eCCl decrease >75% or creatinine ≥ 4 mg/dl

UO < 0.5 mL/kg/h x 24 hr or anuria x 12 hrs

Outcome Variable Loss Persistent ARF= complete loss of renal

function >4wk ESRD End Stage Renal Disease

eCCL (estimated creatinine clearance) = k x height in cm/SCr AKIN diagnostic criteria of AKI: Abrupt reduction (within 48hr) of kidney function defined as an absolute increase in serum creatinine 0.3mg/dl or 50% increase in serum creatinine from baseline or reduction of urine output <0.5ml/kg/hr of >6hr applied in clinical context and after fluid resuscitation. No structural criteria have been used for classification.

Staging of AKI according to AKIN Stage Serum Creatinine

Criteria Urine output Criteria

1 Increased creatinine 0.3mg/dL or 150-200%

increase

UO < 0.5 mL/kg/h > 6 hr

2 Increased creatinine 200%

over baseline UO < 0.5 mL/kg/h >12

hr

3 Increased creatinine 300% over baseline or increase

4mg/dL with an acute increase 0.5mg/dL or need

for RRT

UO < 0.3 mL/kg/h>24 hr or anuria for 12 hrs

Note: Urine output is not kidney specific like creatinine and weight-based criteria is also

misleading. KIDGO criteria (2012): AKI is defined as increase in serum creatinine >0.3mg/dL within 48hrs or increase in serum creatinine >1.5fold from baseline occur within 7days (serum creatinine >50% of reference) or urine output <0.5ml/kg/hr for 6hr.

KIDGO Classification Stage Serum Creatinine Urine output

1 1.5-1.9 of baseline or

≥0.3mg/dL rise increase <0.5mL/kg/h for

6-12h 2 2.0-2.9 baseline <0.5mL/kg/h for

≥12h 3 3.0times baseline or

Increase to >4.0mg/dL or Initiation of RRT or

Decrease in eGFR<35mL/min/1.73m2

≤0.3mL/kg/h ≥24h

New ADQI diagnostic criteria for AKI Stage Functional Criteria Biomarkers

Criteria I Increased creatinine 0.3mg/dL

or 150-200% increase or UO < 0.5 mL/kg/h > 6 hr or mildly

decreased GFR

+

II Increased creatinine 200% over baseline or UO < 0.5 mL/kg/h

>12 hr or moderately decreased GFR

++

III Increased creatinine 300% over baseline or increase 4mg/dL

with an acute increase 0.5mg/dL or acute RRT or UO <

0.3 mL/kg/h>24 hr or anuria for 12 hrs or severely decreased

GFR

+++

Neonatal AKI definition based on KDIGO Stage Serum

Creatinine Urine output

0 No change in SCr or rise ≤0.3 mg/dL

≥ 1.0mL/kg/h for 24h

1 SCr rise ≥ 0.3 mg/dL within 48 h

or SCr rise ≥1.5–1.9 reference SCr

within 7 d

≤1.0mL/kg/h for 24h

2 SCr rise ≤2.0–2.9 reference SCr

(previous value)

≤0.5 mL/kg/h for24h

3 SCr rise ≥3 reference SCr or

SCr ≥2.5 mg/dL or receipt of dialysis

≤0.3 mL/kg/h for 24 h or anuria for 12 h

Defining AKI in neonates is a problem: Renal blood flow received by neonatal kidney at birth 2.5-4%, 6% at 24 hrs of life, 10% at one week and 15-18% at 6weeks of cardiac output as compared to adult who receives 20-25% of cardiac output.



GFR improves from 10 to 20 mL/min/1.73 m2 during the first days of life to 30 to 40 mL/min/1.73 m2by 2 weeks of life and improves steadily over the first few months of life, reaching the adult GFR by 2 years of age. In premature infants, the GFR at birth is lower and increases slowly. Calculate of estimated GFR using Jaffe enzymatic reaction [0.33 x height in cm/SCr mg/dL (mg/dL x 88.4 = µmol/L)] in newborn Urine concentrating capacity is 500-700mOsm (adult 1400mOsm) Newborn serum creatine at birth reflects maternal level and it declines at variable rates Hyperbilirubinemia and cephalosporins interfere with

serum creatinine Estimation Due to risk of blood loss it is not routinely measured frequently Some studies have taken urine output criteria for AKI in neonates Trend of serum creatinine is important assessment tool in at risk neonates Novel biomarkers for neonatal AKI are serum & urinary NGAL, urinary interleukin-18, kidney injury molecule-1, osteopontin, serum cystatin C, and beta-2 microglobulin.

