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AZOTEMIA Dr.Vajehallah Raeesi Assistant Professor Department of Internal Medicine Birjand University of Medical Sciences DR.VAJEHALLAH RAEESI.

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Presentation on theme: "AZOTEMIA Dr.Vajehallah Raeesi Assistant Professor Department of Internal Medicine Birjand University of Medical Sciences DR.VAJEHALLAH RAEESI."— Presentation transcript:

1 AZOTEMIA Dr.Vajehallah Raeesi Assistant Professor Department of Internal Medicine Birjand University of Medical Sciences DR.VAJEHALLAH RAEESI

2 c Normal kidney functions occur through numerous cellular processes to maintain body homeostasis The duration and severity of the disease. The combination of these findings should permit identification of one of the major nephrologic syndromes and will allow differential diagnoses to be narrowed and the appropriate diagnostic evaluation and therapeutic course to be determined DR.VAJEHALLAH RAEESI

3 Initial Clinical and Laboratory Data Base for Defining Major Syndromes in Nephrology SyndromesImportant Clues to DiagnosisFindings That Are Common Acute or rapidly progressive renal failure Anuria Oliguria Documented recent decline in GFR Hypertension, hematuria Proteinuria, pyuria Casts, edema Chronic renal failureAzotemia for >3 months Prolonged symptoms or signs of uremia Symptoms or signs of renal osteodystrophy Kidneys reduced in size bilaterally Broad casts in urinary sediment Proteinuria Casts Polyuria, nocturia Edema, hypertension Electrolyte disorders Nephrotic syndromeProteinuria >3.5 g per 1.73 m2 per 24 h Hypoalbuminemia Edema Hyperlipidemia Casts Lipiduria DR.VAJEHALLAH RAEESI

4 reduction in GFR leading to azotemia alterations of the urinary sediment and/or protein excretion  GFR is important in both the hospital and outpatient settings  GFR is the primary metric for kidney "function," and its direct measurement involves administration of a radioactive isotope (such as inulin or iothalamate) that is filtered at the glomerulus but neither reabsorbed nor secreted throughout the tubule  GFR is related directly to the urine creatinine excretion and inversely to the serum creatinine (U Cr /P Cr ). DR.VAJEHALLAH RAEESI

5  Failure to account for GFR reductions in drug dosing can lead to significant morbidity and mortality from drug toxicities (e.g., digoxin, aminoglycosides)  In patients with chronic progressive renal disease, there is an approximately linear relationship between 1/P Cr (y axis) and time (x axis).  Signs and symptoms of uremia develop at significantly different levels of serum creatinine, depending on the ntpatie (size, age, and sex), the underlying renal disease, the existence of concurrent diseases, and true GFR. DR.VAJEHALLAH RAEESI

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7  Assessment of Glomerular Filtration Rate (GFR  radioactive isotope (such as inulin or iothalamate  Serum creatinine  Urea clearance CrCl = (U vol x U Cr )/(P Cr x T min DR.VAJEHALLAH RAEESI

8  When a timed collection for creatinine clearance is not available, decisions about drug dosing must be based on serum creatinine alone. Two formulas are used widely to estimate kidney function from serum creatinine: (1) Cockcroft- Gault and (2) four-variable MDRD (Modification of Diet in Renal Disease).  Cockcroft-Gault: CrCl (mL/min) = (140 – age (years) x weight (kg) x [0.85 if female])/(72 x sCr (mg/dL)  MDRD: eGFR (mL/min per 1.73 m2) = x PCr (e–1.154) x age (e–0.203) x (0.742 if female) x (1.21 if black). DR.VAJEHALLAH RAEESI

9 can mask significant changes in GFR with small or imperceptible changes in serum creatinine concentration  The gradual loss of muscle from chronic illness,  chronic use of glucocorticoids  malnutrition DR.VAJEHALLAH RAEESI

10 Serum cystatin C has been proposed to be a more sensitive marker of early GFR decline than is plasma creatinine  however, like serum creatinine, cystatin C is influenced by age, race, and sex and additionally is associated with diabetes, smoking, and markers of inflammation DR.VAJEHALLAH RAEESI

11 Once it has been established that GFR is reduced, the physician must decide if this represents acute renal injuryor chronic  clinical situation  history  laboratory data anemia, hypocalcemia, and hyperphosphatemia  Radiographic evidence of renal osteodystrophy ; urinalysis ; and renal ultrasound DR.VAJEHALLAH RAEESI

12  Patients with advanced chronic renal insufficiency ; Proteinuria. nonconcentrated urine (isosthenuria. small kidneys on ultrasound. increased echogenicity and cortical thinningTreatment should be directed toward slowing the progression of renal disease and providing symptomatic relief for edema, acidosis, anemia, Acute renal failure; (prerenal azotemia. intrinsic renal diseases (affecting small vessels, glomeruli, or tubules), or postrenal processes (obstruction to urine flow in ureters, bladder, or urethra) DR.VAJEHALLAH RAEESI

