Acute renal failure (Acute kidney injury)

1. Acute renal failure(Acute kidney injury) Asist. prof. Magdalena Stârcea IVth Pediatric Clinic

2. Definition: AKI (acute kidney injury) is defined as a precipitous and significant (>50%) decrease in glomerular filtration rate (GFR) over a period of hours to days, causing abnormal regulation of fluid, electrolytes, acid–base balance, blood pressure, and removal of waste products. (Has replaced the old term –Acute Renal Failure) Prior to 2004 more than 30 definitions of AKI. We use now the RIFFLE criteria to define AKI.

3. Oliguria is defined as a urine output that is less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL/dailly in adults. • It is one of the clinical hallmarks of renal failure. At onset, oliguria is frequently acute, often the earliest sign of impaired renal function, and poses a diagnostic and management challenge to the clinician. • In most clinical situations, acute oliguria is reversible, and does not result in renal failure. However, identification and timely treatment of reversible causes is crucial, since the therapeutic window may be small. • Important and common co-morbid condition in PICU (pediatric intensive care unit).

4. Paediatric Incidence of AKI • 10% incidence of AKI in patients admitted to PICU (Schneider J, et al: Crit Care Med 2010; 38:933–939) • AKI increases mortality from 10% to 57.1% in patients • with multi-organ failure, • marrow or solid organ transplantation, • extracorporeal membrane oxygenation, or • acute respiratory distress syndrome (Askenazi DJ, et al:. Pediatr Crit Care Med 2011; 12:1–6) Long Term Outcomes At 3 to 5-yr follow-up, because 40% to 50% of paediatric patients who had AKI will show signs of chronic renal insufficiency, indicating that sublethal injury permanently alters the kidneys. (Askenazi DJ, et al: Kidney Int 2006; 69:184–189)

5. In 2004, the Acute Dialysis Quality Initiative group (ADQI) proposes the RIFLE classification of AKI. • In 2007 - Acute Kidney Injury Network (AKIN) classification come out, based on the RIFLE system.

6. Schwartz equation: GFR (ml/min/1.73m2)=  [H(cm)xk]/creatinine k = 0.35 for preterm, < 2500g, < 4 weeks old k = 0.45 for infants 1 to 52 weeks oldk = 0.55 for children 1 to 13 years oldk = 0.55 for adolescent females >13years oldk = 0.70 for adolescent males >13years old Serum creatinine: • Differs with age, sex, dietary intake, muscle mass, etc. • Doesn’t reflect dynamic changes, only increases when there is substantial loss of renal function. • 10 –40% of creatinine is cleared by tubular secretion in the urine –therefore has the potential to hide a considerable decline in GFR.

7. For this reasons is very important to find early markers of AKI. Newer biomarkers include: • Neutrophil Gelatinose Associated Lipocalin (NGAL) • Secreted by renal tubular epithelium and excreted in the urine during normal renal function. • Serum levels rise markedly after epithelial damage following ischaemic or nephrotoxic injury. • Cystatin C - Protein secreted by all nucleated cells - Minimally influenced by weight, sex, race, age, muscle mass. -May rise earlier than serum creatinine may be a better marker of acute renal dysfunction.

8. Kidney Injury Molecule –1 (KIM-1) Is a protein that is highly upregulated in the proximal tubules after ischaemic or toxic AKI. • IL-18. • Induced in the proximal renal tubule after AKI. • Seems to be useful in differentiation of acute tubular necrosis from other types of renal disease. • Is not elevated in chronic kidney disease, UTI and pre-renal failure

9. Classification I. Clinical criteria and depending on diuresis- AKI with oliguria - daily decrease of urinary output and clinical signs of renal dysfunction- AKIwithout oliguria – increase of serum urea and creatinine levels despite normal or even increased urinary volume

10. II. Pathophysiological criteria A. Prerenal failure: renal function disturbance due to a decrease of renal perfusion. Correcting the cause - renal function recovery Causes:1. Decrease the total volume of liquid- gastrointestinal disorders- diabetes insipidus- burns2. Decreased intravascular volume and effective circulatory volume- bleeding- passing the " third space" fluids after shock, trauma, surgery - nephrotic syndrome- shock- heart failure- renal vasoconstriction :PG synthetase inhibitors, CyA, high doses of dopamine / adrenaline in case of shock

