Aute renal failure part one


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Aute renal failure part one

  2. 2. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI ACUTE RENAL FAILURE Acute kidney failure — also called acute renal failure or acute kidney injury — develops rapidly over a few hours or a few days. Acute kidney failure is most common in people who are already hospitalized, particularly in critically ill people who need intensive care. Acute kidney failure can be fatal and requires intensive treatment. However, ARF may be reversible. If you're otherwise in good health, you may recover normal kidney function. DEFINITION------An abrupt increase in the BUN and Creatinine with corresponding problems in handling of fluids, Potassium, Phosphorus, and acid-base balance. This is usually a greater than 50% decline in the GFR. It is a sudden fall in renal function characteristic by azotemia. FOR DIAGNOSIS; raising blood urea nitrogen Raising creatinine concentration. Problems with the Definition : • Serum Creatinine does NOT reflect the degree of renal dysfunction or improvement • Urine output or lack of may also not reflect the degree of dysfunction • A better definition may be Acute Kidney Injury (AKI). Types of Acute Kidney Injury: Acute Renal Failure can be: 1. Oliguric <400 ml/day or 2. Non-Oliguric >400 ml/day Non-Oliguric has a much better prognosis. -In the Pre-Dialysis Era, ARF had a 50------70% Mortality Rate. --Today with Dialysis, ARF still has a 50----70% Mortality Rate . 2
  3. 3. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI Types of Acute Renal Failure: ARF Pre- Renal PostRenal Intrinsic Renal Vascular Glomerular Interstitial Tubular Phases of Acute Renal Failure: Initiation Phase-drop in BP, nephrotoxins, early sepsis—rise in BUN/Cr, decreasing urine output • Oliguric Phase-usually less than 400 ml/da, may require dialysis • Recovery/Diuretic Phase-increasing urine output, decreasing BUN/Cr, Potassium, Phosphorus, and Magnesium . PRE –RENAL ARF: A decreasein either total circulatory volume or effective circulatory volume (I.e. CHF or Sepsis). This leads to activation of the ReninAngiotensin--Aldosterone System and ADH. Thus enhanced Na and H2O reabsorbtion. 1. CAUSES: 40—60% of cases Caused by diminution in the renal blood flow Major causes include: 3
  4. 4. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI 1. GIT loss: DEHYDRATION Diarrhea, vomiting( what ever the cause--- infection like cholera or organic obstruction) intraluminal fluid in bowel obstruction ,intraluminal gut fluid , bowel wall oedema((IBD)),Fistula, Excessive sweating . 2. Sequestration of intravascular volume--- burns ,pancreatitis , sepsis 3. Hepatic: liver cirrhosis , chronic hepatitis 4. Cardiac : CCF , cardiogenic shock , pericardial temponade 5. Hemorrhage: active bleeding with large amount 6. Diuretic phase of ARF or Post-Obstructive Diuresis 7. Medications: Loop diuretics----frosemide , Bumetanide ,Thiazide diuretic ACE-I or ARBs---- commonly seen in CCU after few days of treatment. The prolonged use of diuretic result in loss of concentrating function. Non oliguric prerenal ARF may also caused by inhibition of the effect of antidiuretic hormone(ADH/Vasopresin)on the collecting D. BY LITHIUM CLINICAL FEATURES: 1.History: Sometimes acute kidney failure causes no signs or symptoms and is detected through lab tests done for another reason. It is mandatory to look for unexplained symptoms in a patient who had a risk factor for acute renal injury like organ failure , drug intake , systemic medical illness , HTN or DM. Symptoms are not specific : 1. CNS symptoms---- syncopy, dizziness , fatigue, confusion, seizures , coma 2. UROLOGICAL symptoms--- change of urine frequency and amount ,thirsty 3. H/O fluid loss--- diarrhea , vomiting persistent , bleeding from orifices 4. H/O Fluid retention, swelling in your legs, ankles --CCF , liver cirrhosis with ascitis 5. CARDIAC symtoms--- dyspnea , chest pain H/O use of diuretics 2.Physical examination:  Postural change in pulse and blood pressure 4
