Welcome to Seminar
ACUTE KIDNEY INJURY & CHRONIC KIDNEY DISEASe IN CHILDREN BY- DR. SAMEEKSHYA PRADHANGUIDE- ASSOC. PROF. DR. J .R CHAMPATIRAY
ACUTE KIDNEY INJURY
Rapid deterioration of renal function resulting in retention of nitrogenous wastes and inability of kidney to regulate fluid and electrolyte homeostasis.
In year 2000 the acute dialysis quality initiative (ADQI) proposed RIFLE criteria for defining AKI . Later, Acute Kidney Injury Network (AKIN) classified AKI based on the RIFLE system.
> 3 months
Incidence The precise incidence of AKI in children is not well known. 4-6 % case of AKI seen in general ward and upto 40% in PICU AGE with dehydration & shock is a common cause.In India, malaria, snake bite are also common causes.In PICU, commonly affects children who have sepsis and multiorgan failure.Children undergoing major cardiac surgery and organ transplantation are also at considerable risk.HUS and AGN are important renal causes.Post renal causes of AKI are rare.
EtiologyPre renalIntrinsic or renalPost renal
- Both pre and post renal aki are potentially reversible in early stages but if prolonged can cause renal parenchymal damage.
(A) Pre renal Also calledprerenal azotemia,is characterized by diminished effective circulating arterial volume, which leads to inadequate renal perfusion and a decreased GFR .
Causes of prerenal akiAcute gastroenteritis Hemorrhage ShockCongestive cardiac failure Hepatorenal syndrome (renal vasoconstriction)Sepsis (peripheral vasodilaton)Profound third space loss (burns, Ac. Pancreatitis, nephrotic syndrome, massive ascites)NSAIDs & ACE inhibitors
ReninAngiotensin IIAldosteroneRenal Tubular Na Reabsorption
VasopressinRenal Tubular H2O ReabsorptionUrine VolumeConcentrated UrineUrine Sodium
Decreased Renal PerfusionMechanisms of Sodium and Water Conservation in Prerenal Azotemia
(B) renal CAUSES Obstruction of renal artery or veins - renal vein thrombosis , renal arterial obstruction,Involvement of renal microvasculature HUS , HSP, polyarteritis , collagen vascular diseaseGlomerular causes- AGN ( PSGN ,other infections ), cresentic GN Interstitial causes- acute tubulointerstitial nephritisTubular causes (ATN) Prolongation of pre-renal insult , intravascular hemolysis , sepsis , nephrotoxic agents , multiorgan failure , rhabdomyolysis , snakebite , other envenomations , falciparum malaria , leptospirosis
1.Obstruction of renal arteries and veins
Bilateral renal arterial thrombosis may occur after umbilical artery catheterization in neonates (rarely causes aki usually causes intractable hypertension).Renal vein thrombosis may be a complication of infant of diabetic mother especially following dehydration.In older children renal vein thrombosis may occur with nephrotic syndrome with anasarca and dehydration.Gross hematuria, enlargement of kidney and azotemia are typical manifestation.
2.Involvement of renal microvasculature HUS is a common cause of AKI in chidren. Causes thrombotic microangiopathy2 types- D+HUS and D-HUSCommon causes of D+HUS EHEC(in developed countries),Shigella dysentriae type I (in India)Following dysentery shigella-toxin enters the circulation and leads to endothelial injury in microvasculature . Localized coagulation and deposition of platelet thrombi and fibrin occurs in glomeruli causing decrease in GFR.
3.GLOMERULAR DISEASESPSGN, Post infectious GN, Cresentric GN, Renal vasculitis, IgA nephropathy are important causes in this group.
4.Acute interstitial nephritis Usually occurs due to hypersensitivity reaction to some drugs (ampicillin, cephalosporins, sulfonamides,quinolones, NSAIDs, phenytoin etc)The patient may have fever , arthralgia , rash and eosinophilia : urine often shows eosinophils Renal biopsy should be done if it is strongly suspected.
5.Acute Tubular necrosis Occurs mostly in critically ill infants and children who have been exposed to nephrotoxic agents and/or prolonged hypoperfusion/hypoxia.Common causes of ATN include renal hypoperfusion following volume contraction , severe renal vasoconstriction , nephrotoxic agents , sepsis , shock and hypotension.Renal hypoperfusion prerenal aki(reversible) intermediate stage (slowly reversible) ATN
Mechanism of atn
(c)Post renal It includes a variety of disorders characterized by obstruction of the urinary tract.In a patient with 2 functioning kidneys, obstruction must be bilateral to result in AKI.Relief of the obstruction usually results in recovery of renal function except in patients with associated renal dysplasia or prolonged urinary tract obstruction.
