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Definition of acute renal failure ARF

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					    Definition of acute renal failure (ARF)


ASL is a sudden, often reversible reduction of the
elimination and metabolic function of kidneys,
whose more severe form is associated with
marked reduction of diuresis
                     ARF)
(oligoanuric form of ARF)

Oliguria = diuresis < 300 ml/day
Anuria = diuresis < 100 ml/day

Non-
Non-oligoanuric ARF is associated with a severe
reduction of renal functions. However diuresis is
preserved due to residual function in the preserved
areas of renal tissue
                                     New classification of
                                     acute kidney injury


                                              RIFLE



Molitoris BA et al. (2007) Improving outcomes of acute kidney injury: report of
  an initiative Nat Clin Pract Nephrol 3: 439–442 doi:10.1038/ncpneph0551
          Kriterium: GF                        Kriterium: diuresis
            SKrea zvýšen o 26,4 µmol/l
                                                                                   High
Risk      nebo o 50-100 % (1,5 – 2x proti
           výchozí hodnotě) nebo pokles
                                                Diuréza pod 0,5 ml/h a kg po
                                                   dobu více než 6 hodin         sensitivity
                  GFR o > 25 %

             SKrea zvýšen o 100-300 %
              (tj. 2 – 3x proti výchozí       Diuréza pod 0,5 ml/h a kg po

 Injury        hodnotě) nebo pokles
                    GFR o > 50 %
                                                dobu více než 12 hodin


                SKrea zvýšen o 300 % (3x)
                                                Diuréza pod 0,3 ml/h a
                nebo pokles GFR o > 75 %
                                                 kg po dobu 24 hodin
  Failure       nebo kreatinin 354 µmol/l a
                více s akutním vzestupem o
                   minimálně 44 µmol/l
                                                 nebo anurie po dobu
                                                       12 hodin




    Loss          Persistující akutní renální selhání = kompletní ztráta
                         funkce ledvin po dobu více než 4 týdny
                                                                                 High
                        Konečné stadium onemocnění ledvin                      specificity
       End                 (ESKD) (více než 3 měsíce)
                Early biomarkers of AKI

   Neutrophil gelatinase - associated lipocalin (NGAL)
                  (IL-
    Interleukin 18 (IL-18)
   Cystatin C
                              KIM-
    Kidney injury molecule 1 = KIM-1




      These biomarkers are more usefuI for
      early diagnosis and early therapeutic
       intervention in AKI than creatinine
            Risk factors of acute renal failure

   Sepsis
   Hypovolemia
   Acute pancreatitis
   Rhabdomyolysis
   Hemolysis
   Hepatic insufficiency
   Treatment with aminoglycoside antibiotics
   Treatment with cytostatics
   Artificial ventilation during respiratory failure
   i.v.
    i.v. administration of contrast agents
   Diabetes mellitus
   Paraproteinaemia
        Pathophysiological factors of ARF



   Reduction of blood flow through the cortical layer of
    the kidney

   Change of permeability of the glomerular basal
    membrane

   Tubular reflux of filtrate

   Tubular obstruction
                  Causes of ARF



    Prerenal
    (renal hypoperfusion)

    Renal
    (primary impairment of renal parenchyma)

    Postrenal
    (urological, during urinary tract obstruction)
               ARF - prerenal ethiology (1)

1. Reduction of effective intravascular volume
   Volume depletion
   - blood loss
   - GIT loss (vomiting, diarrhoea, probes, drains)
   - renal loss (diuretics, polyuric conditions)
   - loss through wound areas/skin (burns, sweating)

  Volume redistribution
  - transfer of fluids to the third space (pancreatitis, ascites,
     peritonitis, nephrotic syndrome)
  - peripheral vasodilatation (sepsis, antihypertensives)
               ARF - prerenal ethiology (2)

2. Reduced cardiac output
      (congestive heart failure, cardiomyopathy, myocardial
      infarction, pericardial tamponade, massive pulmonary
                           respiration)
      embolism, artificial respiration)
3. Impaired intrarenal hemodynamics
      prostaglandin synthesis inhibitors (NSAID)
      vasodilators of efferent arteriola (ACE inhibitors)
      vasoconstrictors (Cyclosporine A)
4. Renovascular obstruction
      Atherosclerotic and fibromuscular stenoses and
      closures, venous and arterial thrombosis, dissecting
      aneurysm, vasculitis, external compression
Differential diagnosis of prerenal and renal form of ARF



