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Acute Renal Failure

Acute Renal Failure

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Acute Renal Failure

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    1. Acute Renal Failure Benaya Rozen-Zvi Nephrology and hypertension department Rabin Medical Center

    2. Definition Acute renal failure (ARF) is defined as a precipitous and significant (>50%) decrease in glomerular filtration rate (GFR) over a period of hours to days, with an accompanying accumulation of nitrogenous wastes in the body.

    3. Frequency In the US: ARF is seen in 5% of all hospital admissions and upto 30% of patients admitted to the ICU. Prerenal causes account for about half of all cases. ATN is most common cause out of the intrinsic renal diseases.

    5. ARF vs AKI

    6. R-I-F-L-E

    7. R-I-F-L-E and Mortality

    8. Acute RF vs. Chronic RF Acute RF medical emergency Potentially treatable Prognostic factor Chronic RF Mostly irreversible Refer to nephrologists

    9. Acute RF vs. Chronic RF HISTORY Hypertension Diabetes Family hystory Nocturia, polyuria, proteinuria, hematuria Laboratory Former cratinine values Kidney size Broad waxy casts

    12. Prerenal Disease True volume depletion Advanced liver disease Congestive heart failure Renal arterial disease Renal vasoconstriction (NSAID, Hypercalcemia)

    15. Volume depletion Intravascular volume depletion Hemorrhage Sodium depletion GI urine Redistribution of ECF Third space accumulation Edematous disorders

    16. Liver disease sodium retention, initially manifested as ascites a progressive decline in GFR. Both humoral and hemodynamic factors play a primary role in the development of these problems.

    17. Liver disease sodium retention, initially manifested as ascites a progressive decline in GFR. Both humoral and hemodynamic factors play a primary role in the development of these problems.

    20. CHF Sodium retention early in the course of the disease and a decline in GFR as cardiac function worsens. Neurohumeroral factors and certain therapies may contribute to these problems.

    21. Renal artery stenosis

    22. Renal artery stenosis Bilateral or single functioning kidney Mostly atherosclerotic May Be precipitated by ACE-I or ARB. US Doppler is good screening CT angiography and MRA are limited by the need to give IV contrast.

    25. Prerenal Disease Renal hypoperfusion Decreased RBF and GFR Increased filtration fraction (GFR/RBF) Increased Na and H2O reabsorption Oliguria, high Uosm, low UNa Elevated BUN/Cr ratio Elevated uric acid Low FeNa

    27. FeNa Calculation of fractional excretion of sodium (FeNa) FeNa = (urine Na/plasma Na)/(urine creatinine/plasma creatinine) FeNa <1 % = prerenal ARF FeNa >1% = ATN

    28. Confounding diagnostic variable

    29. Postrenal ARF Ureteral obstruction Retroperitoneal tumor retroperitoneal fibrosis urolithiasis papillary necrosis Urethral obstruction Benign prostatic hypertrophy prostate, cervical, bladder, colorectal carcinoma bladder hematoma bladder stone obstructed catheter neurogenic bladder stricture

    30. Postrenal ARF

    31. Hydronephrosis pitfalls Early ( less then 24 hours) Volume depletion Pelvic scaring Inexperienced operator

    32. Postrenal ARF Urinary obstruction need to be treated rapidly. Renal damage within days Complete loss of kidney within two to three month In case of UTI high risk of septic shock and irreversible renal damage

    33. Intrinsic renal disease

    34. Acute tubular necrosis

    35. Pathophysiology ATN usually occurs after an acute ischemic or toxic event, and it has a well-defined sequence of events. Initiation phase characterized by acute decrease in GFR to very low levels, with a sudden increase in serum Cr and BUN concentrations. Maintenance phase is characterized by sustained severe reduction in GFR and the BUN and Cr continue to rise. Recovery phase, in which the tubular function is restored, is characterized by an increase in urine volume (if oliguria was present) and gradual decrease in Cr and BUN to their pre-injury level.

    37. Ischemic ATN Ischemic ATN is often described as a continuum of prerenal azotemia. Response to fluid repletion can help distinguish between the two. Hypoperfusion initiates cell injury and cell death. mostly in S3 portion of the proximal tubules and thick ascending limb of loop of Henle.

    38. Causes of Ischemic ATN It may be considered part of the spectrum of prerenal azotemia and they have the same causes and risk factors Hypovolumic states hemorrhage, volume depletion from GI or renal losses, burns, fluid sequestration. Low cardiac output states CHF and other diseases of the myocardium, valvulopathy, arrhythmia, pericardial diseases, tamponade.

