prepared by dr abdulbari a mahdi fibms ped nephrology n.
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Acute Kidney injury
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  1. Prepared by: Dr. Abdulbari A. Mahdi FIBMS (Ped. Nephrology) Acute Kidney injury

  2. Acute Kidney Injury Abrupt increase in the blood concentration of creatinine and nitrogenous waste products and by the inability to regulate fluid and electrolyte homeostasis appropriately

  3. A Common, Serious Problem Present in 5% of all hospitalized patients, & up to 30% of ICU patients Incidence is increasing at an alarming rate Mortality rate >50% in dialyzed ICU patients 25% of ICU dialysis survivors progress to ESKD within 3 years

  4. Terminology • More than 30 different definitions • Variety of quoted incidence rates, risk factors, and morbidity and mortality rates • Change in nomenclature of this condition to acute kidney injury (AKI), acknowledging that acute renal dysfunction occurs due to injurious endogenous or exogenous disease processes • Recently, a group of pediatric and adult nephrologists and intensivists founded the Acute Dialysis Quality Initiative and proposed a consensus definition called the RIFLE classification

  5. In 2004, a consensus definition for AKI was proposed by the Acute Dialysis Quality Initiative: the RIFLE criteria - 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

  6. When the achieved designation results from urine output criteria a subscript “o” is added e.g. RIFLE-Fo • A subscript “c” is used to denote the presence of preexisting chronic kidney disease

  7. Pediatric RIFLE criteria • The adult-derived RIFLE definition was modified, and then applied and validated in pediatric patients and renamed as the pediatric RIFLE (pRIFLE) criteria. • pRIFLE stratifies AKI from mild (RIFLE R, risk) to severe (RIFLE F, failure) based on changes in the SCR or estimated creatinine clearance (eCCl) • Estimated creatinine clearance (ml/min/1.73 m2) is calculated using the Schwartz formula: eCCl = k × height / SCR

  8. pRIFLE R – eCCl decrease by 25% • OR urine output is < 0.5 ml/kg/hr for 8 hr

  9. pRIFLE I – eCCl decrease by 50% OR urine output < 0.5 ml/kg/hr for 16 hr

  10. pRIFLE F – eCCL decrease by 75% or eCCl < 35 ml/min/1.73 m2 OR urine output < 0.3 ml/kg/hr for 24 hr or anuric for 12 hr

  11. pRIFLE L – persistent failure > 4 weeks

  12. pRIFLE E – persistent failure > 3 months (ESRD)

  13. Pediatric RIFLE criteria definition and classifications of AKI

  14. Aetiologic Classification • Pre-renal • Renal (intrinsic) • Postrenal (obstructive)

  15. Prerenal failure Decreased true intravascular volume • Dehydration • GIT losses • Salt-wasting renal or adrenal diseases. • Central or nephrogenic diabetes inipidus • Third space losses: sepsis trauma nephrotic syndrome Decreased effective intravascular volume • congestive heart failure • Pericarditis • cardiac tamponade • hepatorenal syndrome

  16. Prerenal Azotemia Pathophysiology Pathophysiology Renal Autoregulation Renal Autoregulation myogenic reflex myogenic reflex glomerulotubular feedback glomerulotubular feedback angiotensin II angiotensin II Sodium and water reabsorption Sodium and water reabsorption aldosterone aldosterone vasopressin vasopressin

  17. Mechanisms of Intrarenal Autoregulation Afferent Maintenance of RBF Arteriolar Resistance Reduced Myogenic Reflex Maintenance Renal and Tubuloglomerular Feedback of Perfusion GFR Pressure Angiotensin II Efferent Maintenance of Arteriolar GHP Resistance

  18. Mechanisms of Sodium and Water Conservation in Prerenal Azotemia Decreased Renal Perfusion Renin Vasopressin Angiotensin II Aldosterone Renal Tubular Na Renal Tubular H2O Reabsorption Reabsorption Urine Volume Concentrated Urine Urine Sodium

