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  2. Emergencies in nephrology • Acute kidney injury (AKI); • Renal colic; • Hypertensive crisis.

  3. Definition of AKI There are more than 35 definitions of AKI (formerly acute renal failure) in literature! • Sudden interruption of kidney function resulting from obstruction, reduced circulation, or disease of the renal tissue; • Results in retention of toxins, fluids, and end products of metabolism; • Usually reversible with medical treatment; • May progress to end stage renal disease, uremic syndrome, and death without treatment.

  4. Definition of Acute Kidney Injury (AKI) based on “Acute Kidney Injury Network”

  5. RIFLE criteria for diagnosis of AKI based on The “Acute Dialysis Quality Initiative” Am J Kidney Dis. 2005 Dec;46(6):1038-48

  6. Epidemiology AKI occurs in ≈ 7% of hospitalized patients. 36–67% of critically ill patients (depending on the definition). 5-6% of intensive care unite (ICU) patients with AKI require renal replacement therapy (RRP). Nash K, Hafeez A, Hou S: Hospital-acquired renal insufficiency. American Journal of Kidney Diseases 2002; 39:930-936. Hoste E, Clermont G, Kersten A, et al.: RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: A cohort analysis. Critical Care 2006; 10:R73. Osterman M, Chang R: Acute Kidney Injury in the Intensive Care Unit according to RIFLE. Critical Care Medicine 2007; 35:1837-1843.

  7. Mortality according to RIFLE Mortality increases proportionately with increasing severity of AKI (using RIFLE). AKI requiring RRT is an independent risk factor for in-hospital mortality. Mortality in pts with AKI requiring RRT 50-70%. Even small changes in serum creatinine are associated with increased mortality. Hoste E, Clermont G, Kersten A, et al.: RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: A cohort analysis. Critical Care 2006; 10:R73. Chertow G, Levy E, Hammermeister K, et al.: Independent association between acute renal failure and mortality following cardiac surgery. American Journal of Medicine 1998; 104:343-348. Uchino S, Kellum J, Bellomo R, et al.: Acute renal failure in critically ill patients: A multinational, multicenter study. JAMA 2005; 294:813-818. Coca S, Peixoto A, Garg A, et al.: The prognostic importance of a small acute decrement in kidney function in hospitalized patients: a systematic review and meta-analysis. American Journal of Kidney Diseases 2007; 50:712-720. .

  8. Increase in Creatinine without AKI • Inhibition of tubular creatinine secretion Trimethoprim, Cimetidine, Probenecid • Interference with creatinine assays in the lab (false elevation) acetoacetate, ascorbic acid, cefoxitin flucytosine

  9. Increase in blood urea nitrogen (BUN) without AKI • Increased production Gl Bleeding Catabolic states (Prolonged ICU stay) Corticosteroids Protein loads (Total parenteral nutrition -Albumin infusion)

  10. AKI • Persons at Risks • Major surgery; • Major trauma; • Receiving nephrotoxic medications; • Elderly.

  11. Major Disease Categories Causing AKI

  12. Prerenal Azotemia • Intravascular volume depletion bleeding, GI loss, Renal loss, Skin loss, Third space loss • Decreased cardiac output chronic heart failure (CHF) • Renal vasoconstriction Liver Disease, Sepsis, Hypercalcemia • Pharmacologic impairment of autoregulation and GFR in specific settings ACEi in bilateral renal artery stenosis, nonsteroidal anti-inflammatory drugs (NSAIDs) in any renal hypoperfusion setting

  13. Intrinsic Renal Azotemia • Large Renal Vessel Disease Thrombo-embolic disease • Renal Microvasculature and Glomerular Disease Inflammatory: glomerulonephritis, allograft rejection Vasospastic:malignant hypertension, scleroderma crisis, pre-eclampsia, contrast Hematologic: Hemolytic-Uremic Syndrome (HUS) & Thrombocytopenic Purpura (TTP), Disseminated intravascular coagulation • ATN Ischemic Toxic • Tubulo-interestitial Disease Acute Interestitial Nephritis (AIN), Acute cellular allograft rejection, viral (HIV, BK virus), infiltration (sarcoid) • Intratubular Obstruction myoglobin, hemoglobin, myeloma light chains, uric acid, tumor lysis, drugs (indinavir, acyclovir, foscarnet, oxalate in ethylene glycol toxicity)

  14. Postrenal azotemia • Stones; • Blood clots; • Papillary necrotic tissue; • Urethral disease; anatomic: posterior valve functional: anticholinergics, L-DOPA • Prostate disease; • Bladder disease; anatomic: cancer, schistosomiasis functional: neurogenic bladder.