Understanding more about terms used in relation to AKI

Functional Criteria Structural Criteria

Acute Kidney Disease (AKD)

AKI, or GFR ≤60mL/min per1.73m2 for <3 months, or decrease in GFR by ≥35% or increase in SCr by >50% for<3

months

Kidney damage for <3 months

Non-Kidney Disease (NKD)

GFR ≥60 mL/min per 1.73m2, Stable SCr No damage

Chronic Kidney Disease (CKD)

GFR <60mL/min per 1.73m2 for >3 months Kidney damage for >3 months

AKI Increase in SCr by 50% within 7 days, or Increase in SCr by 0.3 mg/dL within 2 days, or Oliguria

No criteria

Criteria and Staging of AKD

Stage Serum Creatinine Stage 0 A: Absence of injury or dysfunction

B: Biomarkers or other evidence of injury/repair/regeneration or indicators of loss of renal glomerular or tubular reserve

C: Creatinine <1.5 times baseline but not back to baseline Stage I 1.5-1.9 times baseline Stage II 2.0-2.9 times baseline Stage III 3.0 times baseline or increase in serum creatinine to ≥4.0mg/dL or ongoing need for RRT

Note: Half-life of creatinine increases if GFR decreases and it may take 24-36hrs to rise after renal insult.

Transient AKI: Defined as return of serum creatinine to normal within 24hr AKI Syndrome: It includes no AKI, subclinical AKI, functional AKI, and established AKI on the basis of functional change and damage. Kidney susceptibility: It is defined as kidney frailty, may depend on several systemic conditions and comorbidities such as diabetes and hypertension, previous episodes of AKI, and presence of subclinical CKD (chronic kidney disease) identified by a reduction in RFR-G. Acute Kidney Stress (AKS) also refer as preinjury phase that leads to AKI. AKS may be a condition of very early injury or increased susceptibility to exposures that may or may not lead to AKI. To define

kidney function and the overall potential of nephron mass, the Kidney Stress Test has been used as a measure of the Renal Functional Reserve (RFR). The RFR (glomerular = RFR-G) is the difference between the maximal GFR (stressed) measured after the stimulus (acute oral or intravenous amino-acid load), and the baseline (unstressed GFR). 2-2.5hrs. GFR = Filter fraction x renal plasma flow. Kidney attack This is similar to heart attack. Accurate monitoring of diagnostic criteria of AKI coupled with novel biomarkers may be indicative of kidney attack. Subclinical AKI and Renal Angina: Subclinical AKI is diagnosed when renal damage and dysfunction does not reach a threshold sufficient to



make serum creatinine rise above 0.3 mg/dl in 48 h or when oliguria is rapidly reversed before the 6hr timeframe. Patients may have up to 50 % of the renal mass compromised before creatinine rises. Collectively symptoms, risk factors, novel biomarkers, and minimal rise in serum creatinine are pointer of renal angina. In other words, we may have creatinine increased AKI (CRIAKI) and non-creatinine increase AKI (NCRIAKI). Kidney Specific Severity Score: Various scores like Bullock, Mehta, Liano’, SHARF-II, PICARD, Demirjian may be helpful in assessing kidney disease severity. Biomarkers in assessing kidney injury: Biomarkers help in early prediction of factors that will worsen AKI (helps in prevention, early intervention and avoiding harmful therapy), diagnosis (prerenal, acute tubular necrosis and obstructive nephropathy), need for renal replacement therapy, outcome, and associated mortality. Biomarkers helpful in assessing increased risk of kidney injury: Interleukin-18, Neutrophil gelatinase-associated lipocalin (NGAL), Kidney injury molecule-I (KIM-I), urinary NGAL, GST (glutathione-S-transferase), L-FABP (liver fatty acid binding protein), TIMP2. Kidney damage (primary prevention): Interleukin-18, Serum CysC, Neutrophil gelatinase-associated lipocalin (NGAL), and urinary Kidney injury molecule-I (KIM-I), NGAL Kidney damage (secondary prevention): Serum creatinine, urea, CysC. Decrease GFR: Serum creatinine, urea, Cystatin-C Kidney failure (prognostic markers): Interleukin-6, Neutrophil gelatinase-associated lipocalin (NGAL), Kidney injury molecule-I (KIM-I), urinary NGAL, c-reactive protein (CRP), creatinine, urea.