  19. Intrinsic ARF Intrinsic ARF may be due to the following broad Intrinsic ARF may be due to the following broad categories: categories: ischemic ischemic acute tubular necrosis nephrotoxic nephrotoxic - glomerular changes vascular / glomerular vascular / glomerular - minimal tubular involvement other other

  20. Acute Tubular Necrosis Hypoxic / ischemic ATN • Prolonged prerenal injury OR severe hypoxic insults • Urinalysis → Casts + Epithelial cells Casts ± low grade proteinuria • Urinary indices: inability to conserve Na+ and water • Serum creatinine ↑↑ 0.5 – 2 mg/dl/day • U/S : Normal sized-kidneys with loss of C.M. differentiation • Prognosis ?? → CKD • Recovery + diuretic phase → attention to fluid and electrolyte balance

  21. Acute Tubular Necrosis Nephrotoxic AKI • Antibiotics • Acyclovir, Cidofovir, Indinavir, Foscarnet, Pentamidine, Aminoglycosides and amphotericine B • Organic solvents • Ethylene glycol, Toluene • Poisons • Paraquat, Snake bites • Chemotherapeutic agents • Cisplatin, Ifosphamide • Anti-inflammatory and immunosuppressive agents • NSAIDs, Cyclosporin, Tacrolimus, IVIG, Radiocontrast agents

  22. Acute Interstitial Nephritis • Reaction to drug OR idiopathic • Presentation: • Fever, Arthralgia, Rash, Uveitis, Eosinophilia,Pyuria • Pathogenesis: Hypersensitivity reaction with the development of antitubular basement membrane antibodies • U/S: large echogenic kidneys • Biopsy: Interstitial infiltrates with many eosinophils • Specific therapy → withdrawal of the drug and corticosteroid

  23. Etiology of AIN

  24. Hemolytic Uremic Syndrome • One of the most common causes of community-acquired AKI in young children • Triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency • HUS has clinical features in common with thrombotic thrombocytopenic purpura (TTP) which is also characterized by these features but can include central nervous system (CNS) involvement and fever and can have a more gradual onset • A low platelet count can usually, but not always, be detected early in the illness, but it can then become normal or even high. If a platelet count obtained within 7 days after onset of the acute gastrointestinal illness is not <150,000/mm3, other diagnoses should be considered

  25. Terminology and Classification

  26. Etiology

  27. Microangiophathic hemolytic anemia with fragmented erythrocytes (schistocytes)

  28. Postrenal AKI • Obstructive cause • - Solitary kidney • - Ureters bilaterally • - Urethra • Congenital OR Acquired • Rx: promptly relieve the obstruction

  29. Clinical Approach to AKI: Pre-, Intra-, and Post-Renal History Volume status Ultrasound Urinalysis US shows Hydronephrosis Urinalysis Normal Urinalysis Abnormal Post-Renal Pre-renal Tubulointerstial Disorders Glomerular and Vascular Disorders

  30. Nephrologists Clinical Approach to AKI History Volume Status Ultrasound Urinalysis Normal Urinalysis Hydronephrosis Pre-Renal Post-Renal Vascular Disorders Abnormal urinalysis Low ECF Volume GI losses Hemorrhage Diuretics Osmotic diuresis Altered renal blood flow or hemodynamics Sepsis Heart failure Cirrhosis/Hepatorenal syndrome Hypercalcemia Medications NSAIDs/Cox-2 inhibitors ACE inhibitors Angiotensin II receptor blockers Vascular disease Prostate disease BPH Cancer Pelvic malignancy Stones Stricture Retroperitoneal fibrosis Arterial Renal artery stenosis Renal artery thromboembolism Fibromuscular dysplasia Takayasu arteritis Medium vessel Polyarteritis nodosa Kawasaki disease Small vessel Glomerulonephritis Thrombotic microangiopathies Cholesterol emboli Renal vein Renal vein thrombosis Abdominal compartment syndrome Renal parenchymal disorders Glomerular Disorders Tubulointerstitial Disorders Tubular obstruction Crystals Calcium oxalate (Ethylene glycol, orlistat) Indinivir Acyclovir Methotrexate Tumor lysis syndrome Myeloma cast nephropathy Acute tubular necrosis Ischemic Nephrotoxic Contrast-induced Rhabdomyolysis Acute interstitial nephritis Medication-induced Autoimmune Sjogren syndrome Sarcoidosis Infection-related