  5. 5. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI  A large weight loss may indicate volume depletion  Weght gain may accompany intravascular volume loss with total body volume overload-:-1. SIGNS OF CCF 2. ASCITIS AND OEDEMA 3. CHRONIC STASIS DERMATITIS 4. ULCERS IN THE LOWER LIMBS  Hemodynamic – persistent low pulmonary capillary wedge pressure suggests hypovolemia where as raising or high PCWP suugests CCF and under perfusion.  In a pt with cardiac or pulmonary disease , hemodynamic monitoring plays a rule in diagnosis. WHAT ARE THE DIAGNOSTIC CRETERIA? I. II. III. IV. Signs of volume depletion or third space fluid loss Volume depletion by hemdynamic criteria such as pulmonary capillary wedge pressure. Urinalysis and laboratory findings Response to volume repletion with reversal of azotemia PLUS if oliguric ; increase in urine out put with normalization of urinary indices No evidence of obstruction on ultrasound abdomen if oliguric stage persists. V. POST-RENAL ARF Cause :  2---25% ARF cases .  Generally , the patient is oliguric or anuric.  Due to changes in the obstructing lesions with the patients position, there may be wide variety in urine out put. 1 .Intrauretric obstruction: Stones , blood clots ,pus ,tissue papillary necrosis—DM ,Analgesic drug excess 2.Extraureteric obstruction: A- Most commonly – tumors involving the retroperitoneal lymph nodes Lymphoma , testicular carcinoma , cervical cancer –70% OF female ARF caused by pelvic tumors, colon cancer 5
  6. 6. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI B- 5% -- Retroperitoneal fibrosis from radiation therapy and ergot alkaloids. 3.Lower urinary tract obstruction----neurogenic bladder, prostate hypertrophy 80% of cases, cancer, bilateral renal caliculi ,bladder cancer CLINICAL FEATURES: 1.History: historical features include--A .Nephrolithiasis B .Repeated pyelonephritis ,immune deficiency with fungal disease C . Hematuria , gross hematuria D .Previous pelvic tumour or lymphoma E. Previous abdominal radiation treatment --- fibrosis F. Drug ingestion---- ergot alkaloids G. Dribbling, frequency ,incontinance ,dysuria 2. H/O nausea ,vomiting ,irritability, headache , dyspnea 2.Physical examination: I. II. Bilateral flank pain & tenderness---70---80% Costo vertebral angle tenderness-----ascending infection Signs of inferior vena cava or lymphatic obstruction (( lymphedema)). DIAGNOSTIC FEATURES: History is mandatory for exploration of urological symptoms or significant past medical os surgical history that signifies renal complication, H/O hematouria ,H/O difficulty of urination Laboratory indices similar to prerenal azotemia. Ultrsonography evidence of bilateral hydronephrosis , unilateral hydronephrosis if a single kidney is present , evidence of intraabdominal ,retroperitoneal , pelvic obstructive masses. Evidence of obstructed flow on retrograde pyelography Evidence of bilateral obstructed flow on radiohippurate scans Urinary catheter which once done the patient passed large amount of urine with gradual reduction of renal parameters and improvement of pt day by day. 6