11. B. Intrinsec AKI: Causes1. Causes that produce a severe and prolonged ischemia- shock- respiratory distress syndrome (newborn and preterm infant!)- severe heart failure2. Nephrotoxic causes - antibiotics, hyperuricemia, cisplatin, contrast agents, heavy metals, organic solvents (etilenglycols, teraclorura carbon, methanol, toluene)- rhabdomyolysis, massive hemolysis3. Vascular / glomerular causes - renal artery occlusion, renal vein thrombosis- AGN, rapidly progressive GN- Microvascular (vasculitis): HUS, malignant hypertension C. Postrenal causes: produce a disturbance in urinary elimination • Functional / structural abnormalities of urinary tract :- posterior urethra valve, ureteral obstruction, neurogenic Bladder 2. Won abnormalities: blood clot postbiopsie, trauma, retroperitoneal tumors, stones

12. Pathophysiology AKI (acute kidney injury) causes renal arteriolar vasoconstriction, desquamation of renal tubular cells to form casts, which causes intraluminal tubular obstruction and increased glomerular filtration retropresion. Neutrophils adhere to the endothelium and release proinflamatories mediators. AKI can be classified in terms of pathophysiology of: AKI with oliguria AKI without oliguria, (has a more favorable prognosis) The difference between oliguric and non – oliguric AKI consists in renal aggression intensity. Numerous experimental studies in recent years have shown changes in cellular, molecular and metabolic accompanying loss of kidney function.

13. Prerenal insufficiency • 70% of community-acquired cases of acute renal failure • 60% of hospital-acquired cases • is a functional response of structurally normal kidneys to hypoperfusion. The early phase of renal compensation for reduced perfusion includes autoregulatory maintenance of glomerular filtration rate, via afferent arteriolar dilatation (induced by myogenic responses, tubulo-glomerular feedback, and prostaglandins actions), and via efferent arteriolar constriction (mediated by angiotensin II). The early phase also includes enhanced tubular reabsorption of salt and water (stimulated by the renin-angiotensin-aldosterone system and sympathetic nervous system). Rapid reversibility of oliguria following timely re-establishment of renal perfusion is an important characteristic and usual scenario • prolonged renal hypoperfusion can determinate an undesirable developmentfrom compensation to decompensation. Excessive stimulation of the sympathetic and renin-angiotensin systems can cause profound renal vasoconstriction and ischemic renal injury.

14. Intrinsic renal failure is associated with structural renal damage. This includes acute tubular necrosis (from prolonged ischemia, drugs, or toxins), primary glomerular diseases, or vascular lesions. The pathophysiology of ischemic, acute tubular necrosis is well studied. Ischemia leads to altered tubule cell metabolism (depletion of ATP, release of reactive oxygen species) and cell death with resultant cell desquamation, cast formation, intratubular obstruction, backleak of tubular fluid, and oliguria. In the majority of clinical situations, the oliguria is reversible and associated with repair and regeneration of tubular epithelial cells.

15. There are four stages of the progression of renal injury in AKI: Phase I (initiation) = shown by decreased renal perfusion and ATP depletion Phase II (extension) = lesions of reperfusion can cause new lesions. At this stage appear the extension of inflammation and ischemic effects generating exacerbation of the initial lesions. Proximal tubules regenerated, but the tubules from renal medullary suffering necrosis and apoptosis. Lesion severity installed in this stage will be proportional to the prognosis of the lesion. Phase III (hold) = necrosis and apoptosis remains parallel with inflammation and destruction of the kidney cell. Phase IV (reverse) = occur simultaneously mechanisms of regeneration, repair and cell proliferation previously injured.

16. Postrenal failure is a consequence of mechanical or functional obstruction to the flow of urine. This form of oliguria and renal insufficiency usually responds to release of the obstruction. Mortality/Morbidity: • Mortality rates in oliguric AKI vary widely according to the underlying cause and associated medical condition. It ranges from 5% for patients with community-acquired acute renal failure to 80% among patients with multi-organ failure in PICU. • The most common causes of death are sepsis, cardiovascular and pulmonary dysfunction, and withdrawal of life support. Race: there is no racial predilection. Sex: the sexes are equally affected. Age: oliguria affects all ages. • It is more common in the neonatal and older age groups because of co-morbid conditions, and it is more common in early childhood due to the high incidence of illnesses leading to dehydration.