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14 Novel Biomarkers  BUN and creatinine are functional biomarkers of glomerular filtration rather than tissue injury biomarkers and, therefore, may be suboptimal for the diagnosis of actual parenchymal kidney damage  Kidney injury molecule-1 (KIM-1) :ischemia or nephrotoxins such as cisplatin  Neutrophil gelatinase associated lipocalin (NGAL, also known as lipocalin-2 or siderocalin): 2 hours of cardiopulmonary bypass–associated AKI.  a1-Microglobulin: high levels may predict poorer outcome  Cystatin C: tubular dysfunction  Interleukin-18 (IL-18):Elevated urinary levels found to be early marker of AKI and independent predictor of mortality in critically ill patients 1 -Microglobulin DR.VAJEHALLAH RAEESI

15 Prerenal Failure  40–80% of acute renal failure  any cause of decreased circulating blood volum  reductions in cardiac output from peripheral vasodilation (sepsis, drugs)  profound renal vasoconstriction [severe heart failure, hepatorenal syndrome, drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs)  Patients on NSAIDs and/or ACE inhibitors/ARBs  Normal GFR is maintained in part by the relative resistances of the afferent and efferent renal arterioles  Atherosclerosis, hypertension, and older age can lead to hyalinosis and myointimal hyperplasia, causing structural narrowing of the intrarenal arterioles and impaired capacity for renal afferent vasodilation DR.VAJEHALLAH RAEESI

16 IndexPrerenal AzotemiaOliguric Acute Renal Failure BUN/P Cr ratio >20:110-15:1 Urine sodium (U Na ), meq/L <20>40 Urine osmolality, mosmol/L H 2 O >500<350 Fractional excretion of sodium <1%>2% Urine/plasma creatinine (U Cr /P Cr ) >40<20 DR.VAJEHALLAH RAEESI

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18 Postrenal Azotemia  <5% of cases of acute renal failure  urethra or bladder outlet, bilateral ureteral obstruction, or unilateral obstruction in a patient with a single functioning kidney  diagnosed by renal ultrasound  False-positive : diuresis, renal cysts, extrarenal pelvis  False-negative :obstruction is less than 48 hours in duration or associated with volume contraction, staghorn calculi, retroperitoneal fibrosis, or infiltrative renal diseases  Unilateral obstruction may cause AKI in the setting of significant underlying CKD or in rare cases from reflex vasospasm of the contralateral kidney. DR.VAJEHALLAH RAEESI

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21 Intrinsic Renal Disease  prerenal and postrenal azotemia have been excluded  large renal vessels, intrarenal microvasculature and glomeruli, or the tubulointerstitium  Ischemic and toxic ATN account for 90% of cases of acute intrinsic renal failure  Ischemic ATN : major surgery, trauma, severe hypovolemia, overwhelming sepsis, or extensive burns.  Processes that involve the tubules and interstitium : drug (especially antibiotics, NSAIDs, and diuretics), severe infections (both bacterial and viral), systemic diseases (e.g., systemic lupus erythematosus), and infiltrative disorders (e.g., sarcoid, lymphoma, or leukemia).  Occlusion of large renal vessels including arteries and veins is an uncommon cause of acute renal failure  Diseases of the glomeruli (glomerulonephritis and vasculitis) and the renal microvasculature (hemolytic-uremic syndromes, thrombotic thrombocytopenic purpura, and malignanthypertension DR.VAJEHALLAH RAEESI

22 Nephrotoxin-Associated Aki  All structures of the kidney are vulnerable to toxic injury, including the tubules, interstitium, vasculature, and collecting system  risk factors for nephrotoxicity include older age, chronic kidney disease (CKD), and prerenal azotemia.  Contrast Agents: rise in SCr beginning 24–48 hours following exposure, peaking within 3–5 days, and resolving within 1 week  Antibiotics:AKI typically manifests after 5–7 days of therapy  Chemotherapeutic Agents:Cisplatin and carboplatin -Ifosfamide may cause hemorrhagic cystitis - mitomycin C and gemcitabine  Toxic Ingestions:Ethylene glycol-Melamine-Aristolochic acid  Endogenous Toxins: myoglobin, hemoglobin, uric acid, and myeloma light chains DR.VAJEHALLAH RAEESI

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24 Diagnostic Evaluation  AKI is currently defined by a rise of at least 0.3 mg/dL or 50% higher than baseline within a 24–48-hours period  or a reduction in urine output to 0.5 mL/kg per hour for longer than 6 hours  History and Physical Examination  Urine Findings  Blood Laboratory Findings DR.VAJEHALLAH RAEESI