  15. AKI Stages • Onset – 1-3 days with ^ BUN and creatinine and possible decreased urinary output (UOP); • Oliguric – UOP < 400/d, ^BUN, Crest, Phos, K, may last up to 14 d • Diuretic – UOP ^ to as much as 4000 mL/d but no waste products, at end of this stage may begin to see improvement • Recovery – things go back to normal or may remain insufficient and become chronic

  16. Initial diagnostic tools in AKI • History and Physical exam • Detailed review of the chart, drugs administered, procedures done, hemodynamics during the procedures. • Urinalysis protein, blood, crystals, infection • Urine microscopy casts, cells (eosinophils) • Urine lytes • Renal imaging Ultrasound, Mag-3 scan, Retrograde Pyelogram • Markers of CKD iPTH, size<9cm, anemia, high phosphate, low bicarb • Renal biopsy

  17. 5 Key Steps in Evaluating AKI • Obtain a thorough history and physical; review the chart in detail; • Do everything you can to accurately assess volume status; • Always order a renal ultrasound; • Look at the urine; • Review urinary indices.

  18. Prevention of AKI in ICU • Recognition of underlying risk factors • Diabetes • CKD • Age • Hypertension (HTN) • Cardiac/liver dysfunction • Maintenance of renal perfusion • Avoidance of hyperglycemia • Avoidance of nephrotoxins Dennen P, Douglas I, Anderson R,: Acute Kidney Injury in the Intensive Care Unit: An update and primer for the Intensivist. Critical Care Medicine 2010; 38:261-275.

  19. Antibiotics • Aminoglycosides (10-15% Incidence of Acute Tubular Necrosis) • Occurs in 10-20% patients on 7 day course • Results in non-oligurics; increased Creatinine • A single dose early in septic course is usually safe • Sulfonamides • Amphotericin B (Incidence 80-90%) • Levofloxacin • Ciprofloxacin • Rifampin • Tetracycline • Acyclovir (only nephrotoxic in intravenous form) • Pentamidine • Chemotherapy and Immunosuppressants • Cisplatin • Methotrexate • Mitomycin • Cyclosporine • Heavy Metals • Mercury Poisoning • Lead Poisoning • Arsenic Poisoning • Bismuth • Lithium related kidney disorders • Polydipsia and Nephrogenic Diabetes Insipidus • Acute Renal Failure • Dialysis indications: Creatinine >2.5 or Seizures, ALOC, Rhabdomyolysis • Chronic kidney disease with fibrosis • AntiHyperlipidemics • Statins • Gemfibrozil • Associated with Acute Renal Failure due to Rhabdomyolysis • Fenofibrate (Tricor) • Increases Serum Creatinine without significant decrease in GFR • Serum Creatinine rise is reversible on stopping Fenofibrate • Chemotherapy • Cisplatin • Ifosphamide • Causes Fanconi's Syndrome • Miscellaneous Drugs • Chronic Stimulant Laxative use • Resulting chronic volume depletion and Hypokalemia causes nephropathy • Radiographic contrast • ACE Inhibitors • Expect an increase of Serum Creatinine in Chronic kidney disease • NSAIDs • Aspirin • Low dose Aspirin reduces Renal function in elderly • Decreased Creatinine Clearance after 2 weeks of use • Changes persisted for at least 3 weeks off Aspirin • Mesalamine (Asacol, Pentasa) • Mesalamine is an NSAID analog and has systemic absorption from the bowel • Penicillins and Cephalosporins • Hypersensitivity (fever, rash, arthralgia) • Sulfonamides • Vasculitis reaction • NSAIDs • Nephrotic Syndrome type reaction • Rifampin • Diuretics (Thiazides and furosemide) • Allopurinol • Cimetidine • Ciprofloxacin • Dilantin