17. Clinical History: • Careful evaluation of the patient's history and physical examination often reveals the cause. This is especially important in prerenal and postrenal processes, since early diagnosis and treatment frequently results in complete recovery. • Fluid losses • Recent history of diarrhea or vomiting should be sought since this is the most common cause in children. • Less commonly, fluid loss may result from traumatic hemorrhage, burns, or following polyuric states such as diabetes insipidus and diabetes mellitus. • Loss of intravascular fluid volume into the interstitial space accompanies surgery, shock syndromes, and nephrotic syndrome. Children with fluid losses may complain of thirst, dizziness, palpitations, and fatigue, and there may be a history of weight loss.

18. Drugs • A detailed history of recent medications should be obtained. In the presence of mild prerenal insufficiency, administration of medications that impair renal autoregulation can precipitate oliguric ARF. • Cyclosporine, tacrolimus, and contrast agents are direct, afferent arteriolar constrictors that interfere with the myogenic response. • NSAIDs inhibit the renal synthesis of vasodilatory prostaglandins. They are an important cause when administered to febrile children with intercurrent dehydration. • Drugs that induce direct tubular necrosis include aminoglycosides, amphotericin B, cyclosporine, tacrolimus, antineoplastic agents (methotrexate, cisplatin), and contrast agents. • Acyclovir and sulfonamides can precipitate within the tubular lumen and result in obstruction. • In addition, a large number of medications, especially penicillins, cephalosporins, sulfonamides, ciprofloxacin, NSAIDs and diuretics, can cause interstitial nephritis. • History of ingesting undercooked meat may suggest hemolytic-uremic syndrome.

19. Endogenous tubular toxins • Myoglobin (following crush injuries, myositis, and prolonged grand mal seizures) • Hemoglobin (hemolysis) • Uric acid (tumor lysis syndrome) • Symptoms of glomerular disease • Many children have a history of gross hematuria and edema. An antecedent streptococcal infection may suggest a post-infectious glomerulonephritis, and a history of bloody diarrhea often precedes the hemolytic-uremic syndrome. • Children with fever, joint complaints, and skin rashes who present with oliguria, should be suspected to have systemic lupus erythematosus or allergic interstitial nephritis. • A history of recurrent sinusitis or lower respiratory tract infections may suggest Wegener granulomatosis, and hemoptysis may suggest Goodpasture disease.

20. Symptoms of urinary tract obstruction • Complete absence of urine output • Alternating periods of polyuria and oligo-anuria • Poor urinary stream or dribbling • Symptoms of chronic renal failure • Although oliguria is usually acute at initial presentation, it may also be a presenting symptom of chronic renal failure. • Children may have additional symptoms suggestive of previous renal disease such as frequent urinary tract infections, hematuria, proteinuria, hypertension, edema, fatigue, pallor, anorexia, and bone pain.

21. Physical: • Signs of intravascular volume depletion - Tachycardia - Orthostatic hypotension - Decreased skin turgor - Dry mucous membranes • Signs of AKI • Children may present with edema, anemia, and signs of congestive heart failure such as hepatomegaly, gallop rhythm, and pulmonary edema. • Hypertension is common, especially in acute glomerulonephritis, and may be secondary to volume overload and alterations in vascular tone. • Although many children with hypertension are asymptomatic, it is common to encounter patients with signs of congestive heart failure, visual disturbances, or encephalopathy.

22. Signs specific to the underlying renal disease • A butterfly rash on the face and joint swelling are highly suggestive of systemic lupus erythematosus. • Henoch-Schönlein disease presents with a characteristic purpuric rash over the buttocks and extensor surface of the lower extremity. • Acute interstitial nephritis may be accompanied by fever, arthralgias, and fleeting maculopapular or urticarial rashes. • A variety of skin rashes may be detected in vasculitides. • Oliguria with palpable kidneys during infancy suggests renal vein thrombosis, polycystic kidneys, multicystic dysplasia, or hydronephrosis. In older children, enlarged kidneys should also raise the suspicion of tumors. A transplanted kidney that is tender to palpation is indicative of rejection.

23. Signs of postrenal failure • Poor urinary stream, urinary dribbling, and a palpably enlarged urinary bladder are indicative of obstruction. Diagnosis may be strengthened by re-establishment of urine output after gentle passage of a catheter. • The external genitalia may reveal meatal stenosis or urethral trauma. Patients with indwelling urinary catheters that develop oliguria should undergo flushing of the catheter to rule out blockage.