Source of biomarkers production: This will help in knowing the site of renal injury or damage.

Baseline Reference Range of Biomarkers Biomarker

Source Tests Unit Reference range:

Healthy

NGAL Serum ELISA ng/mL 86.3 ± 43.0 (men)

88.9 ± 38.2 (women)

56.71 ± 17.57 1.7 ± 0.5 0.4-100

Urine ELISA ng/mL 5.7-17.7 11.94 ± 8.09

0.8-28.9 (men)

1.9-316.7 (women)

Cystatin C

Serum Nephelometri

c immunoassay/ELISA

mg/L 0.53-0.95 0. 85 ± 0.21

Urine Nephelometri

c immunoassay/ELISA

mg/L 0.051-0.28 0.02-0.11

KIM-1 Urine ELISA pg/mL 59-2146 395.1 ± 398.8 31.0-1000.0 31.0-1736.5

IL-18 Urine ELISA pg/mL 1.4-1.8 3.0-108.6 6.2-311.1

L-FABP Urine ELISA ng/mL μg/g

Cr

3-400

5.67 (2.74-8.21)

NAG Urine Colorimetry

U/g 0.75-0.90 U/g 1.06 ± 0.1

U/g (children)

Evaluation of a Patient with AKI

Find out the aetiology (prerenal, intrinsic, vascular,

postrenal, obstructive), community or hospital

acquired (usually multifactorial) etiology, and

predisposing factors

Life threatening conditions

Diagnostic workup

Serum creatinine and blood urea nitrogen or urea

GFR

Urea clearance

Cystatin-C



Urine examination including chemistry

Urine albumin/creatinine ratio

Variables in differentiating AKI

Acid-base assessment Serum biochemistry Complete blood count with platelet value Liver enzymes Serum albumin Coagulation profile Creatinine kinase Autoimmune workup

Microbiology: C3 and C4 level, anti-sterptolysin O, blood and stool culture, antinuclear antibodies, antineutrophilic cytoplasmic antibodies, hepatitis A and HIV serology

Creatinine kinase Plasma and urine biomarkers Interleukin-18 Neutrophil gelatinase-associated lipocalin (NGAL) Kidney injury molecule-I (KIM-I) Drug or toxin level Renal echography, ultrasound, doppler study, cysto-urethrogram and MRI Kidney biopsy Nephrotoxic drugs causing AKI Early biomarkers to detect AKI: [TIMP-2, IGFBP7 (stress biomarkers)], KIM-1, NGAL, cystatinC, IL-18, IL-8, hepcidin Goals of treatment Prevention Fluid & electrolytes

Preventing & managing complications Nutritional support Renal Replacement Therapy Treatment Fluid Resuscitation: Prevention of AKI should be target of management of AKI. Assess volume status. Give one bolus in case of hypovolemia of normal saline 10-20mL/kg over 30min and may be repeated twice if necessary until urine output is established and if no urine output and it may be followed by single dose of furosemide (2-mg/kg/IV). Fluid responsive AKI will respond to it. Children with volume overload >10% are candidate for renal replacement therapy. Child with euvolemia and oliguria and not responding to fluid challenge one should suspect intrinsic renal injury. Avoid nephrotoxins exposure. Use of mannitol, diuretics, dopamine, natriuretic peptides and fenoldopam are controversial in prevention of AKI.

