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Medicine 5th year, 1st lecture (Dr. Kawa Husain)
 

Medicine 5th year, 1st lecture (Dr. Kawa Husain)

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The lecture has been given on Dec. 2nd, 2010 by Dr. Kawa Husain.

The lecture has been given on Dec. 2nd, 2010 by Dr. Kawa Husain.

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    Medicine 5th year, 1st lecture (Dr. Kawa Husain) Medicine 5th year, 1st lecture (Dr. Kawa Husain) Presentation Transcript

    • Renal failure
    • Function of the kidneys
      The kidneys are responsible for:
      1- removing wastes from the body.
      2-regulating electrolyte balance and blood pressure.
      3- converting Vit D into its active form.
      4-stimulating RBC production by synthesizing erythropoietin.
    • Renal failure
      Failure of the excretory function of the kidneys,leading to retention of nitrogenous waste products of metabolism.
      Failure of the regulation of fluid & electrolytes status .
      Failure of the endocrine function of the kidney.
    • Acute renal failure :
      Refers to a sudden and usually reversible loss of renal function, which develops over a period of days or weeks.
      Chronic renal failure :
      Refers to an irreversible deterioration in renal function which classically develops over a period of years
    • ACUTE RENAL FAILURE
    • ACUTE RENAL FAILURE
      Acute renal failure (ARF) refers to a sudden and usually reversible loss of renal function ( rapid decline in glomerular filtration rate), which develops over a period of days or weeks and is usually accompanied by a reduction in urine volume.
      (>50%) decrease in glomerular filtration rate (GFR) over a period of hours to days, with an accompanying accumulation of nitrogenous wastes in the body.
      There are many possible causes and it is frequently multifactorial. The clinical picture is often dominated by the underlying condition (e.g. septic shock, trauma).
    • ARF complicates approximately 5% of hospital admissions and up to 30% of admissions to intensive care units.
      Oliguria (urine output 400 mL/d) is a frequent but not invariable clinical feature (50%).
      ARF is usually asymptomatic and diagnosed when biochemical monitoring of hospitalized patients reveals a recent increase in blood urea and creatinine concentrations.
    • Causes of ARF
      • Pre-renal cause.
      • Intrinsic renal cause.
      • Post-renal cause.
      • Systemic diseases
      acting via one or more of these 3 categories.
    • Causes of ARF
      Acute Renal Failure
      Pre-renal
      Intrinsic renal
      Post-renal
      Tubular
      Interstitial
      Vascular
      Glomerular
    • nephron
      the functional unit of the kidney
      • capable of forming urine
      • has two major components:
      glomerulus
      tubule:
      proximal
      loop of Henle
      distal
      collecting
    • Causes of ARFPre-renal ARF
      Accounts for 60-70% of cases of ARF
      Represents physiologic response to mild-moderate renal hypoperfusion
      Renal parenchymal tissue is not damaged therefore rapidly reversible upon restoration of RBF and glomerular filtration pressure
      Elderly and those with pre-existing renal disease at increased risk
    • Causes of ARFPre-renal ARF
      I. Absolute decrease in effective blood volume( Hypovolemia):
      A. Hemorrhage, burns, dehydration
      B. GI fluid loss: vomiting, surgical drainage, diarrhea
      C. Renal fluid loss: diuretics, osmotic diuresis (e.g., diabetes mellitus), hypoadrenalism
      D. Sequestration in extravascular space: pancreatitis, peritonitis, trauma, burns, severe hypoalbuminemia
      II.Relative decrease in blood volume ( ineffective arterial volume ) Hypotention.
      A.Congestive heart failure
      B. Systemic vasodilatation: sepsis, antihypertensives, , anaphylaxis .
      C.Liver failure.
      E. massive pulmonary embolus.
    • Causes of ARF Pre-renal ARF
      III.Arterial occlusion (Renal artery occlusion stenosis):
      Bilateral thromboembolism.
      Thromboembolism of a solitary kidney.
    • Causes of ARF Intrinsic Renal Causes
      Accounts for 25-40% of cases of ARF
      Types:
      ATN ( Acute Tubular Necrosis ) 85%
      Interstitial nephritis 10%
      Acute glomerulonephritis <5%
      Intrarenal vascular disease <5%
    • Causes of ARFIntrinsic Renal Causes
      I-. Acute tubular necrosis
      A. Ischemia B. NephrotoxinsC.Sepsis syndrome
      A. Ischemia
      As for severeprerenal ARF (hypovolemia, low cardiac output, renal vasoconstriction, systemic vasodilatation), obstetric complications (abruptioplacentae, postpartum hemorrhage)
    • B. Nephrotoxins
      1. Exogenous:
      Antibiotics (aminoglycosides, cephalosporin , amphotericin B )
      Iodinated contrast agents.
      Chemotherapy (e.g., cisplatin )
      Organic solvents (e.g., ethylene glycol)
      2. Endogenous:
      Intratubular pigments ( hemoglobinuria as in hemolysis, myoglobinuria as in rhabdomyolysis).
      Intratubular proteins (myeloma) .
      Intratubular crystals( uric acid, oxalate) ( tumor lysis syndrome ).
    • Causes of ARFIntrinsic Renal Causes
      II. Interstitial nephritis
      A. Allergic: antibiotics (e.g., -lactams, sulfonamides, trimethoprim, rifampicin), nonsteroidal anti-inflammatory agents, diuretics, captopril
      B. Infection: bacterial (e.g., acute pyelonephritis, leptospirosis), viral (e.g., cytomegalovirus), fungal (e.g., candidiasis)