24. Lab studies • Urinalysis • freshly voided urine sample is a rapid and inexpensive way of distinguishing prerenal from intrinsic renal failure. • In prerenal failure, a few hyaline and fine granular casts may be seen with little protein, heme, or red cells. Heme-positive urine in the absence of erythrocytes suggests hemolysis or rhabdomyolysis. • In intrinsic renal failure, hematuria and proteinuria are prominent. Broad, brown granular casts are typically found in ischemic or toxic acute tubular necrosis, and red cell casts are characteristically seen in acute glomerulonephritis. The urine in acute interstitial nephritis shows white cells, especially eosinophils and white cell casts.

25. Urinary indexes • Simultaneous measurement of urinary and serum sodium, creatinine, and osmolality can help differentiate between prerenal azotemia, in which the reabsorptive capacity of tubular cells and concentrating ability of the kidney are preserved, or even enhanced and intrinsic renal failure, in which these functions are impaired due to structural damage. • In prerenal failure, urine specific gravity is high (greater than 1020), the ratio of urinary to plasma creatinine is high (greater than 40), ratio of urinary to plasma osmolality is high (greater than 1.5), and the urinary-sodium concentration is low (less than 20 mEq/L). • The opposite findings are encountered in intrinsic renal failure, which are urine to plasma creatinine ratio less than 20, urine-to-plasma osmolality less than 1.1, and urine-sodium concentration greater than 40 mEq/L. • The fractional excretion of sodium (FeNa) is the percentage of filtered sodium that is excreted. %FeNa = [(U/P)Na]/[(U/P)Cr] x 100 • The %FeNa is typically less than 1% in prerenal azotemia and greater than 2% in intrinsic renal failure.

26. Introduced by the KDIGO in 2012, specific criteria exist for the diagnosis of AKI.

27. BUN and serum creatinine • In prerenal failure, there is a marked elevation of BUN and a BUN/Cr ratio greater than 20. This reflects increased proximal tubular reabsorption of urea. The hallmark of established AKI is a daily increase in serum creatinine (0.5-1.5 mg/dL/d) and in BUN (10-20 mg/dL/d). • Serum sodium • Hyponatremia is a common finding that is usually dilutional, secondary to fluid retention and administration of hypotonic fluids. • Less common causes of hyponatremia include sodium depletion (hyponatremic dehydration) and hyperglycemia (serum sodium concentration decreases by 1.6 mEq/L for every 100 mg/dL increase in serum glucose above 100 mg/dL). • Acid-base balance • The impaired renal excretion and decreased tubular reabsorption and regeneration of bicarbonate results in metabolic acidosis with a high anion gap. • Severe acidosis can develop in children who are hypercatabolic (shock, sepsis) or who have inadequate respiratory compensation.

28. Serum potassium • Hyperkalemia is an important complication because of reduced glomerular filtration, reduced tubular secretion, metabolic acidosis (each 0.1 unit reduction in arterial pH raises serum potassium by 0.3 mEq/L), and associated catabolic state. • Hyperkalemia is most pronounced in patients with excessive endogenous-potassium production including rhabdomyolysis, hemolysis, and tumor lysis syndrome. • Hyperkalemia represents a life-threatening emergency that must be treated promptly and aggressively, primarily due to its depolarizing effect on cardiac conduction pathways. • Symptoms may include malaise, nausea, and muscle weakness.

29. Serum phosphate and calcium • Hyperphosphatemia and hypocalcemia frequently complicate oliguric AKI. The phosphate excess is secondary to reduced renal excretion and can result in hypocalcemia and calcium phosphate deposition in various tissues. • Hypocalcemia results from hyperphosphatemia-impaired gastrointestinal calcium absorption due to inadequate active vitamin D production by the kidney, skeletal resistance to the calcemic action of parathyroid hormone, and coexistent hypoalbuminemia. • Acidosis increases the fraction of total calcium in the ionized form; thus, overzealous bicarbonate therapy in can decrease ionized calcium. • Severe hypocalcemia results in tetany, seizures, and cardiac arrhythmias

30. Complete blood count (CBC) • Anemia is a result of dilution and decreased erythropoiesis. Microangiopathic hemolytic anemia with schistocytes and thrombocytopenia are indicative of hemolytic-uremic syndrome. • Patients with oliguria that is secondary to systemic lupus erythematosus may display neutropenia and thrombocytopenia. • Eosinophilia is consistent with allergic interstitial nephritis. • Prolonged ARF can result in functional platelet disorders. • Coagulation studies: disseminated intravascular coagulation associated with sepsis. • Creatine kinase, myoglobinuria: markedly elevated creatine kinase and myoglobinuria suggest rhabdomyolysis.