Fluid therapy

400 mL/m2/day 5-10% dextrose

OR

< 6mo 40 mL/kg/day

6mo- 5yr 30 mL/kg/day

5yr -10yrs 20 mL/kg/day

Adolescent 10 mL/kg/day

Test Prerenal AKI Renal AKI Post Renal Acute

Glomerular Nephritis

Acute Tubular Nephritis

Acute Interstitial Nephritis

Serum BUN/Creatine ratio

>20:1 >20:1 <20:1 <20:1 >20:1

FENa (%) (U/P Na/U/P Creatinine x 100)

<1

>1

>1 <1 Variable

Urine sodium Specific gravity Osmolality

<10-20 >1.020 >500

Neonate >400

<20 <1.010

Variable

>20 >1.020

>250-300 Neonate <350

variable >1.020

variable

Variable >1.020 <400

U/P creatinine >40 <20 Urine analysis Hyaline cast Red cells,

dysmorphic red cells

Granular, renal tubular casts

White cells, white cell casts

Normal, red cells, white

cells, crystal Low molecular weight protein

Low High

Novel urinary biomarkers

Low High

FEurea (%) <35 >35 FEuric acid (%) <7 >15



Sodium intake should be restricted and potassium and phosphate should not be given until evidence of low value.

Replace urine output with N/2DS mL/mL

Colloids vs Crystalloids vs Albumin: Still debate is continuing. Evidence of the superiority of buffered solutions over chloride-rich solutions is present and later should be used with caution in AKI, especially in patients at increased risk for AKI Maintain age appropriate mean arterial pressure (MAP) Use vasopressor (noradrenaline) and inotropes if systematic perfusion is inadequate (early use within 1-6hrs is preferred). Vasopressin may be tried in some cases. Prevent volume overload as it is well known factor to increase mortality. Congestive failure: Use inotropes e.g. Dobutamine Use of prostaglandins is controversial Drugs known to cause AKI: Prerenal azotaemia Cox-2 inhibitors, diuretics and antihypertensive Glomerular diseases Hydralazine therapy, propylthiouracil, interferon Acute tubular necrosis Aminoglycosides, amphotericin B, acetaminophen, vancomycin, radiocontrast agents, herbicides, intravenous immunoglobin Acute interstitial nephritis Loop and thiazide diuretics, NSAIDS, phenytoin, cimetidine, cephalosporins, quinolones, PPI, sulphona-mides, vancomycin. Intratubular obstruction Acyclovir, methotrexate, high dose oral phosphate, sulphonamide antibiotics Small vessel Diseases ACE inhibitors, NASID, calcineurin inhibitors. Quinine, oral contraceptives, mitomycin C, vascular endothelial inhibitor growth factors Postrenal obstruct ruction NSAID, compound analgesics, anticholinergics Treat sepsis (50% AKI): follow SWOT approach Drugs for intrinsic renal disease; Trials undergoing research Alkaline phosphatase (sepsis-associated AKI) L-Carnitine (sepsis-associated AKI) Remote ischemic preconditioning (post-operative AKI) p53-targeted siRNA (post–cardiac surgery AKI) Extracorporeal devices (dialysis-requiring AKI) Vitamin D (hospitalized AKI) Uremic toxin absorption/pentoxifylline (hospital-acquired AKI) Evidence of benefit: Search is on α-Melanocyte-stimulating hormone Atrial natriuretic peptide (ANP)

Calcium channel blockers (CCB) Diuretics Dopamine Erythropoietin Insulin growth factor (IGF) Replace urine output with N/2DS mL/mL Twice daily weight monitoring Glycaemic control (110-149mg/dL) Hyponatremia: Serum Sodium < 130 mEq/L Fluid restriction Serum Sodium < 120 mEq/L Raise sodium to 125mEq/L

Metabolic acidosis: Renal dysfunction and secondary to systemic disease are major contributors to metabolic acidosis. Keep a watch on fluid overload and hypertension. Corrected with sodium bicarbonate if pH < 7.2 or HCO3- <12mEq/L only or dialysis.

Symptomatic hypocalcaemia: Calcium gluconate (10%) 0.5-1.0 mL/kg diluted over 30-60 min

Hyperkalaemia: Management should target in removing potassium, moving potassium inside the cells and membrane stabilization.

Hyperphosphatemia secondary to reduced glomerular filtration may be treated using non-calcium phosphate binders and dietary restriction

Nutrition: AKI is hypercatabolic state and need adequate nutrition therapy. 400Kcal/m2/day or 20-30Kcal/kg/d (1-1.3 times of basal metabolic rate), high biological protein, low phosphorus and potassium diet, CHO >70%, Fat 10-20%, and Protein 1-2 gm/kg (1.2-1.7 in CRRT). Add vitamin C and water-soluble vitamins including folic acid and thiamine. Have reasonable glycaemic control (110-150mg/dL).