  31. Treatment of AKI Aims of treatment: Maintenance of Fluid and Electrolyte Homeostasis Preventing Life-threatening Complications Avoiding Further Kidney Injury Providing Apprpriate Nutrition RRT in most severe forms of AKI

  32. The treatment of AKI divided into: • nondialytic therapy (supportive therapy and medical management) • dialytic therapy . • The nondialytic therapy: • to date the only effective nondialytic treatment of AKI entails: • 1. Restoration of adequate renal blood flow • 2. Avoidance of nephrotoxic medications or those that interfere with renal compensatory mechanisms • 3. Assurance that renal perfusion has been maximized before exposure to nephrotoxic agents.

  33. 1- Vasoactive agents: a- dopamine : • . the use of “renal dose” dopamine(0.5-5 μg / kg / min) to improve renal perfusion after an ischemic insult has become very common in ICU(in the absence of hypertension). • . dopamine increases renal blood flow by promoting vasodilatation and may improve urine output by promoting natriuresis. b- ANP: an atrial natriuretic peptide, it increases the GFR by dilating afferent arterioles while constricting efferent arterioles and so improve GFR , urinary out put .

  34. 2- Diuretics therapy : • Stimulating urine output eases management of AKI, but the conversion of oliguric to nonoliguric AKI has not been shown to alter the course of the disorder. • Diuretics therapy have no value in patient with established anuria. • These agents act by altering tubular function but it should be recognized that the increase in urine flow does not represent an improvement in renal function nor does it affect the natural history of the disease that precipitated the AKI.

  35. 1. Mannitol(0.5-1 g/kg delivered over 30 minutes) may increase intratubular urine flow to limit tubular obstruction and may limit cell damage by preventing swelling or by acting as a scavenger of free radicals or reactive oxygen molecules. • S.E. of mannitol a. Lack of response to therapy can precipitate congestive heart failure, particularly if the child’s intravascular volume is expanded before mannitol b. Lack of excretion may result in hyperosmolarity. 2. Furosemide (Lasix) (1-5 mg / kg / dose) • . increases urine flow rate to decrease intratubular obstruction • . inhibits Na-K ATP ase, which limits oxygen consumption in already damaged tubules with a low oxygen supply . • S.E. of Furosemide is ototoxicity. Continuous in fusions may be more effective and may be associated with less toxicity than bolus administration.

  36. 3- Fluid Balance: • Depending on the cause of AKI and the presence or absence of associated symptoms such as vomiting or diarrhea, children with AKI may present with hypovolemia, euvolemia, or fluid over loadandpulmonary edema. • Patients with salt-wasting renal disease, diarrhea or vomiting may present with fluid deficits that need correction to a euvolemic state, whereas patients with oliguria or anuria more commonly present with hypervolemia and need fluid restriction and/or acute fluid removal to achieve a euvolemic state. • In some oliguric patients it may be imposible to distinguish whether oliguria is due to hypoperfusion (hypovolemia) or impending ATN . so evaluation of the urine may prove helpful in this regard

  37. . in patient with hypovolemia • 1- urine is concentrated (urine osmolality >500mOsm / kg) because increase reabsorption of water • 2- urinary Na conc. < 20 m Eq / L because Na reabsorption increase • 3- Fractional excretion of sodium (F.E.Na) is usually <1% • 4- increase serum BUN to creatinine ratio due to increase tubular reabsorption of urea. • 5- Increase urine to plasma creatinine ratio because the creatinine is not reabsorbed.