  7. 7. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI INTRA-RENAL FAILURE  30---50% of ARF.  Direct insult to the kidney . May be a result of vascular, Glomerular, interstitial, or tubular causes.  Final common pathway of untreated prerenal or postrenal failure. TWO TYPES: 1.Primary parenchymal disease 10 ----20% ARF 2.Acute tubular necrosis ((ATN)) Vasomotor changes produce tubular ischemia -----------------tubular dysfunction--tubuloglomular feed back------------- decrease GFR CAUSES: 1.Primary renal disease: i. ii. iii. iv. v. Vascular : Post stertococcalGlomerulonephriris SLE Polyarteritis nodosa wegners granulomatosis Scleroderma Good pastures syndrom Malignant HTN IgA BURGERS HEMOLYTIC UREMIC SYNDROME renal artery stenosis RENAL EMBOLIZATION THROMBOTIC THROMBOCYTOPENIC PURPURA Tubulo-interstitial diseases: Myeloma proteins Hypercalcemia Hypokalemia Allergic interstitial nephritis---nonsteroidal –antiinflammatory, b-lactamase-penicillins Crystallization within the tubular lumen: Oxylate crystals Urate crystals ( hyperuricemia 18—20mg/dl ) Methtrexate derivatives Tumor lysis syndrome---- urate , calcium phosphate Post –angiogram ,CABG , sustained hypotension Rhabdomyolysis 7
  8. 8. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI ACUTE TUBULAR NECROSIS Pathophysiology---Hypoxia of the tubular microvasculature leads to tubular necrosis and loss of reabsorbtion and secretory abilities of the tubules . Afferent and Efferent Arteriolar Vasoconstriction • Mesangial Contraction WITH Release of Reactive Oxygen species, NO, ATII, PG’s, Catecholamines • Tubular Necrosis due to tubular obstruction and back-leak With Cellular Edema • Increased free Ca++ WITH Release of compartmentalized enzymes • Destruction in Cytoskeleton • Reperfusion injury from reactive Oxygen species, WBC’s, Complements, and cellular debris TYPES OF ATN: A. 1. 2. 3. 4. 5. 6. ISCHEMIC TUBULAR NECROSIS : Hypotention Surgery ---cardiovascular or abdominal surgery. Sever burns Sever muscle injury or extreme physical exertion. Sepsis , aortic cross –clamping Prerenal azotemia . B.TOXIC TUBULAR NECROSIS: Substances, such as medicines that are toxic to the kidneys. Many substances that are not toxic to the kidneys in a healthy person may become toxic in a person who has existing kidney problems or another condition that increases his or her risk of acute renal failure, such as heart failure, diabetes, or multiple myeloma. 1. 2. 3. 4. 5. Heavy metals Myoglobin (rabdomylosis) Hemoglobin(extensive hemolysis) Medications (aminglycoside) Halogenated alkanes . 8
  9. 9. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI DIAGNOSTIC FEATURES:  1RY Parenchymal disease---.Urinanalysis .Severe hypertension is common .No evidence of obstruction on USS abdomen  No signs ,symptoms, hemodynamic indications of ongoing hypovolemia or persistent ARF following correction of hypovolemia.  Urinalysis and laboratory finding  No evidence of obstruction  No response to volume repletion CLINICAL FEATURES: History---1. H/O URTI suggests post infectious glomerulonephritis Fever , rash or pleuritic pain may point to vasculitis 2. H/O drug intake NSAID ,ANTICOAGULANTS ,ANTIBIOTIC ,CIMETIDINE ,DIURETIC, CYCLOPHOSPHAMIDE, METHOTREXATE, AMINOGLYCOSIDE, RADIOLOGIC CONTRAST MATERIAL. 3. H/O sepsis --- once there is no cause 4. H/O blood transfusion--- hemolysis ,transfusion reaction ,microangiopathic hemolysis 5. Rhabdomylosis---unconscious or seizures. Hypokalemia/hypophosphatemia cause it. 6. Examination may find evidence of vasculitis. Rashes are often present. Sclerodectaly---scleroderma HTN---85% 7. H/O preexsisting prerenal azotemia may point to progression to ATN. 8. Hypotension does not need to be documented in postsurgical patient ,60 year in order for the physign to suspect ATN RECOMMENDED DIAGNOSTIC APPROACH: i. Urinalysis: Red blood cell casts -----evaluate autoimmune disease ii. Urine osmolality –(Uosm) Specific gravity of limited value in ATN (affected by glucose or protein). 1. Pre-renal--- 90% have Uosm more than500mosm/l 2 .Post renal ARF --- INITIAL like prerenal azotemia Persistent obstruction ---- tubular damage---low Uosm 9