                   Normal
                   Normal        Prerenal    Renal


  Spec. gravity    1015 – 1025   > 1020      1010

  UNa mmol/L       15 – 40       < 20        > 30

  FENa %           1–3           <1          >3

  Ukr/Pkr µmol/L   20 – 60       > 40        < 20
           ARF from primary renal causes (1)
1. ARF on the basis of tubular damage
   Acute tubular necrosis (ATN) - 60% of all ARF
        - Ischemic (prolonged hypoperfusion in prerenal ARF)
                                (toxo-infectious-
        - In septic conditions (toxo-infectious-hypovolemic shock)
        - Nephrotoxicity - ATB
                          - Cytostatics and immunosuppresives
                         - Organic solvents, glycols, fungi
                         - Heavy metals
                         - Radiocontrast agents
                         - Rhabdomyolysis (hematin from myoglobin
                            is harmful to the cells of proximal tubule)
                         - Incompatible blood transfusions
        - In pregnancy and after delivery
   Intratubular obstruction
        - Acute urate nephropathy
        - Primary and secondary hyperoxaluria
        - Deposit of proteins (multiple myeloma)
Acute tubular necrosis
Reparation phase of acute tubular necrosis
           ARF from primary renal causes (2)
2. ARF on the basis of interstitial damage
    Acute interstitial nephritis after drugs (antibiotics, analgesics,
     antiphlogistics, diuretics, anticonvulsants)
    Acute infectious interstitial nephritis (bacterial infections –
     including Weil’s disease, viral and parasitic infections)
    Affection of interstitium in hemoblastoses and system diseases
    (myelo-
    (myelo- and lymphoproliferative diseases, SLE)
3. ARF due to glomerular and vascular lesions
           post-
    Acute post-streptococcal GN
                 post-
    Other acute post-infectious GN
    Rapidly progressing GN
    Primary system vasculitis
    Primary chronic glomerulopathies
    Secondary chronic glomerulopathies
    Malignant hypertension (primary and secondary)
Acute interstitial nephritis
Leukocytary cylinder
               ARF from postrenal causes

   Urolithiasis (cave solitary kidney)
   Prostate (hypertrophy, tumor, inflammation, lithiasis)
   Tumors (pelvis, ureter, urinary bladder, compression)
   Papillary
    Papillary necrosis
    (analgetics,                              mellitus)
    (analgetics, urate nephropathy, diabetes mellitus)
   Ligature of ureter
    (gynaecological and surgical complications)
   Retroperitoneal haematoma (trauma, surgery)
   Urology examination
                         membranes,
    (oedema of mucous membranes, contrast agents)
   Retroperitoneal fibrosis
   Major blood coaguls and necrotic tissues
    (biopsy, surgery, necrosis)
   Lymphocela (surgery, transplantation)
   Atonia or rupture of urinary bladder
Ultrasound
Ultrasound image of hydronephrosis
IVP in bilateral hydronephrosis
Dilatation of ureters in urinary tract obstruction
Acute urate nephropathy
       Nephropathy caused by myoglobinuria
                     Etiology

   Use of higher amount of ethyl alcohol
   Hypothermia
   Pressure necroses of skeletal muscles
   Traumatic damage of skeletal muscles
   Drugs (statins) and toxins
   Metabolic myopathy
   Extreme bodily exertion
   Infection (including HIV)
   Coma, immobilization
      Nephropathy caused by myoglobinuria
                 Pathogenesis

   Reduction of renal perfusion with decrease of
    intravasal volume which leads to activation of
        renin-
    the renin-angiotensin system
   Binding of NO that causes vasodilatation
    to myoglobin contributes also to renal
    vasoconstriction
   Production of castings in renal tubuli
   Toxic influence of a heme component on
    renal tubuli due to a damage of lipid
    structures of the cell membrane by
    lipoperoxidation
            Diagnosis of rhabdomyolysis


