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1、Acute Kidney Injury-Acute renal failure,Jiang Huajun. M.D, Ph.D Dept. of Nephrology, Union Hospital. HUST drhuajunjiang ,The Early Report of ARF,The disease seems in general to come on suddenly. The peculiar symptom is a sudden diminution of secretion of urine, which soon amounts to a complete suspe
2、nsion of it. The affliction is probably at first considered as retention; but the catheter being employed, the bladder is found to be empty. . . after several days, the patient begins to talk incoherently, and shows a tendency to stupor. This increases gradually to perfect coma, which in a few days
3、more is fatal. . . ” John Abercombie (1780 1828) sudden (i.e.,hours to days) reduction in urine volume,Profile,Rapid decrease in renal function over days to weeks, causing a accumulation of nitrogenous products in the blood. Often results from major trauma, illness, or surgery but in some cases is c
4、aused by a rapidly progressive, intrinsic renal disease. Symptoms include anorexia, nausea, and vomiting, progressing to seizures and coma if the condition is untreated. Fluid, electrolyte, and acid-base disorders develop quickly. Diagnosis is based on laboratory tests of renal function, including s
5、erum creatinine, renal failure index, and urinary sediment . Other tests are needed to determine the cause. Treatment is directed at the cause but also includes fluid and electrolyte management and sometimes dialysis,Epidemiology,Variable (inconsistent definitions, different population) Based on new
6、 definition, AKI occurs approximately 7% in hospitalized patients Mortality: Variable depend on etiology,The Modern Understanding of ARF,ARF to AKI Definition is based on absolute increase in serum creatinine (Scr) and oliguria,New concepts in Definition,Whats the new definition? Early single-center
7、 and multicenter Cohort studies , administrative database studies Definitions were different Hou et al. Am J Med 74: 243248, 1983,New concepts in Definition,The Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8:R204-R212,De,Decrease in
8、 GFR,RIFLE criteria,New concepts in Definition,An new precise operational definition of AKI is intended to emphasize the reversible nature of most renal insults,Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11:R31,AKIN criteria,In 48
9、 hours,New concepts in DefinitionKDIGO criteria,New concepts in Definition,New Biomarkers Cystatin C Neutrophil gelatinaseassociated lipocalin (NGAL) Kidney injury molecule-1 Interleukin 18,Pathophysiology,Endothelial injury from vascular perturbations Direct effect of nephrotoxins Abolishment of re
10、nal autoregulation Formation of inflammatory mediators,Pathophysiology,Tubular obstruction necrosis and apoptosis of tubular cells Increased tubuloglomerular feedback elevated intracellular calcium levels from tubular damage cause a series of cellular-level alterations,Etiology,Pre-renal Underperfus
11、ion of kidneys results from volume depletion, fluid sequestration, or inadequate perfusion pressures (heart failure, cirrhosis, or sepsis) hypoperfusion of functioning kidney leads to enhanced reabsorption of Na and water, resulting in oliguria with high urine osmolality and low urine Na,Etiology-pr
12、erenal,Etiology,Renal (tubular, interstitial, glomerular, vascular) Tubule ATN Ischemia (prolonged or severe prerenal state) Nephrotoxic,Etiology,Interstitium Acute interstitial nephritis (AIN) -drug induced -certain infections: pyelonephritis, papillary necrosis -neoplastic disorders,Etiology,Glome
13、rulus Primary Infectious Rheumatologic Vasculitic antineutrophilic cytoplasmic antibody antinuclear antibody test antistreptolysin O complement levels c-reactive protein cryoglobulin erythrocyte sedimentation rate hepatitis panel (ie, specifically for hepatitis B and C) renal biopsy,Etiology,Postren
14、al (10% of AKI) Urinary tract obstructions (within or outside) stones, tumors, retroperitoneal fibrosis Ultrasonography,Etiology-postrenal,CausesExamples Tubular precipitationuric acid (tumor lysis), sulfonamides, , acyclovir, methotrecxate, Ca oxalate (ethylene glycol ingestion), myeloma protein, m
15、yoglobin Ureteral obstructionIntrinsic: calculi, clots, slougher renal tissue, fungus ball, edema, malignancy, congenital defects Extrinsic: malignancy, retroperitoneal fibrosis, ureteral trauma during surgery or high impact injury Bladder obstruction Mechanical: prostatic hypertrophy or cancer, bla
16、dder cancer, urethral strictures, phimosis, urethral valves, obstructed indwelling urinary catheter Neurogenic: anticholinergics, upper or lower motor neuron lesion,Symptoms and signs,Of the underlying illness or surgical procedure that precipitated renal deterioration. Uremia symptoms: anorexia, na