    39. Causes of Ischemic ATN Systemic vasodilation sepsis, anaphylaxis DIC Renal vasoconstriction cyclosporine, norepinephrine, epinephrine, amphotericin B, etc Hyperviscosity syndrome Impaired renal autoregulatory responses cyclooxygenase inhibitors

    40. Nephrotoxic ATN Most of the pathophysiological features of ischemic ATN are shared by the nephrotoxic forms and it has the same three phases. Nephrotoxic injury to tubular cells occurs by multiple mechanisms including direct toxicity, intrarenal vasoconstriction, and intratubular obstruction.

    41. Exogenous toxins Aminoglycosides: 10-30% of patients getting aminoglycosides develop ATN. Risk factors include preexisting liver disease, renal disease, concomitant use of other nephrotoxins, advanced age, shock, female sex and a higher level 1 hr after the dose. Toxicity presumably more common with 3 doses/day than a single daily dose (as the drug uptake by tubules is saturable phenomenon). Amphotericin B: The likelihood of toxicity is in direct proportion to the total dose administered and is more common if > 3 grams is administered.

    42. Exogenous Toxins Radiocontrast media: Iodinated contrast media causes vasoconstriction as well as a direct toxic effects on tubular cells. Patients at increased risk include diabetes, baseline renal insufficiency, large contrast load, history of HTN, older age and presence of proteinuria. Cyclosporine and tacrolimus: Can cause ARF as well as chronic interstitial nephritis. Sulfa drugs, acyclovir and indinavir cause ARF by tubular obstruction due to crystal formation in the tubular lumen Others: Cisplatin, methotrexate and foscarnet, etc.

    43. Prevention Radiocontrast dye: Out of all the agents/modalities that have been investigated for prevention of CIN, only the following have been shown to be of some benefit: 1.Hydration with isotonic saline infusion. Typically, isotonic sodium chloride solution (0.9%) administered at a rate of 100 mL/h 12 hours before and 12 hours after the administration of the dye load is most effective, especially in the setting of prior renal insufficiency and diabetes mellitus.

    44. Prevention 2. Low osmolal and iso-osmolal nonionic contrast media are also associated with lower incidence of CIN. 3. N-acetylcysteine has been used with success in high-risk patients to prevent contrast-induced nephrotoxicity. 4. Using lower doses of contrast media, avoiding volume depletion and NSAIDs, both of which can cause renal vasoconstriction are some other useful measures.

    45. Endogenous Toxins Crystals: Acute crystal-induced nephropathy is encountered in conditions where crystals are produced endogenously due to high cellular turnover (i.e. uric acid, calcium phosphate), as seen in certain malignancies or the treatment of these malignancies (tumor lysis syndrome). However, this condition is also associated with ingestion of certain toxic substances, such as ethylene glycol. Multiple myeloma: This condition causes renal failure by several mechanisms, such as prerenal azotemia due to volume contraction, cast nephropathy due to increased light chain proteins precipitated into the tubular lumen, hypercalcemia and uric acid nephropathy.

    48. Acute Interstitial nephritis Significant cause of acute renal failure series of 109 patients from a large center biopsied for unexplained renal impairment with normal sized kidneys AIN accounted for 29 of 109 (27%) cases

    51. Acute Interstitial nephritis A review of three series that totaled 128 pts (71%) Drugs, with antibiotics responsible for 1/3 (15%) Infection-related (8%) Idiopathic (5%) Tubulointerstitial nephritis and uveitis (TINU) syndrome (1%) Sarcoidosis

    52. Clinical Course Most of the time 7-14 days from exposure May be accompanied by fever, rush and eosinophilia Leukocituria without hematuria.

    54. Diagnostic Studies CBC Urinalysis w/microscopy Hansel stain Urine electrolytes (FeNa usually >1%) Renal ultrasound Gallium scan Gold standard is renal biopsy

    55. Urine Sediment

    56. Treatment Discontinue offending agent!! Most cases improve spontaneously Prednisone (1mg/kg/day) for minimum of 1-2 weeks followed by slow taper for total of 4-6 weeks Solumedrol 0.5-1g/day for three days if more severe ARF

    57. Glomerulonephritis Vasculitis (ANCA associated, anti GBM, cryogloblinemic) Post infectious SLE HSP

    58. Cholesterol emboli

    59. Cholesterol emboli Affect patient with wide spread atherosclerotic disease Renal failure develops several days after intra-arterial manipulation. May be spontaneous or related to anticoagulation. May be associated with fever, weight loss, eosinophilia and livido reticularis

    62. Typical HUS (neuraminidase, T antigen exposure)(neuraminidase, T antigen exposure)

    63. Typical HUS 2/4 children never recovered GFR after HUS 2/4 evolved from recovery with proteinuria 2/4 children never recovered GFR after HUS 2/4 evolved from recovery with proteinuria