  20. AKI • Subjective symptoms • Nausea • Loss of appetite; • Headache; • Lethargy; • Tingling in extremities.

  21. AKI • Objective symptoms • Oliguric phase – • vomiting • disorientation, • edema, • ^K+ • decrease Na • ^ BUN and creatinine • Acidosis • uremic breath • CHF and pulmonary edema • hypertension caused by hypovolemia, anorexia • sudden drop in UOP • convulsions, coma • changes in bowels

  22. AKI • Objective systoms • Diuretic phase • Increased UOP • Gradual decline in BUN and creatinine • Hypokalemia • Hyponatriuemia • Tachycardia

  23. AKI • Diagnostic tests • Histoty&Physical (examenation) • BUN, creatinine, sodium, potassium. pH, bicarb. Hgb and Hct • Urine studies • Ultrasound of kidneys • Kidneys, ureters, and bladder (KUB) • Abdomen and renal CT • Retrograde pyelogram

  24. Prevention of Contrast-Induced Nephropathy • Avoid use of intravenous contrast in high risk patients if at all possible. • Use pre-procedure volume expansion using isotonic saline (?bicarbonate). • N-Acetylcysteine • Avoid concomitant use of nephrotoxic medications if possible. • Use low volume low- or iso-osmolar contrast Dennen P, Douglas I, Anderson R,: Acute Kidney Injury in the Intensive Care Unit: An update and primer for the Intensivist. Critical Care Medicine 2010; 38:261-275.

  25. Prevention of AKI in hepatic dysfunction • Intravenous albumin significantly reduces the incidence of AKI and mortality in patients with cirrhosis. • Albumin decreases the incidence of AKI after large volume paracentesis. • Albumin and terlipressin decrease mortality in HRS. Sort P, Navasa M, Arroyo V, et al.: Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. New England Journal of Medicine 1999; 341:403-409. Gines P, Tito L, Arroyo V, et al.: Randomised comparative study of therapeutic paracentesis with and without intravenous albumin in cirrhosis. Gastroenterology 1988; 94:1493-1502. Gluud L, Kjaer M, Christensen E: Terlipressin for hepatorenal syndrome. Cochrane Database Systematic Reviews 2006; CD005162.

  26. Management of AKI in ICU • Treatment is largely supportive in nature maintain renal perfusion • Correct metabolic derangements • Provide adequate nutrition • ? Role of diuretics • RRT remains the cornerstone of management of minority of patients with severe AKI

  27. Maintaining renal perfusion • Human kidney has a compromised ability to autoregulate in AKI. • Maintaining haemodynamic stability and avoiding volume depletion are a priority in AKI. Kelleher S, Robinette J, Conger J: Sympathetic nervous system in the loss of autoregulation in acute renal failure. American Journal of Physiology 1984; 246: F379-386.

  28. Maintaining renal perfusion • The individual BP target depends on age, co-morbidities (HTN) and the current acute illness. • A generally accepted target remains MAP ≥ 65. Bourgoin A, Leone M, Delmas A, et al.: Increasing mean arterial pressure in patients with septic shock: Effects on oxygen variables and renal function. Critical Care Medicine 2005; 33:780-786

  29. Volume resuscitation – which fluid? • no statistical difference between volume resuscitation with saline or albumin in survival rates or need for RRT. Finfer S, Bellomo R, Boyce N, et al.: A comparison of albumin and saline for fluid resuscitation in the intensive care unit. New England Journal of Medicine 2004; 350: 2247-2256.

