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• Acute renal failure (acute kidney injury)


  Abrupt loss of kidney function that results in: decline in glomerular filtration rate (GFR) manifested by oliguria, anuria, retention of urea and other nitrogenous waste products, and dysregulation of extracellular volume and electrolytes

  
• Acute kidney injury (AKI)


  • Traditionally manifested by an elevated or a rise in serum creatinine, but creatinine is often a delayed and imprecise test to accurately estimate GFR in failing kidneys

  
• RIFLE classification of AKI


  A consensus definition based on changes in serum creatinine and urine output
• RIFLE stages


  • R = Risk for renal dysfunction
  • I = Injury to the kidney
  • F = Failure of kidney function
  • L = Loss of kidney function
  • E = End-stage renal disease

  
• RIFLE definition


  Increase in serum creatinine by ≥1.5 times baseline within seven days
• AKIN definition


  Increase in serum creatinine by 0.3 mg/dL or ≥1.5 times baseline within 48 hours
• Etiology of AKI


  • Pre-renal causes
  • Intrinsic renal disease
  • Postrenal AKI

  
• Pre-renal AKI


  • GFR decreased significantly, increased salt and water absorption in the tubules, tubules have intact function, oliguria is universal, normal renal perfusion restores urine flow and GFR

  
• Causes of intrinsic AKI

  • Tubular injury (acute tubular necrosis)
  • Renal vascular diseases
  • Interstitial diseases
  • Glomerulonephritides

  
• Postrenal AKI


  Due to bilateral urinary tract obstruction
• Causes of postrenal AKI

  • Renal calculi
  • Clots
  • Neurogenic bladder
  • Medications that cause urinary retention
  • Congenital obstructive renal anomalies

  
• Clinical presentation of AKI

  • Depends on the cause: pre-renal AKI shows signs of dehydration, intrarenal AKI shows edema, hematuria, hypertension, postrenal AKI shows colicky abdominal pain, oliguria, palpable urinary bladder
• Physical findings in pediatric AKI

  • Signs of intravascular volume depletion
  • Signs of fluid overload
  • Renal disease due to systemic causes
  • Palpably enlarged kidneys
  • Signs of obstruction

  
• Lab abnormalities in AKI

  • Anemia
  • Thrombocytopenia
  • Hyponatremia
  • Metabolic acidosis
  • Elevated BUN, creatinine, uric acid, potassium, phosphate
  • Hypocalcemia
  • Low C3 level
  • Rise of ASO
  • ANA positive
• Urinary indices in pre-renal vs intrinsic AKI

  Pre-renal AKI: elevated specific gravity, elevated urine osmolality, low urine sodium, low fractional excretion of sodium

  Intrinsic AKI: low specific gravity, low urine osmolality, high urine sodium, high fractional excretion of sodium
• Management of AKI


  Treatment of underlying cause

  Treatment of complications
• Treatment of pre-renal AKI

  Prompt correction of hypoperfusion with isotonic fluid, blood transfusion, IV albumin, correct cardiac failure, inotropes

  
• Treatment of intrarenal AKI

  Give fluid, if no urine output give diuretics, fluid and salt restriction, specific treatment for underlying cause
• Treatment of postrenal AKI

  Catheterize and relieve obstruction, remove cause of obstruction
• Treatment of AKI complications

  • Hypertension
  • Edema
  • Hyperphosphatemia
  • Hypocalcemia
  • Hyponatremia
  • Hyperkalemia
• Chronic kidney disease (CKD)

  Kidney damage for greater than or equal to 3 months, as defined by structural or functional abnormalities of the kidney, with or without decreased GFR

  
• GFR


  Glomerular filtration rate, varies with age, gender and body composition
• Stages of CKD


  • Stage 1: GFR > 90 ml/kg/1.73 BSA

  Stage 2: GFR 60 to 90 ml/kg/1.73 BSA

  Stage 3: GFR 30 to 60 ml/kg/1.73 BSA

  Stage 4: GFR 15 to 30 ml/kg/1.73 BSA

  Stage 5 (ESRD): GFR < 15 ml/kg/1.73 BSA
• Abnormalities on kidney biopsy


  Definition continues...

  
• GFR


  • GFR < 60 ml/mn/1.73m2 for >= 3 months, with or without the other signs of kidney damage described above
  • GFR varies with age, gender and body composition of a child
  • Creatinin tend to increase only when the kidney lost 50% its function
• Normal GFR by age

  • 1 week (M, F): 41 + 15
  • 2-8 week (M, F): 66 +25
  • > 8 week (M, F): 96 + 22
  • 2-12 years (M, F): 133 + 27
  • 13-21 years (M): 140 + 30
  • 13-21 years (F): 126 + 22
• Classification of stages of CKD

  • Stage 1: GFR > 90 ml/kg/1.73 BSA, renal parenchymal disease present
  • Stage 2: GFR 60 to 90 ml/kg/1.73 BSA, usually no symptoms but may develop biochemical abnormality at the end of the lower GFR
  • Stage 3: GFR 30 to 60 ml/kg/1.73 BSA, Biochemical abnormalities and plus will have anorexia and poor growth
  • Stage 4: GFR 15 to 30 ml/kg/1.73 BSA, Symptoms more severe
  • Stage 5 (ESRD): GFR < 15 ml/kg/1.73 BSA, Renal replacement Rx required