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26 Oliguria and Anuria  Oliguria refers to a 24-h urine output <400 mL  anuria is the complete absence of urine formation (<100 mL) . Anuria can be caused by total urinary tract obstruction, total renal artery or vein occlusion, and shock.  Cortical necrosis, ATN, and rapidly progressive glomerulonephritis occasionally cause anuria.  Oliguria can accompany any cause of acute renal failure and carries a more serious prognosis for renal recovery in all conditions except prerenal azotemia. DR.VAJEHALLAH RAEESI

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28 Proteinuria  The dipstick measurement detects only albumin and gives false-positive results when pH >7.0 and the urine is very concentrated or contaminated with blood  proteinuria that is not predominantly albumin will be missed by dipstick screening.  healthy individuals excrete <150 mg/d of total protein and <30 mg/d of albumin. However, even at albuminuria levels <30 mg/d, risk for progression to overt nephropathy or subsequent cardiovascular disease is increased  When the total daily excretion of protein is >3.5 g, hypoalbuminemia, hyperlipidemia, and edema (nephrotic syndrome  A hypercoagulable state may arise from urinary losses of antithrombin III, reduced serum levels of proteins S and C, hyperfibrinogenemia, and enhanced platelet aggregation DR.VAJEHALLAH RAEESI

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30 Hematuria  Isolated hematuria without proteinuria, other cells, or casts is often indicative of bleeding from the urinary tract  Hematuria is defined as two to five RBCs per high-power field (HPF) and can be detected by dipstick.  A false-positive dipstick for hematuria (where no RBCs are seen on urine microscopy) may occur when myoglobinuria is present, often in the setting of rhabdomyolysis  Common causes of isolated hematuria include stones, neoplasms, tuberculosis, trauma, and prostatitis. Gross hematuria with blood clots is usually not an intrinsic renal process; rather, it suggests a postrenal source in the urinary collecting system  A single urinalysis with hematuria is common and can result from menstruation, viral illness, allergy, exercise, or mild trauma  Persistent or significant hematuria (>3 RBCs/HPF on three urinalyses, a single urinalysis with >100 RBCs, or gross hematuria) is associated with significant renal or urologic lesions in 9.1% of cases DR.VAJEHALLAH RAEESI

31  Even patients who are chronically anticoagulated should be investigated  The suspicion for urogenital neoplasms in patients with isolated painless hematuria and nondysmorphic RBCs increases with age  Hematuria with pyuria and bacteriuria is typical of infection  Hypercalciuria and hyperuricosuria are also risk factors for unexplained isolated hematuria  The RBCs of glomerular origin are often dysmorphic  The most common etiologies of isolated glomerular hematuria are IgA nephropathy, hereditary nephritis, and thin basement membrane  Hematuria with dysmorphic RBCs, RBC casts, and protein excretion >500 mg/d is virtually diagnostic of glomerulonephritis. Even in the absence of azotemia, these patients should undergo serologic evaluation and renal biopsy DR.VAJEHALLAH RAEESI

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33  Hyperkalemia  a. Restriction of dietary potassium intake  b. Discontinuation of potassium-sparing diuretics, ACE inhibitors, ARBs, NSAIDs  c. Loop diuretics to promote urinary potassium loss  d. Potassium binding ion-exchange resin (sodium polystyrene sulfonate)  e. Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote entry of potassium intracellularly  f. Inhaled beta-agonist therapy to promote entry of potassium intracellularly  g. Calcium gluconate or calcium chloride (1 g) to stabilize the myocardium DR.VAJEHALLAH RAEESI

34  Metabolic acidosis  a. Sodium bicarbonate (if pH 15 mmol/L)  b. Administration of other bases e.g., THAM  c. Renal replacement therapy . Nephrotoxin-specific  a. Rhabdomyolysis: consider forced alkaline diuresis  b. Tumor lysis syndrome: allopurinol or rasburicase DR.VAJEHALLAH RAEESI

35 Cirrhosis and Hepatorenal Syndrome  Albumin may prevent AKI in those treated with antibiotics for spontaneous bacterial peritonitis.  The definitive treatment of the hepatorenal syndrome is orthotopic liver transplantation  Bridge therapies that have shown promise include terlipressin (a vasopressin analog), combination therapy with octreotide (a somatostatin analog) and midodrine (an 1-adrenergic agonist), and norepinephrine, all in combination with intravenous albumin (25–50 mg per day, maximum 100 g/d). DR.VAJEHALLAH RAEESI

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41 Classification of Chronic Kidney Disease (CKD STAGE GFR, mL/min per 1.73 m >90 a 90 b 60–89 30–59 15–29 <15 DR.VAJEHALLAH RAEESI

42 خسته نباشید DR.VAJEHALLAH RAEESI


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