   Clinical picture: Rigid and painful muscles,
    muscular oedema and weakness
   Laboratory findings: ↑ myoglobin,
                  (at
    myoglobinuria (at urine pH of < 5.6 myoglobin
                     haematin),
    changes to toxic haematin), ↑ urea, ↑ creatinine,
    ↑ CPK, ↑ LDH, hyperkalaemia, hypocalcaemia,
    hyperphosphataemia
   EMG (muscle lesions)
   Histological muscular examination
            Nephropathy caused by myoglobinuria
                       Management


   Infusion of crystalloids to maintain duresis above
    300 ml/h. If a diuretic response is not present
    Furosemid is administered in high doses
   Alcalization of urine with infusions of sodium
    hydrogen carbonate
    (“bicarbonate diuresis” has a protective effect especially during tubular
    lesions due to rhabdomyolysis or haemolysis)
   Treatment of hyperkalaemia
   Haemoelimination therapy
   Parenteral or enteral nutrition
   Prevention and therapy of complicated infections
      Definition of contrast induced nephropathy

   Acute worsening of renal function qualified either by
    absolute increase of serum creatinine by more than
    44.2 µmol/L or by relative increase by more than
    25% above the level before administration of a
    contrast agent
                                                24-
    Acute increase of serum creatinine during 24-48
                                  3-
    hours with a maximum after 3-5 days after
    administration of a contrast agent
   Elimination of other causes of renal failure
   Due to development of vascular surgery and
    intervention cardiology the number of cases of
    contrast nephropathy has increased
        Nephropathy after radiocontrast substances
                    Pathogenesis (1)

   Intrarenal vasoconstriction leading to
    ischaemia of medullar structures
   Direct toxic effect of a contrast substance
    on the cells of the proximal tubule
   Intratubular obstruction
   Tissue damage caused by free oxygen
    radicals
   Induction of apoptosis
        Nephropathy after radiocontrast substances
                     Patogenesis (2)

   After administration of ionic radiocontrast
            short-
    agents short-term (minutes) vasodilatation
    occurs, which is followed by strong
    vasoconstriction lasting several hours and
    with prolonged reduction of blood flow and
    glomerular filtration
   The main location of damage to renal tissue
    is the external medular zone and therefore
    nephrotoxic acute tubular necrosis is
    concerned
         Risk factors of contrast nephropathy

    Risk factors of a patient        Risk factors of
        (<
    Age (< 70 years)                 a radiocontrast agent
   Gender (female)                 Osmolality
   Preexisting renal disease        1.G. = hyperosmolality
    (the most serious risk           (1 500 -1 800 mOsm/kg)
    factor)
    factor)                                  hypo-
                                     2.G.= hypo-osmolality
   Diabetes mellitus                (780 mOsm/kg)
               risk)
    (twice the risk)                         iso-
                                     3.G = iso-osmolality
   Reduced ejection fraction       Non-
                                     Non-ionising contrast
   Risk medication                  agents have a smaller
   Low level of serum albumin       toxicity than ionising ones
    and natrium                     Dose of a contrast agent (a
   Multiple myeloma                 dose up to 70 ml is
                                     considered safe, a dose
                                     above 5 ml/kg is considered
                                     a risk)
         Nephropathy after radiocontrast substances
            Preventive and therapeutic measures

   If a patient does not belong to a risk group it is not
    necessary to perform any specific measures
   Correction of all susceptive risk factors
   Sufficient hydration and adjustment of possible
    intravascular hypovolemia
    (FS NaCl 150 ml/hour 3 hr before and 6 hr after
                   300-                examination)
    examination, 300-500 ml during examination)
   Adjustment of medication before administration of a
    contrast agent (cave drugs which limit renal blood
    flow – NSA, aminoglycosides, ACE inhibitors)
                   non-
    Preference for non-ionic substances with low
    osmolality
                      N-
    Administration of N-acetylcystein before and after
    application of a radiocontrast agent
                N - acetylcestein (NAC)

   Antioxidant agent that affects intracellular
    mechanisms of cell stress and increases
    production of NO (vasodilation effect)
   Reduces apoptosis and necrosis of tubular
    cells
   Indication of NAC in nephrology: Prevention of
    contrast nephropathy, paracetamol intoxication and
                   ischemic-
    prophylaxis of ischemic-reperfusion damage
            600-
    Dosage: 600-1200 mg orally or i.v. one day
    before and one day after X-ray examination
         Nephropathy after radiocontrast substances
                   Elimination methods