  30. Volume resuscitation – how much fluid? • Fluid conservative therapy decreased ventilator days and didn’t increase the need for RRT in Acute Respiratory Distress Syndromepatients. • Association between positive fluid balance and increased mortality in AKI patients. Wiedeman H, Wheeler A, Bernard G, et al.: Comparison of two fluid management strategies in acute lung injury. New England Journal of Medicine 2006; 354:2564-2575. Payen D, de Pont A, Sakr Y, et al.; A positive fluid balance is associated with worse outcome in patients with acute renal failure. Critical Care 2008; 12: R74

  31. Which inotrope/vasopressor? • There is no evidence that from a renal protection standpoint, there is a vasopressor agent of choice to improve kidney outcome. Dennen P, Douglas I, Anderson R,: Acute Kidney Injury in the Intensive Care Unit: An update and primer for the Intensivist. Critical Care Medicine 2010; 38:261-275.

  32. Renal vasodilators? • renal dose dopamine (<5 μg/kg of body weight/min) increases renal blood flow and, to a lesser extent, GFR. Dopamine is unable to prevent or alter the course of ischaemic or nephrotoxic AKI). Furthermore, dopamine, even at low doses, can induce tachy-arrhythmia’s, myocardial ischaemia, and extravasation out of the vein can cause severe necrosis. Thus, the routine administration of dopamine to patients for the prevention of AKI or incipient AKI is no longer justified. Lauschke A, Teichgraber U, Frei U, et al.: “Low-dose” dopamine worsens renal perfusion in patients with acute renal failure. Kidney 2006; 69:1669-1674. Argalious M, Motta P, Khandwala F, et al.: “Renal dose” dopamine is associated with the risk of new onset atrial fibrillation after cardiac surgery. Critical Care Medicine 2005; 33:1327-1332.

  33. Is there a role for Fenoldopam in prevention or treatment of AKI in ICU setting? Dopamine-1 receptor agonist, lack of Dopamine-2, and alpha-1 receptor effect, make it a potentially safer drug than Dopamine! Reduces in hospital mortality and the need for RRT in AKI Reverses renal hypoperfusion more effectively than renal dose Dopamine So far so good specially in cardiothoracic ICU patients, awaiting more powered trials in other groups! J Cardiothorac Vasc Anesth. 2008 Feb;22(1):23-6. J Cardiothorac Vasc Anesth. 2007 Dec;21(6):847-50 Am J Kidney Dis. 2007 Jan;40(1):56-68 Crit Care Med. 2006 Mar;34(3):707-14

  34. Is there a role for diuretics in the treatment of AKI in ICU setting? Loop diuretics may convert an oliguric into a non-oliguric form of AKI that may allow easier fluid and/or nutritional support of the patient. Volume overload in AKI patients is common and diuretics may provide symptomatic benefit in that situation. However, loop diuretics are neither associated with improved survival, nor with better recovery of renal function in AKI. JAMA. 2002 Nov 27;288(20):2547-53 Crit Care Resusc. 2007 Mar;9(1):60-8

  35. NAC • The most recent trials seem to confirm a potential positive preventive effect of N-acetylcysteine (NAC), particularly in contrast-induced nephropathy (CIN), NAC alone should never take the place of IV hydration in patients at risk for CIN; fluids likely have a more substantiated benefit. (150 mg/kg in 500 mL saline (0.9%)] over 30 min immediately before contrast exposure and followed by 50 mg/kg in 500 mL saline (0.9%) over the subsequent 4 h )

  36. EPO • Erythropoietin (EPO) has tissue-protective effects and prevents tissue damage during ischaemia and inflammation, and currently trials are performed with EPO in the prevention of AKI post-cardiac surgery, CIN and post-kidney transplantation.

  37. AKI • Nursing interventions • Monitor input/output, including all body fluids • Monitor lab results • Watch hyperkalemia symptoms: malaise, anorexia, parenthesia, or muscle weakness, EKG changes • watch for hyperglycemia or hypoglycemia if receiving total parenteral nutrition or insulin infusions • Maintain nutrition • Safety measures • Mouth care • Daily weights • Assess for signs of heart failure • Skin integrity problems • The nurse questions orders for potentially nephrotoxic drags, and the ordered dose is validated before the client receives the drag.

  38. The nurse • The primary nursing diagnosis and collaborative problems for the client with acute renal failure are Excess Fluid Volume, Potential for Pulmonary Edema, and Potential for Electrolyte Imbalances.