      C. Infiltration: lymphoma, leukemia, sarcoidosis
      D. Idiopathic
    • Causes of ARF Intrinsic Renal Causes
      III. Disease of glomeruli ( Acute Glomerulonephritis)
      PostinfectiousGlomerulonephritis.
      Anti-basement membrane antibody disease
    • IV. Vascular :
      Vasculitis.
      Malignant hypertension.
      Microscopic polyarteritis.
      Causes of ARF Intrinsic Renal Causes
    • Causes of ARF Post-renal Causes of ARF
      Account for 5% of cases of ARF
      ARF occurs when both urinary outflow tracts are obstructed or when one tract is obstructed in a patient with a single functional kidney.
      -Bladder outlet obstruction
      -Bilateral ureteral obstruction ( unusual ).
      Ureteral obstruction in a solitarey kidney.
      ( obstruction by : Calculi, blood clot, sloughed papillae, cancer, external compression e.g., retroperitoneal fibrosis)
      -Urethra stricture .
    • Types of Acute Renal Failure
      REVERSIBLE PRE-RENAL ACUTE RENAL FAILURE
      When haemodynamic disturbances produce acute renal dysfunction that has the potential to be rapidly reversed
      ( reversable ),by early recognition and treatment .
      ESTABLISHED ACUTE RENAL FAILURE (ATN )
      May develop following severe or prolonged under-perfusion of the kidney (pre-renal ARF).
      In such cases, the histological pattern of acute tubular necrosis is usually seen.
    • REVERSIBLE PRE-RENAL ACUTE RENAL FAILURE
      When haemodynamic disturbances produce acute renal dysfunction that has the potential to be rapidly reversed
      ( reversable ),by early recognition and treatment .
    • REVERSIBLE PRE-RENAL ACUTE RENAL FAILURE
      Pathogenesis
      The kidney can regulate its own blood flow and GFR over a wide range of perfusion pressures.
      When the perfusion pressure falls-as in hypovolaemia, shock, heart failure or narrowing of the renal arteries-the resistance vessels in the kidney dilate to facilitate flow. Vasodilator prostaglandins are important.
      ( this mechanism is markedly impaired by NSAIDs ).
      If autoregulation of blood flow fails, the GFR can still be maintained by selective constriction of the post-glomerular (efferent) arteriole. This is mediated through the release of renin and generation of angiotensin II, which preferentially constricts this vessel. (ACE inhibitors interfere with this response) .
      More severe or prolonged under-perfusion of the kidneys may lead to failure of these compensatory mechanisms and hence an acute decline in GFR..
    • The renal tubules are intact and become hyperfunctional; that is, tubular reabsorption of sodium and water is increased, partly through physical factors associated with changes in blood and urine flow and partly through the influence of angiotensins, aldosterone and vasopressin.
      This leads to the formation of a low volume of urine which is concentrated (osmolality > 600 mOsm/kg) but low in sodium (< 20 mmol/l).
      These urinary changes may be absent in patients with impaired tubular function, e.g. pre-existing renal impairment, or those who have received loop diuretics
    • Clinical assessment
      Features of the underlying cause
      There may be marked hypotension and signs of poor peripheral perfusion, such as delayed capillary return.
      Pre-renal ARF may occur without systemic hypotension, particularly in patients taking NSAIDs or ACE inhibitors .
      Postural hypotension(a fall in blood pressure > 20/10 mmHg from lying to standing) is a valuable sign of early hypovolaemia.
      The cause of the reduced renal perfusion may be obvious, but concealed blood loss can occur into the gastrointestinal tract, following trauma (particularly where there are fractures of the pelvis or femur) and into the pregnant uterus.
      Large volumes of intravascular fluid are lost into tissues after crush injuries or burns, or in severe inflammatory skin diseases or sepsis.
      Metabolic acidosis and hyperkalaemiaare often present.
    • DIAGNOSIS OF PRE-RENAL ACUTE RENAL FAILURE:
      • A compatable history.( bleeding , burn , dehydration……)
      • The clinical findings.( hypotention , decrease urine output , metabolic acidosis …)
      • A progressive increase in blood urea & plasma creatinine.
      hyperkalemia.
      • Urineosmolality > 600 mOsm/kg
      Urine sodium < 20 mmol/l.
      Urine/plasma urea ratio of > 10:1
    • MANAGEMENT OF PRE-RENAL ACUTE RENAL FAILURE:
      Establish and correct the underlying cause of the ARF.
      If hypovolaemia is present, restore blood volume as rapidly as possible (with blood, plasma or isotonic saline (0.9%), depending on what has been lost).
      Monitoring of the central venous pressure or pulmonary wedge pressure as an adjunct to clinical examination may aid in determining the rate of administration of fluid.
      Critically ill patients may require invasive haemodynamic monitoring to assess cardiac output and systemic vascular resistance, and the use of inotropic drugs to restore an effective blood pressure .
      Correct metabolic acidosis.
      Restoration of blood volume will correct acidosis by restoring kidney function.
      Isotonic sodium bicarbonate (e.g. 500 ml of 1.26%) may be used.
    • PROGNOSIS OF PRE-RENAL ACUTE RENAL FAILURE
      If treatment is given sufficiently early, renal function will usually improve rapidly; in such circumstances residual renal impairment is unlikely.
      In some cases, however, treatment is ineffective and renal failure becomes established