  10. 10. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI iii. 3. ATN—90% have Uosm less than 350 mosm/l Loss of the concentrating ability with tubular dysfunction 4.Uosm/Posm: The overlap range (Uosm 350 to 500 mosm/l) is not diagnostically useful. 90% of patients with ATN have Uosm/Posm less than 1.07 90% of patients with prerenal azotemia have Uosm/Posm more than 1.25 BUN and creatinine: 1. Creatinine---with complete cessation of glomerular filtrate , serum creatinine increase by a bout 1mg/dl/day Daily increase is less in patients with decreased muscle mass( older) More 2.5mg/dl/day in young muscular males. 2. Urea: Urea is freely filtred and variably absorbed. Reabsorption is proportional to water flow in tubules ,the presence of ADH , local tubular damage, peritubular blood flow. Production of urea is affected by hepatic disease Decrease BUN-- LOW PROTEIN DIET  STARRVATION  HEPATIC FAILURE Increase BUN ( hypercatabolism)--      BURNS SEPSIS INFECTION GLUCOCORTICOID USE TRAUMA POSTSURGICAL The rate of BUN rises with complete recession of glomerular filtration --- 24-60mg/ml/d IV -- plasma BUN/creatinine ratio:  Routine urea is increased greatly in prerenal and post renal uremia.  BUN/Creatinine ratio more than 20/1 is present in 80% of renal and postrenal azotemia.  Intrarenal ARF &ATN are characterized by proportionate BUN/ CRET 10/1 10
  11. 11. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI V-- URINE CREATININE: 1. Urine creatinine : Is a marker of ability to concentrate urine as creatinine is filtred without reabsorption 2. Ucreatinine /P creatinine  ˂ 10----------85% of pt with ATN  ˂ 20------85% OF PT with prerenal ARF VI --Urine sodium (U Na): 1. The ability to conserve Na in proportional to the amount filtered is a marker of intact tubular function . 2. UNa ˂ 20meq /l occurs in 90% of prerenal azotemia ˂ meq/l is found in 90% of pt with ATN 40 VII—Fractional exertion of sodium( EF Na) 1.A more sensitive test is the calculated EF Na U Na /P Na x P creat /U creat 2. 90% of prerenal azotemia 90% of ATN ˂ 1% ˂ 2% 3. EF Na less than 1% Common in renal parenchymal disease ,particularly glomerulonephritis as tubules retain function and attempt to compensate in response to diseased glomeruli. VIII Other laboratory tests: 1. A clue to presence of tubuloischemic necrosis ----------- hyperchloremic acidosis of rapid onset 2. Myoglobin levels in urine may confirm rabdomyolysis 3. A SEVER ANION GAP METABOLIC ACIDOSIS WITH OXALATE CRYSTALS IN URINE MAY INDICATE ETHYLENE GLYCEROL TOXICITY. 4. Hyperchloremic acidosis with hyperkalemia--- 80% of pt w post obstructive dieresis 11
  12. 12. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI IX ULTRSOUND: 1. 85% of case , the cause of obstruction can be detected by USS (ureter,kidney,pelvis) 2. If the index of suspicion of obstruction is high (single kidney , kidney transplant ,abdominal mass), retrograde pyelogram may be indicated. 12