17、usea, vomiting, weakness, myoclonic jerks, seizures, confusion and coma. PE: edema, palpable bladder etc,Diagnosis,Suspected when urine output falls or serum BUN and Scr rise Seek an underlying cause Laboratory tests: CBC, BUN/Scr, electrolytes, urine tests and other needed by cause determination,Di
18、agnostic Evaluation,IndexPrerenalPostrenalATN AGN U/P osmolality 1.511.511.5 11.5 Urine Na (mmol/L) 4040 0.040.02 22 1,Adapted from Miller TR, et al: urinary diagnostic indices in acute renal failure,U/P: urine/plasma Renal failure index: U/P Na + U/P creatinine,Special Scenarios,Contrast-induced ne
19、phropathy (CIN) increase in serum creatinine levels that is 25% or higher (0.5 mg/dL) within 72 hours of contrast media administration risk factors for CIN include older age, diabetes, underlying chronic CKD, multiple myeloma, and volume depletion. Vasomotor alterations ,free radical formation prehy
20、dration, temporary discontinuation of ACE inhibitors, angiotensin receptor blockers, and diuretics,Special Scenarios,Sepsis 19% in moderate sepsis, 23% in severe sepsis, and 51% in septic shock AKI+sepsis: 70% mortality rate versus 45% among patients with AKI alone nitric oxide synthases, cytokines,
21、 chemokines, and adhesion molecules early goal-directed therapy, hemodialysis,Treatment,Varied and depend on etiologic factors Prerenal azotemia from volume depletion is usually responsive to isotonic saline repletion ATN requires the discontinuation of nephrotoxic agents,maintenance of optimum hemo
22、dynamics, and close surveillance for complications of renal dysfunction (eg, acidosis, electrolyte abnormalities) Postrenal etiologies dictate obstruction removal,Treatment,Emergency treatment Life-threatening complications Pulmonary edema: O2, IV vasodilators Hyperkalemia: IV infusion of 10%Ca gluc
23、onate 10ml, dextrose 50g, insulin 510 units. Severe acidosis ( pH7.2 ) IV NaHCO3 ( 150mEq in 1 L of 5% D/W,Treatment,Fluid control Daily water intake= sensible dehydration volume (previous 24 hours) + insensible dehydration endogenic water (1g protein: 0.4ml; lipid: 1ml; glucose: 0.6ml) insensible d
24、ehydration endogenic water 5001000ml/d,Treatment,Numerous pharmacologic agents: insulin-like growth factor 1, thyroxine, atrial natriuretic peptide,dopamine, and loop diuretics, effective in preventing or ameliorating experimental AKI. none of these substances has been translated successfully to cli
25、nical practice. clinical management of AKI is primarily supportive,Treatment: Nutritional support,NUTRITIONAL STATUS IN AKI Patients with AKI in the ICU, even more than other critically ill patients, are at risk of nutritional depletion evaluation in this clinical condition is difficult as most of t
26、he commonly utilized traditional nutritional tools are often misleading protein-energy wasting (PEW) a condition of decreased body stores of protein and energy fuel stores (i.e., lean body mass and fat masses) biochemical (such as albumin or prealbumin), body weight loss, decreased muscle mass low e
27、nergy and protein intakes,International Society of Renal Nutrition and Metabolism (ISRNM,Treatment: Nutritional support,AKI is associated with alterations of water, electrolyte and acid-base metabolism, and also with specific changes in protein, carbohydrate and lipid metabolism hyperglycemia and in
28、sulin resistance proteolysis of skeletal muscle proteins with increased amino acid turnover and negative nitrogen balance altered lipid metabolism TG,VLDL TC, HDL, LDL,Treatment: Nutritional support,NUTRIENT REQUIREMENTS IN AKI Macronutrients depends more on the severity of underlying disease, preex
29、isting nutritional status and acute/chronic comorbidities, than on AKI itself,Treatment: Nutritional support,GOALS OF NUTRITIONAL SUPPORT IN AKI ensure the delivery of energy and protein in such amounts as to prevent protein-energy wasting preserve lean body mass and nutritional status avoid further
30、 metabolic derangements and complications improve wound healing support immune function and to reduce mortality,Treatment: replacement therapy,RRT is the central component of care for patients with severe AKI. generally accepted indications for RRT include volume overload, hyperkalemia, metabolic acidosis, and overt uremic symptoms,Treatment: replacement therapy,For decades, continuous renal replacement therapies (CRRTs) such as continuous venovenous hemofiltration (CVVH) were thought to offer bett
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