  39. Potential for Pulmonary Edema • Nursing interventions: • Assess the client for early signs of pulmonary edema. • Monitor serum electrolyte levels, vital signs, oxygen saturation levels, hypertension.

  40. Case 1 • 26 yo F is involved in a motor vehicle accident, with multiple fractures, blunt chest and abdominal trauma. She was briefly hypotensive on arrival to emergency department, received 6L normal saline and normalized BP. Non contrast CT showed small retroperitoneal hematoma. On day#2 her SCr is 0.9 mg/dl, lipase is elevated and tense abdominal distension is noted. Ultrasound showed massive ascites. UOP drops to <20 cc/hr despite of 10 L total IV intake. On day#3, SCr is 2.1mg/dl, CVP is 17, UNa is 10 meq/L, with a bland sediment. What is the cause of her AKI? What bedside diagnostic test and therapeutic intervention is indicated?

  41. Bladder pressure was 29 mmHg • UOP and SCr improved with emergent paracenthesis. • Dx: Abdominal Compartment Syndrome causing decreased renal perfusion from increased renal vein pressure.

  42. Case 2 • 59 yo M, s/p liver transplant in 2001 and acute on chronic rejection, now decompensatedEnd Stage Liver Disease, is admitted with worsening ascites, hepatic encephalopathy and GI bleed (which is now controlled). The only medications he has been receiving are Lactulose and omeprazole. He has been hemodynamically stable with average BP~100/70 mmHg.He had a 3.5 L paracenthesis on day 2. His SCr has been slowly rising from 1.2 to 4.7 mg/dl within the 2nd to 4th day of admission and his UOP has dropped to 150 cc/day. His daily fractional excretion of sodium(FeNa) is <1% despite of 2 L fluid challenge. His Urine sediment is blend. His renal ulyrasound is normal. What is the cause of his AKI?

  43. Patient required hemodialysis (HD). • He had a second liver transplant and came off HD after the surgery with stable SCr of 1.4 mg/dl. • Dx: Hepatorenal Syndrome (HRS)

  44. Hepatorenal Syndrome Major diagnostic criteria: No improvement with at least 1.5 L fluid challenge SCr >1.5 mg/dl or GFR< 40 cc/min Absence of proteinuria (<500 mg/d) Other causes are rouled out (obstruction, ATN, etc.) Minor diagnostic criteria: Urine volume < 400 cc/day UNa < 10 meq/L SNa < 130 meq/L Urine RBC < 50/hpf

  45. Case 3 • 45 yo M with CHF and Bipolar Disorder on Lithium for 10 years, admitted for abdominal pain after a heavy meal, which turned out to be due to acute cholecyctitis. He was kept nil per oson D5 ½ normal saline 50 cc/hr. Next morning he felt well but thirsty and hungry, BP=120/80, input/output=1200/4500. His SCr rose from 1.2 to 1.9 mg/dl. SNa 149 meq/L. UNa 10 meq/L. UOsm 190 mOsm/Kg. What is the cause of his AKI?

  46. Patients intravenous fluids was changed to ½ normal saline, replacing 80% of UOP per hour. SCr and SNa improved to baseline in 2 days. • Dx: Prerenal azotemia secondary to renal free water loss in DI.

  47. AKI • Medical treatment • Hemodialysis • Yugular, subclavian approach • Femoral approach • Peritoneal dialysis • Continous renal replacement therapy (CRRT) • Can be done continuously • Does not require dialysate

  48. Indications for RRT • Still evolving….Generally accepted • Oliguria/Anuria • Hyperammonemia • Hyperkalemia • Severe acidemia • Severe azotemia • Pulmonary Edema • Uremic complications • Severe electrolyte abnormalities • Drug overdose with a filterable toxin • Anasarca • Rhabdomyolysis

  49. Hemodialysis (HD) • Client selection • Dialysis settings • Works using passive transfer of toxins by diffusion • Anticoagulation needed, usually heparin treatment

  50. Access to HD • HD catheter, dual or triple lumen, or arteriovenous shunt for temporary access