   Haemodialysis is considered ineffective
    (Pathogenetically the most important are the changes in
    haemodynamics which occur immediately after the
    administration of a contrast agent and therefore subsequent
    haemodialysis, which is aimed at the removal of a contrast
    agent from the blood compartment is ineffective)

   Prophylactic haemofiltration reduces the risk of
    contrast nephropathy, especially in patients with
    preexisting CHRI and in cardiac patients who are at
    risk of pulmonary oedema

   Performance of haemofiltration removes the
    contrast agent, leads to optimisation of hydration
    and stabilisation of circulation
                      Examination in ARF
 Medical history
surgery, trauma, pregnancy, shock, toxic substances, blood transfusions,
contrast agents, nephrotoxic substances, etc.
 Physical examination
HR, BP, hydration, examination per rectum
 Laboratory examination
Na, K, Ca, P, KM, urea, creatinine, osmolality, glycaemia, Astrup, blood
count, spec. gravity of urine, Na in urine/24 hr., Ukr/Pkr, FENa
 Urinanalysis
diuresis, urine – chemically + sediment, K, Na, urea, creatinine,
osmolality
 Central venous pressure
 Renal sonography
 Hospitalization at Intensive Care Unit
                  moni
urinary catheter, monitoring balance
                     Phases of ARF


1.   Phase of initial damage

2.   Phase of early diuresis
     (diuresis exceeds 300 mL/day, low level of GF, high
     level of nitrous catabolites)

3.   Phase of late diuresis
     (polyuria, decrease of nitrous catabolite level, gradual
     normalization of GF)

4.   Phase of reparation
     (normalization of glomerular and subsequently
     tubular function – impairment of concentration ability
              3-
     persists 3-12 months)
                    Complications of ARF

1. Organ complications
   - gastrointestinal tract impairment
    stress ulcer, erosive gastritis, enterorrhagia
   - uremic pericarditis
    symptom of insufficient therapy, danger of rapid occurrence of
    haemorrhagic exsudate with a risk of tamponade, regular
                      check-
    echocardiography check-ups are necessary
   - haematology complications
    anemia (hemodilution, hemolysis, bleeding),
    thrombocytopathy, trombocytopenia, coagulation factor disorders
    (sepsis, drugs, toxins, DIC)
   - neurological disorders
    lethargy, somnolence, increased irritability, confusion, cramps
2. Metabolic complications
3. Infectious complications
             Therapeutic approaches in ARF

                   life-
  Management of life-threatening conditions and complications
 Elimination of the cause of ARF
 Conservative therapy
      fluids according to the balance and CVP, Dopamine (2-4  (2-
      μg/kg/min.), Furosemid
 Adjustment of ion disorders
 Ensuring the need for nutrients and energy
                                    (40-
      Energy 167 – 209 kJ/kg/day (40-50 kcal)
      Proteins 0.8 – 1.2 g/kg/day
      Sugars 6 – 8 g glucose/kg/day
      Fats 1 g fat/kg/day
                                                                     long-
      Substitution of trace elements and vitamins only in case of long-
      term parenteral nutrition (parenteral, enteral and oral nutrition)
 Treatment of complications of ARF
 Dialysation techniques (CAVH, CVVH, haemodialysis,
                              haemofiltration, peritoneal dialysis)
            Indications for dialysis in ARF

   Clinically expressed uraemia
   Hyperhydration
   Oligoanuria > 3 days
   Severe metabolic acidosis
   Hyperkalaemia > 6 mmol/L
   Urea > 35 mmol/L
   Creatinine > 600 μmol/L
   Hypercalcaemia > 4,5 mmol/L
   Hyperuricaemia > 1000 μmol/L
                      Prognostic factors of ARF

   Etiology of ASL

   Renal damage grade
    (oliguria, creatinine, frequency of dialysis)

   Number and grade of organs affected concomittantly

   Age

   Preexisting disease (diabetes, CAD, hepatic lesion)
   Complications            - infectious (septicaemia, pulmonary infections,
                                            urological infections)
                             - metabolic (catabolism, dehydration, ionic dysbalance)

                                     (cardio-
                             - organ (cardio-respiratory failure, gastrointestinal
                                      complications, CNS disorders, pancreatitis, burns)

				
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