  13. 13. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI X Nuclear studies: 1. Flow studies (glucoheptonadte) Measure renal perfusion and exclude vascular problems 2. Hippurate functional studies Measure renal function Suggest or confirm the presence of ATN Diagnose obstruction Suggest renal transplant rejection XI IV urpgraphy:  Limited by fear of exacerbating ARF & difficulty of giving dye to patient with marginal Marginal fluid status. XI Renal biobsy: Indication---- oliguria that persists for longer than 3 weeks OR when treatable disease is strongly suspected TEST PRERENAL AZOTEMIA OSMOLALITY ATN ˂ 500mosm/l POSTRENAL ˂ 350mosm/l ˂ 500mosm then derease Uosm/Posm ˂ 1.25 ˂1.07 BUN/CREAT (PLASMA) ˂ 20/1 10/1 Ucreat / P creat ≥ 20 ≤ 10 variable UNa ≤ 20 ≥ ≥100 post obs ˂ 1% ˂ 2% FE Na variable ˂ 20/1 40 variable 1. Duration <3 months 2. Oliguria <400 ml urine/24 hours 3. Absolute increase Scr by 0.5 or 1.0 mg/dl or relative increase 25% 4. Cockcroft – Gault Equation 13
  14. 14. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI (140-age) x wt(kg) -----------------------Serum Cr x 72 SUMMARY OF INITIAL EVALUATION: a. Consider possible etiologies and direct evaluation b. Medications should always be suspected c. Standard Blood Testing : a. Electrolyte/renal panel, Ca2+, Phosphate, Mg2+, Albumin b. Complete Blood Count c. Foley catheter to rule out bladder obstruction AND take sample of urine. 1. Urine for electrolytes, dipstick and microscopic analysis a. Osmolality, creatinine, Na+, K+, Clb. Urine spot protein to creatinine ratio (normal is <0.2) c. Pigment: Hemoglobin (myoglobin) d. Cells, Casts, Crystals, Organisms e. Consider Urine culture 2. More informative for the cause: i. Renal/Pelvic Sono - stones, hydronephrosis, mass ii. Consider Abdominal radiograph if ultrasound is not done to rule out stones iii. ESR, ASO titer, ANA, C3/C4 Anti-GBM Abs iv. Renal Biopsy in rapidly progressing disease v. ANCA and Anti-GBM diseases - consider cyclophosphamide + glucocorticoids vi. Idiopathic rapidly progressive glomerulonephritis often ANCA positive (other inflammatory diseases such as bacterial endocarditis can given ANCA+) WHAT OTHER THE DIFFERENT TYPES OF GN?(( pathological)) 1. Glomerular Involvement : 14
  15. 15. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI a. Diffuse: all glomeruli in a section are diseased b. Focal: some glomeruli in a section are diseased c. Segmental: parts of individual glomerulus affected 2. Focal Glomerulonephritis:  a. Some glomeruli are dead( necrosis, collapse, sclerosis ).  B .Acute or chronic inflamation is often seen. 3. Crescent Glomerulonephritis (very poor prognosis)  Crescent (moon shaped) formation in glomerulus  Affected glomeruli are non-functional  Focal and Segmental Glomerulosclerosis: portions of many glomeruli are destroyed 5. Minimal Change Glomerulonephritis :  Glomeruli appear okay, but function is poor  Electron microscopic evidence of basement membrane disease  Response to glucocorticoids is usually very good 6. IgA Deposition:  IgA nephropathy  Deposition of IgA immune complexes  Differential includes Systemic Lupus (SLE) and Henoch-Schonlein Purpura (HSP) 7. Proliferative Glomerulonephritis  Increase in mesangeal cell number  Usually follows insults (eg. Post-Streptococcal)  May be seen in collagen vascular disease, SLE. 8. Collapsing Glomerulonephritis     Major form seen in HIV nephropathy Usually late stage Rapid progression to renal failure (weeks-months) No effective therapy to date 15
  16. 16. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI 9. Tubular Necrosis  Tubular cells die and slough off basement membrane  The dead tubular cells form casts which can occlude lumen  Glomular basement membrane may also be damaged MANAGEMENT OF ARF: A. Renal Diet : Low phosphate, potassium, sodium, and protein High calcium and vitamin D diet Various multivitamin formulas available for renal patients, eg. Nephrovit®. Low protein diet may slow progression slightly in chronic renal disease Phosphate and Calcium Dangerous if product of Calcium and Phosphage > ~70 (mg/dl) (will lead to precipitation) If product is close to 70, then phosphate should be lowered with aluminum compounds These compounds should be given with meals to bind the phosphate directly If product is <60, then calcium should be given 500-1000mg po tid with meals If calcium is low but phosphate normal, then calcium should be given before meals Consider using 1,25 dihyroxyvitamin D supplements B. AVOIDABLE COMPLICATIONS SHOULD BE FOLLOWER. 16