Hypertension: Labetalol: 0.25 – 1 mg/kg/dose intermittently and 0.4 – 1.0 mg/kg/hr as infusion Nicardipine: 0.5-3.0 mcg/kg/min as infusion Nitroprusside: 0.5-8.0 mcg/kg/min as infusion Hydralazine: 0.1 – 0.4 mg/kg/dose IV intermittently Remote Ischemic Preconditioning (RIP) Role of NAC in AKI is controversial Use of loop diuretics, fenoldopam, calcium channel blocker, theophylline is also controversial Statins: Further studies are required Rehabilitation Furosemide stress test: 2hour urine output following 1mg/kg furosemide in clinically euvolemic patients in early AKI may help in identifying severity and progression of AKI. Drugs modification in Renal Failure Drug pharmacokinetics and pharmacodynamics is altered in AKI (renal clearance and metabolism, absorption, hepatic metabolism, altered protein binding, decreased GI motility, effect of vasopressor on



gut, drugs increasing gastric pH, drug distribution, alteration in volume of distribution, capillary leak, altered tubular function, reduced drug clearance are some of mechanism for altered response in AKI). Loading dose to be given similar to normal dose and depends on volume of distribution. Drugs with narrow spectrum of activity and therapeutic range should be given in reduced dose. AKI is dynamic state so the drug half-life keeps on changing If peritoneal dialysis is one no drug modification is required. Maintenance dose: Normal creatinine Dosing interval = ------------------------- x normal interval Patient creatinine OR Patient creatinine Dose = ------------------------- x normal dose Normal creatinine Calculation of GFR GFR = Length in cm x (K/PCr)

K Age

0.45 < 1yr

0.55 Child < 13yrs

0.7 Adolescent male

0.55 Adolescent female

Estimation of glomerular filtration rate using

Schwartz formula = Length in cm x K ------------------------ Serum creatinine mg/dL K Age 0.33 Low birth weight ≤1year 0.45 Full term ≤1yr 0.55 Child <13yr 0.70 Adolescent male

0.55 Adolescent female

Modified Schwartz formula = 0.413 x Length in cm

---------------------------

Serum creatinine mg/dL

Counahan-Barratt

0.43 x length in cm

----------------------------

Serum creatinine mg/dL

Schwartz using creatinine and cystatin-C

39.1 x (serum creatinine mg/dL)0.516 x (1.8/cystatin-C)0.294 x (30xBUN)0.169 x (1.099) if male x

height/1.4)0.188

MDRD formula = 170 x (serum creatinine-0.999) x (age-

0.176) x (BUN-0.170) X (Serum albumin +0.318) X (0.762 if female) x (1.180 if Black) Modified MDRD formula = 186.3 x (serum creatinine-1.154) x (age-0.0293) x (0.742 if female) x (1.21 if Black)

Normal GFR in Neonates, Children, and Adolescents

Age Mean GFR ± SD mL/min/1.73m2

29-34 weeks GA -1week postnatal age

15.3± 5.6

29-34 weeks GA -2-8week postnatal age

28.7±13.8

29-34 weeks gestational age >8week postnatal age

51.4

1week term males and females

41±15

2-8 weeks term males and females

66±25

>8 weeks term males and females

96± 22

2-12 years (males and females)

133±27

13-21 years (males) 140±30 13-21 years (females) 126±22

Some equations used to assess renal functions Fractional excretion of sodium FENa = UNa/PNa x Pcr/Ucr x 100 Renal failure index = (UNa x 100)/Ucr/Pcr Creatinine clearance = k x height (cm)/Pcr

Urinary protein and albumin excretion Age Timed

protein collection (mg/m2/h

r

Spot urine protein/cr

eatinine (mg/mg)

Spot urine albumin/creatinine

(mg/mmol)

