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Acute kidney injury chronic kidney disease

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Text of Acute kidney injury chronic kidney disease
Urine formation
•Creatinine •Urea / Blood urea nitrogen •Glomerular filtration rate •Renal clearance
•Breakdown product of creatine phosphate (energy reservoir) •Usually produced at constant rate (depending on muscle mass) • Excreted unchanged by the kidneys: • glomerular filtration - mostly • proximal tubular secretion – minor
• Little to no tubular reabsorption • 45-90 μmol/L (0.5 - 1.0 mg/dL) for women; 60-110 μmol/L (0.7 - 1.2 mg/dL) for men
Urea / Blood urea nitrogen
•Urea – produced in the liver as a waste product of protein digestion •BUN – the mass of nitrogen within urea / volume •Normal range 1.8-7.1 mmol/L urea (6–20 mg/dL BUN) • Increased urea/BUN – decreased kidney function • High protein diet • Hypovolemia • Hemorrhage • Fever • Increased catabolism
BUN-to-creatinine ratio
• To determine the cause of acute kidney injury or dehydration •Principle: • Both urea and creatinine are freely filtered through glomeruli
• Reabsorption of urea (not creatinine) can be regulated (up or down)
BUN:Cr Urea:Cr Location Mechanism
BUN reabsorption is increased. BUN is disproportionately elevated relative to creatinine in serum. Dehydration or hypoperfusion is suspected.
10-20:1 40-100:1 Normal or Postrenal (after the kidney)
Normal range. Can also be postrenal disease. BUN reabsorption is within normal limits.
<10:1 <40:1 Intrarenal (within kidney)
Renal damage causes reduced reabsorption of BUN, therefore lowering the BUN:Cr ratio.
•BUN and creatinine will not be raised above the normal range until 60% of total kidney function is lost • Therefore, more accurate methods are useful
Glomerular filtration rate
•Volume of blood filtered per minute •ml/min/1.73m2 • Flow rate of filtered fluid through the kidneys
• Estimated GFR (eGFR) – serum creatinine • Sex, age, weight, height, race
Creatinine clearance
•Approximation of GFR •Volume of blood plasma that is cleared of creatinine per unit of time
Estimated clearance
Acute kidney injury
• Loss of kidney function that develops within 7 days •Previously: acute renal failure •Wide spectrum of injuries, not just failure •Common in critically ill patients • 13-18% of all people admitted to hospital
• 1802 ischuria renalis • 1909 Bright’s disease – a consequence of toxic agents, pregnancy, burn, trauma or operations • First WW – war nephritis • Second WW – acute tubular necrosis • 1951 – acute renal failure • 2004 – acute kidney injury
•RIFLE – risk, injury, failure, loss, end-stage kidney disease •AKIN – Acute Kidney Injury Network group
Biomarkers of AKI
• Urine dipstick • Blood • Protein • Leukocytes • Nitrites • Glucose
• Urine microscopy • Red cell casts • Dysmorphic red cells • Tubular epithelial cells
• Ultrasound • Auto-immune profile • Biopsy
Precipitating factors for AKI
Ischemic AKI
• The most common •High susceptibility of kidney to ischemic injury • Structural associations between renal tubules and blood vessels in outer medulla • vasoconstriction • epithelial injury (low ATP) – necrosis or apoptosis • activation of inflammatory processes
•All segments of nephron can be affected, but proximal tubular cells are most commonly injured
Consequences of AKI
Consequences of AKI
Distal organ injury
Kidney-lung interactions
Cardiorenal syndrome
Hepatorenal syndrome
•Rapid decrease in kidney function in individuals with cirrhosis or fulminant liver failure • 1. Altered liver function • 2. Abnormalities in circulation – constriction of vessels in kidneys and dilation in splanchnic circulation (intestines) • 3. Kidney failure
•Vasopressors • Norepinephrine, vasopressin
Outcomes after AKI episode
• 1. Full recovery and return of renal function to baseline • 2. Incomplete recovery of renal function resulting in CKD • 3. Exacerbation of pre-existing CKD accelerating progression to ESKD • 4. Non-recovery of renal function leading to ESKD
Animal models of AKI
Chronic kidney disease
•Progressive loss of kidney function over a period of months or years •Previously: chronic renal failure •Definition: • Decreased kidney function - less than 60 ml/min/ 1,73m2 OR
• Markers of kidney damage OR • Both • At least 3 months duration • Regardless of cause
Markers od kidney damage
Risk factors
•Accumulation of nitrogenous wastes (uremia) • neurological disorders (uremic encephalopathy) • uremic frost
•Mineral bone disease – disturbed vitamin D, calcium and phosphate metabolism •Renal hypertension •Anemia •Reduced RBC survival and iron deficiency •Alterations in water, acid-base and electrolyte balance
Diabetic nephropathy
•Changes in glomerular structures •Damage to blood vessels •Decreasing filtration rate • Increasing blood volume
Glomerular vessels
•Often by chance findings • Screening tests • Severe symptoms
•Renal fibrosis as a response to injury •Replacement of functional tissue by fibrotic tissue
•Renal replacement therapy • Hemodialysis (diffusion) • Peritoneal dialysis • Hemofiltration (convection – increased hydrostatic pressure)
• Hemodiafiltration • Kidney transplantation
•Blood pressure target in CKD patients
Animal models of CKD
•No independent entities
•AKI is a risk factor for CKD •CKD is a risk factor for AKI •Both are risk factors for cardiovascular disease
Acute-on-chronic kidney disease
•AKI occurs on the background of pre-existing CKD •CKD as risk factor for AKI •Most common causes: • Systemic infection • Drugs – diuretics, ACE-inhibitors • Dehydration • Urinary tract obstruction
• Diagnosis of AKI based on • sCr levels OR urine volume
•Most common causes of AKI include • Ischemia, sepsis, hypovolemia, drugs
• Diagnosis of CKD based on • Decreased kidney function - less than 60 ml/min/1,73m2 OR • Markers of kidney damage OR • Both • At least 3 months duration
• Prognosis of CKD based on • eGFR and proteinuria
• Two major causes of CKD are • Diabetes and hypertension

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