  17. 17. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI 1.Acidosis Renal tublar acidosis (RTA) is common in early renal failure Oral bicitra (citrate replaces bicarbonate) may be used Bicitra is contraindicated in edematous states due to high sodium content 2.Hyperuricemia Check uric acid levels Uric acid deposition in renal tubules may worsen progression of renal failure Allopurinol may be given (100-200mg po qd) to attempt normalization of uric acid       3.Hypertension ACE inhibitors generally contraindicated in moderate to severe renal failure Calcium blockers such as nifedipine can be used. Labetolol is also very effective but patient should have LV EF>50% and no bronchospasm Consider Hydralazine for afterload reduction Pure alpha-adrenergic blocking agents may be effective, but tachyphylaxis may occur Diuretic improve hypertension/ volume overload 4. Volume overload Attempt to maximize cardiac output and improve intravascular volume Diuretics often worsen renal failure but may be necessary to prevent pulmonary edema In general, potassium sparing diuretics should be avoided (high risk hyperkalemia) Dopamine or mannitol can be tried, but are usually not effective Albumin infusions are probably not helpful, but may help diuresis in low albumin states Dialysis may be required particularly in severe volume overload situations     5. Protein Load Reducing protein load is thought to reduce azotemia . Appears to slow progression of CRF. Patients with moderate renal disease - some decrease in progression on low protein diet . Patients with severe renal disease show no benefit on low protein diet . Hospital inpatients with ARF ~50% mortality rate. 6.Newer Agents 17
  18. 18. ARF –DEFINITION,CAUSES, DIAGNOSIS AND MANAGEMENT 2014 BY DR. MAGDI AWAD SASI      Atrial natriuretic factor (ANF)= dilators + diuretic ANF (Auriculin®) ? efficacy in oliguric ARF ANF may increase renal dysfunction in diabetics receiving radiocontrast Brain derived natriuretic factor (BDNF) may be effective some patients Other vasodilators (eg. calcium channel blockers) are not effective  Investigation renal growth/regeneration factors 8. Dialysis Indications: 1. 2. 3. 4. 5. 6. 7. 8. 9. Severe fluid overload Refractory hypertension Uncontrollable hyperkalemia Nausea, vomiting, poor appetite, gastritis with hemorrhage Lethargy, malaise, somnolence, stupor, coma, delirium, asterixis, tremor, seizures, Pericarditis (risk of hemorrhage or tamponade) bleeding diathesis (epistaxis, gastrointestinal (GI) bleeding and etc.) Severe metabolic acidosis Blood urea nitrogen (BUN) > 70 – 100 mg/dl o o o o o C. Volume Overload Hemofiltration or hemodialysis can be used to allow recovery of kidney after ARF Average duration of need for these therapies was 9 days in ARF After this time, kidneys regain function and increase urine output Native kidneys may continue with minimal function for 6-12 months of hemodialysis After that, native kidneys usually shut down permanently      D. Kidney Transplantation Excellent (and improving) results with cadaveric grafts. Living Related Donor kidneys superior to CRT New kidney usually placed in extraperitoneally in the pelvis Cyclosporin ,Prednisone, OKT3, mycophenolic acid, FK506 immunosuppression Combined Kidney Pancreas transplant in Diabetic ESRD patients 18