6-24mo <4 <0.5 <30 >24mo <4 <0.2 <30

Renal functions monitoring in critical care: Strict hourly input and output chart Volume status and fluid responsiveness, CVP, cardiac output, ECG and daily weight monitoring Serum biochemistry, cystatinC, LFT, RFT, blood gas and coagulation profile Peripheral blood film Urine analysis Lung USG and x-ray for fluid USG abdomen for ascites ECHO Renal replacement therapy Indications for RRT in children with AKI are; Pulmonary oedema Persistent anuria or oliguria Refractory hypertension Severe hypo/hypernatremia



Refractory hyperkalaemia or evidence of cardiac toxicity >6.5meq/L Refractory metabolic acidosis pH≤7.2 Toxins removal/uraemia Large fluid requirement Differentiating AKI form Chronic Kidney Disease Study of old records Clinical Symptomatology Renal ultrasonography: (decrease in length/thinning of cortex) Anaemia Urine output Risk Factors for CKD in AKI AKI Stage/Severity Need for RRT Repeated episodes Age Low serum albumin Intrinsic renal disease-etiology Duration of AKI Consequences of AKI Volume overload, decreased oncotic pressure, uraemia, and infiltration of lungs by neutrophils may lead to congestive cardiac failure, pulmonary oedema, pleural effusion, a secondary hypertension, abdominal compartment syndrome, gut ischaemia, gut and pulmonary bleeding, and acute lung injury (organ-cross task). Acid-base abnormalities affect various receptors leading to hyper-glycaemia, increased protein break-down, acute lung injury, decreased cardiac output, hyperchloremia. White cell dysfunction and decreased oxidative stress clearing may be responsible to infection and delayed wound healing. Hyponatremia is responsible to CNS manifestations and hyperkalaemia for cardiac arrhythmias Increased destruction and synthesis of red cells and decreased production of erythropoietin, von Willebrand factor are contributing factors for anemia and bleeding Nervous system manifestations may result as liver failure, malnutrition, uraemia, and acidosis and drug metabolism. Increased volume, decreased albumin binding and elimination may be associated with drug toxicity. Complications of AKI Cardiovascular: Pulmonary oedema, arrhythmias, pericarditis, hypertension Metabolic: Hyperkalaemia, hyponatremia, hyper-phosphatemia, hypocalcaemia, metabolic acidosis Neurological: Altered sensorium, seizures, coma

Gastrointestinal: Nausea, vomiting, bleed, ulcer Infectious: Pneumonia, sepsis Haematological: Anaemia, bleeding Suggested Readings 1. Geary DF, Schaefer F. Pediatric Kidney Disease.2nd ed. USA: Springer-Verlag Berlin Heidelberg; 2016 2. Ostermann M and Joannidis M. Acute kidney injury 2016: diagnosis and diagnostic workup. Critical Care 2016 20:299 3. Thomas ME, Blaine C, Dawnay A, Mark A, Devonald J, Ftouh S, Laing C, Latchem S, Lewington A, David V, Ostermann MM. The definition of acute kidney injury and its use in practice. Kidney International (2015) 87, 62–73; 4. Moore PK, Hsu RK, and Liu KD. Management of Acute Kidney Injury: Core Curriculum 2018. Am J Kidney Dis. 2018: 72(1): 136-148. 5. Awdishu L, and Wu SE, Acute Kidney Injury. CCSAP 2017 Book 2 • Renal/Pulmonary Critical Care 6. Feehally J, Floege J, Tonelli M, Johnson R. Comprehensive Clinical Nephrology. 6th ed. China: Elsevier; 2019 7. Ronco C, Bellomo R, Kellum JA, Ricci Z. Critical Care Nephrology.3rd ed. Philadelphia: Elsevier; 2019 8. Reilly RF Jr, Perazella MA. Nephrology in 30 days.2nd ed. China: MacGraw Hill; 2014 9. Straaten HMO, Forni LG, Groeneveld ABJ, Bagshaw SM, Joannidis M. Acute Nephrology for the Critical Care Physicians. London: Springer; 2015 10. Deep A, Goldstein SL. Critical Care Nephrology and Renal Replacement Therapy in Children. Switzerland: Springer; 2018

How to cite this article: Kundan M., Acute Kidney Injury: Clinical Update; Jour. Pedia. Medi. 2019; 1(1). Source of Support: Nil, Conflict of Interest: None declared

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