31. Serologies • Decreased complement levels (C3, C4) are characteristic of acute post-streptococcal glomerulonephritis but can also be seen in lupus nephritis and membranoproliferative glomerulonephritis. A suspected diagnosis of acute post-streptococcal glomerulonephritis can be confirmed by detection of elevated anti-streptococcal titers. The presence of antinuclear antibodies is suggestive of lupus nephritis, and antineutrophil cytoplasmic antibodies indicate vasculitis. • Virology: hepatitis B and C; HIV • The news markers of AKI include cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1) and interleukin-18 (IL-18). None have yet been recommended for routine use.

32. Imaging Studies: • Renal ultrasound very important • Exceptions may include children with unmistakable prerenal failure from dehydration who promptly respond to fluid resuscitation, or those with mild renal insufficiency secondary to a nephrotoxin who respond to discontinuing the medication. • Ultrasound provides important information regarding kidney size and echogenicity, renal blood flow, collecting system, and bladder wall. • Children with acute intrinsic renal failure display echogenic kidneys that may be enlarged. With prolonged renal failure, renal cortical necrosis may result in decreased kidney size. Bilateral, small scarred kidneys are indicative of chronic renal disease. • Congenital disorders, such as polycystic kidney disease and multicystic dysplasia, are easily detected. Stones and tumors that can cause obstruction may also be detected. • A Doppler study is critical in the evaluation of vascular obstruction.

33. Other imaging studies • A voiding cystourethrogram is indicated with suspected bladder outlet obstruction. • A radionuclide renal scan may be useful in the assessment of transplant rejection and obstruction. • A chest radiograph may be indicated if pulmonary edema is suspected. • An echocardiogram may be useful in the presence of congestive heart failure. ECG • The earliest sign is appearance of tall peaked T waves. • Subsequent findings include the following: • Prolongation of the PR interval • Flattening of P waves • Widening of QRS complexes • ST segment changes • Ventricular tachycardia • Terminal ventricular fibrillation

34. Renal biopsy • AKI without obvious cause (no toxic or sepsis, or hypertension) • Important hematuria and / or proteinuria • Extrarenal signs directing to systemic disease or vasculitis (articular manifestations, respiratory or skin) • Suspected interstitial nephritis immunoallergic, especially when the suspected drug should be continued • progressive installation of AKI • Oliguria or anuria persisting for 2 or 3 weeks

35. SIGNS OF GRAVITY INAKI 1. Level of uremic poisoning - urea> 50 mmol / l, creatinine> 1000 umol / l, confusion, drowsiness 2 Overload hydrosodée: > 10% of basal weight, pulmonary edema, pleural or pericardial efusions 3 Water intoxication - hyponatremia <120 mmol / l, confusion, coma 4 Superinfection (pneumonia, catheter or urinary catheter) 5 Gastrointestinal bleeding, stress ulcer, hematoma at puncture 6 Severe metabolic acidosis • bicarbonatémie <10 mmol / l, pH <7.20 7 Hyperkalemia • potassium> 6 mmol / l, ECG signs 8. Hyperphosphatemia and hypocalcemia • P> 3 mmol / l (risk of precipitation intratubular) • Calcium <1.8 mmol / l (convulsion, tetany)

36. TREATMENT Medical Care: • Prevention • In clinical situations where renal hypoperfusion or toxic injury is anticipated, therapy with fluids, mannitol, diuretics, and renal-dose dopamine are used to prevent, or reverse, renal injury. These maneuvers are able of converting the oliguric state to a nonoliguric AKI, which is more easily managed. • Vigorous fluid administration has been successfully employed to prevent AKI following cardiac surgery, cadaveric renal transplantation, hemoglobinuria, myoglobinuria, hyperuricosuria, radiocontrast infusion, and therapy with amphotericin B or cisplatinum. • A trial of intravenous mannitol or furosemide should be attempted in a patient with oliguria for less than 48 hours who has not responded to adequate hydration. The benefit of renal-dose dopamine therapy iscontroversial. • Once oliguria is established, mannitol may precipitate congestive heart failure, the risk of ototoxicity from furosemide, and adverse hemodynamic changes from dopamine are significant.