Causes of post renal akiPosterior urethral valvesUreteropelvic junction obstructionUreterovesicular junction obstructionUreteroceleTumorUrolithiasisHemorrhagic cystitisNeurogenic bladder
Clinical evaluation HISTORY -H/o blood loss, diarrhea, vomitting prerenal aki.Past h/o pharyngitis with gross hematuria, edema, hypertension acute PSGN.Dysentery, petechiae, pallor- HUS.Sudden passage of dark red urine, pallor and jaundice with h/o drug exposure acute intravascular hemolysis (G6PD def.).Rash with arthritis SLE or HSP.H/o prolonged hypotension or exposure to nephrotoxic drugs ATN.Exposure to certain drugs f/b fever, rash, arthralgia and rising S.creat acute TINH/o poor urinary stream with palpable UB or kidney obstructive uropathy.Abdominal colic,hematuria, dysuria urinary tract stones.
PHYSICAL EXAMINATION - Obtaining a thorough physical examination is extremely important . Clues may be found in any of the following Skin Eyes Ears Respiratory system Cardiovascular system Abdomen
Skin :- Palpable purpura - Systemic vasculitis Maculopapular rash - Allergic interstitial nephritis
Eye :- Uveitis interstitial nephritis and necrotizing vasculitis. Ocular palsy - ethylene glycol poisoning or necrotizing vasculitis
Ear :- Hearing loss - Alport disease and aminoglycoside toxicity Mucosal or cartilaginous ulcerations Wegeners granulomatosis
Respiratory system :- rapid and deep breathing met. Acidosis basal creps - volume overload
Cardiovascular examination :Pericardial friction rub - Uremic pericarditisIncreased JVP, Gallop rhythm, pitting edema- CHF due to volume overload.
Abdomen :Renal angle tenderness nephrolithiasis, papillary necrosis, renal artery or vein thrombosis. Distended bladder urinary obstruction.F/s/o chronic liver disease with ascites with prerenal aki hepatorenal syndrome
invesigationsUrine R/MCBC with CPS24 hour urinary protien Blood urea and S. creatinine levelSerum electrolytesThroat swab C/S ASO titer C3 level Serum calcium Serum phosphate Serum uric acid ANAABG
Imaging Ultrasound of KUB - evaluates renal size, able to detect masses, obstruction, stonesChest x-rayDTPA DMSA
Renal biopsy Indicated in Patient in whom the etiology is not identified.Unremitting AKI lasting longer then 2-3 wks or in assessing the extent of renal damage and outcome.Suspected drug induced AKI in a patient receiving therapy with a potentially nephrotoxic drugs.
Urinary indicesPRE-RENAL INTRINSIC URINARY SODIUM (mEq/l) < 20 > 40 Urinary osmolality (mOsm/kg) > 500 < 300Blood urea to creatinine ratio >20:1 < 20:1Urine to plasma osmolality ratio >1.5 < 0.8 1.2 Fractional excretion of sodium < 1 > 1
Biomarkers for early diagnosis Biomarkers that indicate renal injury before rise in S.creatinine values would be helpful in pts. at high risk of aki like children undergoing major surgery or organ transplant, neonates with hypoxia,sepsis or multi organ failure. Examples are:Neutrophil gelatinase associated lipocalin(NGAL)Interleukin -18Kidney molecule1(KIM -1)Cystatin -C
MANAGEMENT The basic principles of management include Treatment of life-threatening complications Maintenance of fluid and electrolyte balance Supportive care Dialysis & CRRT Specific management of underlying disorder
a. Management of Life threatening complicationsSuch complications are Hyperkalemia Fluid overload with heart failureHypertensive emergenciesProfound acidosisSevere anemia
1. Hyperkalemia (>6meq/l): ECG changes- peaked T waves, widening of QRS interval, ST depression, arrythmia, arrest.Emergency measures(>7meq/l with ECG changes)Calcium gluconate 0.5-1 ml/kg over 5 to 10 minsSalbutamol(5-10mg)nebulizationGlucose (50%)0.5-1 gm/kg with 0.1-0.2 unit/kg insulin Less urgent(>6meq/l) deplete body potassium( stop exogenous sources of potassium, sodium polystyrene sulfonate resin-kayexalate, 1g/kg orally decreases S.K+ by 1meq/L)
2.Fluid overload :fluid restriction Insensible water loss(300ml/m)+UO+extrarenal fluid lossReplace insensible loss by 10%D and UO & extrarenal loss by N/2D5.
3.Pulmonary Edema Oxygen Dopamine (5-10) mcg /kg /min infusion in min fluidFrusemide (2-4)mg /kg IV
4.Hypertension Symptomatic- Nitroprusside 1-8 mcg/kg/min, Frusemide 2-4 mg/kg IVAsymptomatic- Nifedipine 0.3-0.5 mg/kg PO5.Severe metabolic acidosispH