  38. by contrast in patient with ATN 1- Dilute urine is (osmolality<350mOsm / kg) 2- urine Na conc.>40 mEq / L 3- FE Na > 1% 4- Urine creatinine to plasma creatinine ratio dose not increase above 20:1 ratio. 5- The serum BUN to creatinine ratio does not increase

  39. Assessment of the patient for fluid balance • . Weight, BP, heart rate, skin turgor and capillary refill are each used to assess the intravascular volume. • 1- in children who are intravascularlyvolume depleted, 10-20 ml / kg of normal saline can be infused to reestablish intravascular volume (dehydrated pt. generally void with in 2 hours) . • If U.O.P. does not increase and azotemia does not improve after fluid resuscitation, then catheterization of the bladeler and central venous pressure monitoring may be necessary to further guide fluid therapy. This achieved through the use of central venous catheter that positioned in the central venous area of the right heart is satisfactory guide to the speed of fluid administration; the CVP normally between 2 and 12 cm H2O. If clinical and laboratory evaluations show that the patient is adequately hydrated, then aggressive diuretic therapy may be considered.

  40. 2- for fluid overload, fluid restriction and/or fluid removal with dialysis or hemofiltration may be instituted if the child does not respond to diuretic therapy. • . when intravascular volume normalized, euvolemia can be maintained by providing the child with fluid to replace normal water losses from the skin, respiratory tract, and GIT (insensible losses, 400 ml / m2 / 24hr. + UOP) • . excess losses need to be accounted for as well and replaced with the appropriate fluid. • In general, glucose containing solutions (10-30%)with out electrolytes are used as maintance fluids . the composition of the fluid may be modified in accordance with the state of electrolyte balance. • . daily weight measurements, BP, accurate fluid input & output records, physical examination and nutritional needs of the child guide ongoing fluid therapy.

  41. 4-Electrolyte and Acid-Base Balance: • 1. Na+ Balance • . mild hyponatremia is very common in AKI due to hyponatremic dehydration but fluid overload with dillutionalhyponatremic is much more common. • . if the serum Na level is >120 m Eq / L , fluid restriction or removal by dialytic therapy corrects the serum Na. • . However, if the serum Na level is <120 m Eq / L , the child is at higher risk for seizures due to hyponatremia and correction to a Na level of approximately 125m Eq / L with hypertonic saline should be considered. • The amount of Na required can be calculated by the following formula:(125-PNa ) (wt. in kg) (0.6) = mEq Na • The required amount is usually infused over several hours to ovoid rapid correction of serum Na level . • Rapid correction of the serum Na conc. In adults with chronic hyponatermia has been associated with Neurologic injury, particularly central pontinemyelinolysisalthongh the incidence of such injury in children is unknoun .

  42. 2. K+ balance: • Common and potentially life threatening. • . kidney tightly regulates K+ balance and excretes approximately 90% of dietary K+ intake. • a. decrease filtration b. impaired tubular secretion. c. altered distribution of K+ by acidosis, which shifts potassium from the intracellular to the extracellular compartment d. release of intracellular K+ due to the associated catabolic state. • True hyperkalemia results in disturbances of cardiac rhythm by its depolarizing effect on the cardiac conduction pathways . • ECG: → Tall, peaked T waves are the first manifestation of cardiotoxicity, and prolongation of the PR interval, flattening of P waves & widening of QRS complexes are later abnormalities. Severe hyperkalemia leads to ventricular tachycardia and fibrillation. • . symptoms of hyperkalemia include malaise, nausea & progressive muscle weakness. • . Treatment of hyperkalemia is indicated if cardiac conduction abnormalities are noted or if the K+ levels are higher than 6 to 7 mEq/L.

  43. Table : Treatment of Hyperkalemia

  44. 3. acidosis: • . as long as the Child’s CNS is intact, respiratory compensation provides partial correction of the acidosis. But if the child is obtunded, respiratory compensation may be compromised, which results in severe acidosis. • . severe acidosis (arterial pH <7.15, serum Hco3 <8 mEq / L “m.mol. / kg”) may increase myocardial irritability and requires treatment to raise the PH to 7.20 which approximates a serum Hco3 level to 12 mEq / L. • . severe acidosis can be treated with intravenous or oral NaHCO3, oral sodium citrate solutions, and/or dialysis . • . it is important to consider the serum total and ionized Ca level • . because of the risks involved in the rapid infusion of alkali, the acidosis should be corrected only partially by the IV route according to the correction formula : • mEqNaHCO3required =0.3×wt(kg)×(12-serum HCO3{mEq/L}) • . the remainder of the correction should be accomplished only after normalization of the serum Ca and phosphorus level may be made by oral administration of NaHCO3tablets or Na citrate solution.