37. Fluid management • The major goal of fluid management is to restore and maintain normal intravascular volume. This is accomplished by determination of input and output, body weights, vital signs, skin turgor, capillary refill, peripheral edema, cardio-pulmonary examination, serum sodium, and FeNa. • Children with intravascular volume depletion require prompt and vigorous fluid resuscitation. Initial therapy includes normal saline or lactated Ringer's at 20 mL/kg over 30 minutes, which can be repeated twice if necessary. • Potassium administration is contraindicated until urine flow is established. This therapy should result in increased urine output within 4-6 hours. If oliguria persists (confirmed by bladder catheterization), central venous monitoring may be required to guide further management. • Oliguria with volume overload requires fluid restriction and intravenous furosemide. Failure to respond to furosemide suggests the presence of acute tubular necrosis rather than renal hypoperfusion, and fluid removal by dialysis or hemofiltration may be required, especially if signs of pulmonary edema are evident.

38. Hyperkalemia • K < 6.0 mmol / l- stop the K sparing therapy, food restriction (restriction dried fruit, bananas, citrus fruits, beans, dried peas, green vegetables, potatoes) • K - 6.0 - 6.5 mmol / l :- hydration- Slow bolus Ca gluconate 10% , 0.5 ml / kg, ECG monitoring- PIV SG 10-30 % 1ml/kg ( rapid insulin 1U/5g glucose)- Sorbitol 70 % + Kayexalate the 1g/kgc/po , 2ml/kg- Where AR < 18 mmol / l - 8.4 % Na bicarbonate , 2mEq/kg/day in 4 parts- K repeated after 6 hours • K > 6.5 mmol / l :- Continuous ECG monitoring- Salbutamol nebuliser- Emergency hemodialysis

39. Other electrolytes and acid-base balance • The primary treatment of hyponatremia is free water restriction; however, serum sodium less than 120 mEq/L, or accompanied by central nervous system dysfunction, may require 3% sodium chloride infusion. • Management of hyperphosphatemia includes dietary restriction and oral phosphate binders (calcium carbonate or calcium acetate). • Hypocalcemia usually responds to the oral calcium salts used for control of hyperphosphatemia but may require 10% calcium gluconate infusion if severe. • Mild metabolic acidosis is treated with oral sodium bicarbonate or sodium citrate. Severe acidosis (pH less than 7.2), especially in the presence of hyperkalemia, requires intravenous bicarbonate therapy. It should be recognized that bicarbonate therapy requires adequate ventilation (to excrete carbon dioxide produced) to be effective and that it may precipitate hypocalcemia and hypernatremia.

40. Hypertension Antihypertensive therapy : • hipertensive encephalopathy :- Diazoxide iv bolus 5mg/kg/dosis - Na nitroprusside : 0.5 - 8μg/kg/min , iv- Furosemide: 1 - 2mg/kg , iv slow • severe hypertension without encephalopathy :- Minoxidil 0,1 - 0,2 mg / k g / day , max 5mg/24 hours- Ca channel blockers : from 0.25 to 0.5 mg / kg / dose , max 1-2mg/kg/zi Warning: angiotensin converting enzyme inhibitors may furtherreduce glomerular filtration and beta-blockers may exacerbatehyperkalemia ! • acute pulmonary edema: hemodyalisis • mild hypertension usually responds to salt restriction and diuretics. • moderate asymptomatic hypertension is most commonly treated with oral or sublingual calcium channel blockers or with intravenous hydralazine.

41. Dialysis • The general goal of dialysis is to remove endogenous and exogenous toxins, and to maintain fluid, electrolyte, and acid-base balance until renal function returns. • The indications for acute dialysis are not absolute, and the decision to use this modality depends on the rapidity of onset, duration, and severity of the abnormality to be corrected. • The choice between hemodialysis and peritoneal dialysis depends on the overall clinical condition, availability of technique, etiology of the renal failure, institutional preferences, and specific indications or contraindications.

42. Common indications of dialysis include: • fluid overload that is unresponsive to diuretics, • symptomatic acid-base/electrolyte imbalances (especially hyperkalemia) that are unresponsive to medications • refractory hypertension • symptomatic uremia (central nervous system symptoms, pericarditis, pleuritis). • If adequate nutrition cannot be achieved because of fluid restriction, early institution of ultrafiltration or dialysis should be considered. Surgical Care: patients with oliguria secondary to obstruction frequently require urologic care. The site of obstruction determines the therapy.