  
• Estimation of GFR


  Patients with CKD have variable clinical presentation<|>Some can have symptoms directly referable to kidney disease (hematuria, flank pain)<|>Others will have extra renal symptoms like edema, HTN, and signs of uremia<|>Most patients are asymptomatic and are noted during routine examination with raised creatinin or proteinuria<|>Estimation of GFR is very important to assess the degree of renal impairment and to follow the course of the disease<|>The glomerular filtration rate (GFR) is equal to the sum of the filtration rates in all of the functioning nephrons<|>It gives an approximate measure of functioning nephrons

  
• Creatinin


  Mostly used to estimate GFR<|>Serum level varies with the age and the muscle mass of a patient<|>It tends to be secreted during severe renal insufficiency<|>For standardization, GFR is corrected based on the BSA of average adult which is 1.73m2 of 70kg wt
• Schwartz Formula


  1. Clearance of Cr ml/mn/1.73 m2 = k x height (cm) / serum creatinin (mg/dl)

  2. k = 0.33 for LBW infants <1 yr old

  3. k = 0.45 for term infants <1 yr old whose wt is appropriate for gestational age

  4. k = 0.55 for children and adolescent girls

  5. k = 0.70 for adolescent boys
• Etiology of CKD in children

  • Congenital structural malformations of the kidneys (40%)
  • Glomerulonephritis (25%)
  • Hereditary nephropathies (20%)
  • Systemic diseases (10%)
  • Others (5%)

  
• Etiology of CKD in children < 5yrs

  • Congenital renal malformation (renal hypoplasia, dysplasia or obstructive uropathy) (60%)
  • Congenital NS, renal vascular thrombosis, cortical necrosis, FSGS, HUS, PCKD

  
• Pathogenesis of CKD


  1. Hyperfiltration injury: As nephrons lost, the remaining nephrons undergo structural and functional hypertrophy with increased glomerular blood flow. The driving force for glomerular filtration in the surviving nephrons increases, leading to progressive nephronal loss due to direct effect of the elevated hydrostatic pressure on glomerular integrity and toxic effect of increased protein trafficking across the GBM.

  2. Proteinuria: Proteins which traverse the glomerules have direct toxic effect on tubules by enhancing inflammation, enhancing glomerular sclerosis and tubelo interstitial fibrosis. Uncontrolled HTN may worsen the glomerular injury. Hyperphosphatemia- with Ca, precipitate in tubular interstitium and then fibrosis.
• Clinical presentation of CKD

  Stages 1-2 are asymptomatic<|>Some patients with glomerular disease present with hematuria, hypertension, oliguria and edema which persists into later stages<|>Polydypsia and polyuria<|>Anorexia and lethargy, weakness and vomiting<|>Exercise intolerance, Failure to grow<|>Bony deformities from renal osteodystrophy

  
• Lab evaluation of CKD

  Urine dip stick testing: Hematuria and proteinuria suggest glomerular disease. Proteinuria can occur from any cause of CKD due to hyperfiltration of the remaining nephrons in increased intraglomerular pressure. Proteinuria may be absent in cystic or dysplastic kidney diseases.<|>Urine microscopy for red blood cells, red blood cell casts and pus cells.<|>Serum Cr, BUN, calculate GFR<|>CBC including RBC indices and reticulocyte count<|>Serum electrolytes: Na+, K+, Cl-, Ca, Po4, PTH<|>Serum 25,(OH)D3 level<|>Stool for occult blood
• Renal ultrasound


  Echogenicity and size of the kidney could be determined<|>Any structural abnormalities can be assessed like cystic dysplasias and hydronephrosis, presence of stones or calcifications, blood flow to the kidney, the condition of bladder (thickness of the bladder wall, trabeculations, capacity, calculi, intravesical masses, diverticulae)

  
• Other imaging


  Voiding cysto-ureterography (VCUG) if there is hydronephrosis or reflux nephropathy is suspected<|>IVP can be done to see differential function of each kidney and assess the presence and site of obstruction, but should be avoided in advanced kidney disease as it might worsen kidney damage due to contrast nephropathy

  
• Complications of CKD


  • Accumulation of nitrogenous waste products
  • Acidosis
  • Sodium retention
  • Oliguria
  • Urinary concentrating defect
  • Hyperkalemia
  • Renal osteodystrophy
  • Growth retardation
  • Anemia
  • Pericarditis, CMP
  • Hypertension
  • Anemia
  • Infection
  • Neurologic symptoms
  • GI Symptoms
  • Hypertension
  • Hyperlipidemia
  • Impaired glucose tolerance
• Management of CKD


  Treat reversible kidney dysfunction<|>Prevent or slow the progression of kidney disease<|>Treat the complications of CKD<|>Identify and adequately prepare the child/family in whom renal replacement therapy will be required<|>Avoid nephrotoxic drugs<|>Prompt control of BP<|>Reduce proteinuria<|>Nutrition support<|>Close monitoring of patients' clinical and laboratory status

  
• Fluid and electrolyte management

  Low Na & fluid loss: increase fluid & Na intake<|>High Na & fluid overload: Na restriction < 2.4 gm/dy, diuretics<|>Hyperkalemia: restrict diet, loop diuretics, treat acidosis, RRT