  45. 4. Ca + phosphate Balance: • Hyperphosphatemia treated with dietary phosphorus restriction and with oral CaCo3 or other Ca compounds • Dialysis therapy also effectively removes phosphorus, but it cross the dialysis membranes less readily than uncharged molecules such urea or K+ • . The causes of hypocalcemia in AKI is multifactorial • a. hyperphosphatemia . • b. inadequate GI Ca absorption due to in adequate 1,25-dihydroxy vitamin D production by the kidney . • c. Skeletal resistance to the action of PTH • . If hypocalcemia is severe and/or if HCo3 therapy is necessary for hyperkalemia , treatment with 10% calcium gluconate (100mg/kg up to aminimum of 1g , or 1ml/kg up to a maximum of 10 ml) should be given over 30-60 minutes with continuous ECG monitoring . • . hypocalcemia may also be treated by oral administration of CaCo3 or other Ca salts.

  46. 5- Medications: • . when medications are prescribed in AKI, the mechanism of drug elimination and the metabolic pathway of the drug must be considered and adjustments made for renal impairment . • . many drug adjustment tables are based on the level of Renal function (GFR>50ml/min/1.73m2 ,GFR of 20-50ml/min/1.73m2 , or GFR<20ml/min/1.73m2) and it is important to estimate the Child’s level of RF appropriately and to consider the rate of increase in the serum creatinine level rather than the absolute creatinine level . • . To prevent further insults to the kidney it is best to avoid nephrotoxic drugs in ARF , if potentially nephrotoxic drugs are needed it is appropriate to use them while monitoring drug levels and potential adverse effects.

  47. 6- Hypertension: • . HT in AKI is commonly related to volume overload and/or to alterations in vascular tone. • . if HT is releated to volume overload → diuretic therapy if no response then dialysis or hemofiltration. • . antihypertensive drugs may also indicated depending on the degree of BP elevation & the cause of HT • . The choice of antihypertension therapy depends on • a. degree of BP elevation. • b. presence of CNS symptoms of HT • c. presence of associated conditions • d. the cause of AKI • . For the child who has sever HT and/or is encephalopathic IV therapy with Na nitroprusside (beginning dose 0.5-1μg/kg/min) is indicated with monitoring of the serum levels of thiocyanate, a metabolic product of nitroprusside that is excreted by the kidney . • Alternative therapies include IV labetalol (0.5-3.0 mg/kg/h) also diazoxide (1-5mg/kg/dose), enalaprilat (0.005-0.01mg/kg/day) and nicardipine (1-3μg/kg/min) . • . for less sever HT IV hydralazine or sublingual nifedipine can be used , sever hypotension and tissue ischemia after sublingual administration of Nifedipine, which has been observed in adult pts, is uncommon in pediatric patients . • . once the BP is controlled treatment with oral long-acting agents can be initiated.

  48. 7- Nutritional support • . AKI is associated with marked catabolism & malnutrition leading to delayed recovery from AKI • . if GIT is intact and functional, enteral feedings with formula (similac PM 60/40 for Newborns & infants) should be instituted . • . Dilute formula should be given initially and then feedings can be increase and concentrated to achieve optimal calories intake. • . in older children a diet of high-biologic-value protein, low-phosphorus& low-potassium foods can be used. • . infants should receive maintenance calories (120 Kcal/kg/day) and older children appropriate maintenance calories or higher if needed due to the catabolic state and malnutrition. • . if enteral feeding are not possible, then hyperalimentation, usually through a central line, with high concentration of dextrose (25%), lipids (10-20%), and protein (1-2g/kg/day) should be instituted . • . if the child is oliguric or anuric and sufficient caloric intake cannot be achieved while appropriate fluid balance is maintained, dialysis should be initiated earlier than in the usual case.