43. Diet: • Children with oliguric ARF are frequently in a highly catabolic state; therefore, aggressive nutritional support is important. Adequate calories should be given to account for maintenance requirements, and supplements should be provided to combat excessive catabolism. • Protein of high biologic value should be administered in amounts that are sufficient to maintain neutral nitrogen balance, reflected by steady BUN levels. • Oral feeding is the preferred route. Infants should be placed on a low-phosphorus formula, and older children fed a low-phosphorus, low-potassium diet. • Additional calories may be supplied by fortifying foods with polycose and medium-chain triglycerides. • Children who are nauseas or anorexia may benefit from enteral feedings. If enteral feedings are not possible, central intravenous hyperalimentation may be used to deliver concentrated dextrose (25%) and lipids (20%). Activity: children are usually hospitalized; therefore, activity is restricted.

44. Complications: • Infections develop in 30-70% of patients and include the respiratory system, urinary tract, and catheters infections. Impaired defenses, due to uremia and inappropriate use of antibiotics, may contribute to the high rate of infectious complications. • Cardiovascular complications are a result of fluid and sodium retention. They include hypertension, congestive heart failure, and pulmonary edema. • Hyperkalemia results in ECG abnormalities and arrhythmias. • Other complications include the following: • Gastrointestinal (anorexia, nausea, vomiting, and ileus, bleeding) • Hematologic (anemia and platelet dysfunction) • Neurologic (confusion, asterixis, somnolence, and seizures) • Other electrolyte/acid-base disorders (metabolic acidosis, hyponatremia, hypocalcemia, and hyperphosphatemia)

45. Prognosis: • Despite significant advances in supportive care and renal replacement therapy, high mortality rates in the setting of multiorgan failure have not improved in the past few decades. • It must be emphasized that patients die with renal failure; however, they do not die not because of renal failure. The patient succumbs rather than to involvement of other systems during the period of renal insufficiency. • On the other hand, prognosis from prerenal causes, or from acute tubular necrosis in the absence of significant co-morbid conditions, is usually quite good if appropriate therapy is instituted in a timely fashion.

46. Hemolitic uremic syndrome • This is the most common infant cause of AKI (75%). Definition and epidemiology: • HUS is a serious complication of an episode of diarrhea often bloody, may change in 10% of cases to hemolyticanemia, thrombocytopenia and acute renal failure, which are the main characteristics The mortality rate is now less than 5% in literature. Histology: • In the kidney: thromotique microangiopathy lesions of glomerular capillary wall or cortical necrosis. Etiologies: Verotoxin-producing E. coli (VTEC O157 serotipe). Epidemics in summer.

47. Mode of transmission - Contamination is most often food: ingestion of food consumed raw or undercooked. - Beef, especially ground - Raw milk and products made ​​from raw milk - Exceptional consumption of raw vegetables or untreated water (well water, for example) not contaminated animal waste. - Inter-human transmission by fecal-oral transmission within families or communities is possible failure of hygiene measures. - Direct contact with infected animals or their droppings can also be cause.Il be noted that the infectious dose is very low.

48. Clinic:typical HUS is D+ - The most common; especially infants. - Prodromes digestive. - Evolution favorable. a. the invasion phase: non-specific: - Moderate fever; - Gastrointestinal disorders: diarrhea, sometimes bloody; - It takes a few hours to a few days. b. the status phase - Sudden pallor associated with hemolytic anemia; - Bleeding disorders with thrombocytopenia; - AKI with hematuria; - Frequently HTA; - Neurological Signs: convulsion.

49. Paraclinical:- Severe hemolytic anemia and regenerative. - Schizocytosis: constantly found (5-10% of cells); early and ephemeral. - Thrombocytopenia (<100000plaquettes/mm ³). - Signs of AKI. Clinical forms: A. Atypical HUS: - Very rare; - After 3 years; - No seasonal pattern; - Without digestive prodrome; - More severe. B. Secondary HUS. C. family HUS.

50. Treatment: Symptomatic: - Renal failure: peritoneal dialysis or hemofiltration. - Hypertension. - Anemia: red blood cell transfusion. Specific: fresh frozen plasma; IV immunoglobulin. Surveillance - sequelae (hypertension, CKD). Complications of HUSD+• Death in the acute phase - 2% • Convulsions, drowsiness, stupor, coma • Gastrointestinal disease: ulcerative colitis, ileitis necro - haemorrhagic • Pancreatitis• Hepatic Impairment • Heart feailure