    65. A Classification of TMA (Thrombotic Microangiopathy) ADAMSTS13: due to intrinsic deficiency or development of autoantibodies against ADAMSTS13; low ADAMSTS13 leads to failure to cleave large vWF multimers, which leads to unmitigated platelet-multimer binding to the endothelium and a microvascular occlusion. Quinine due to development of drug-induced antibodies against platelets and other hematological cell lines as well as against endothelium; Patients with cobalamin-C deficiency usually present in the early days and months of life with failure to thrive, poor feeding, and vomiting. Rapid deterioration occurs due to metabolic acidosis, gastrointestinal bleeding, hemolytic anemia, thrombocytopenia, severe respiratory and hepatic failure, and renal insufficiency. It is likely that some die undiagnosed. Besides the early fulminant course, a more protracted disease can manifest later in childhood and adolescence. Renal biopsy showed a chronic TMA. Serum homocysteine can be 10 times normal values and urinary methylmalonic acid markedly increased but correct with daily hydroxycobalamin administration ADAMSTS13: due to intrinsic deficiency or development of autoantibodies against ADAMSTS13; low ADAMSTS13 leads to failure to cleave large vWF multimers, which leads to unmitigated platelet-multimer binding to the endothelium and a microvascular occlusion. Quinine due to development of drug-induced antibodies against platelets and other hematological cell lines as well as against endothelium; Patients with cobalamin-C deficiency usually present in the early days and months of life with failure to thrive, poor feeding, and vomiting. Rapid deterioration occurs due to metabolic acidosis, gastrointestinal bleeding, hemolytic anemia, thrombocytopenia, severe respiratory and hepatic failure, and renal insufficiency. It is likely that some die undiagnosed. Besides the early fulminant course, a more protracted disease can manifest later in childhood and adolescence. Renal biopsy showed a chronic TMA. Serum homocysteine can be 10 times normal values and urinary methylmalonic acid markedly increased but correct with daily hydroxycobalamin administration

    66. Complement and Atypical HUS

    69. Plasma Therapy

    70. Diagnosis

    71. Urine output

    72. Urinalysis

    73. Red Blood Cell Cast Two examples of red blood cell casts, typical of glomerular bleeding.Two examples of red blood cell casts, typical of glomerular bleeding.

    74. Dysmorphic Red Blood Cells Dysmorphic red blood cells are best viewed under phase-contrast microscopy (as in this example). Note the blebs and punched-out centers (arrows).Dysmorphic red blood cells are best viewed under phase-contrast microscopy (as in this example). Note the blebs and punched-out centers (arrows).

    75. White Blood Cell Cast Note the clear cell outlines and granular cytoplasm.Note the clear cell outlines and granular cytoplasm.

    76. Renal Tubular Epithelial Cell Cast

    77. Pigmented Granular Casts Pigmented granular (muddy brown) casts are characteristic of acute tubular necrosis. Although the exact pathogenesis of cast formation is not known, the major component is Tamm-Horsfall glycoprotein, a strongly anionic macromolecule secreted by the ascending thick limb of Henle. Hyaline and waxy casts are also prominent in this particular urinary sediment.Pigmented granular (muddy brown) casts are characteristic of acute tubular necrosis. Although the exact pathogenesis of cast formation is not known, the major component is Tamm-Horsfall glycoprotein, a strongly anionic macromolecule secreted by the ascending thick limb of Henle. Hyaline and waxy casts are also prominent in this particular urinary sediment.

    78. Urinalysis

    79. Complete blood count

    80. Urine indices

    81. Acute Renal Failure Urinary Indices As discussed, the main differential in the oliguric patient with acute renal failure is between pre-renal azotemia (PR) and acute tubular necrosis (ATN). Although a careful history and physical examination coupled with a careful urinalysis will often distinguish between these two conditions, the use of urinary electrolytes provides further information. The basis of the urinary electrolytes is the different tubular responses to salt and water conservation. Tubular function with pre-renal azotemia is normal allowing maximum tubular sodium and water reabsorption resulting in a concentrated urine that is low in sodium. In acute tubular necrosis, tubular dysfunction leads to sodium wasting and an inability to concentrate the urine. The ratio of urine to plasma creatinine concentrations (U/P)Cr has also been proposed as a discriminating marker. In pre-renal ARF, UCr is high due to water reabsorption without Cr reabsorption and PCr is usually only mildly increased resulting in a high (U/P)Cr ratio. In ATN, the UCr is lower due to an inbility to concentrate the urine and the PCr is increased in prpoprtion to the degree of renal failure so the U/P cr is generally lower than that seen in pre-renal azotemia. Unfortunately, as shown in the slide, there is considerable overlap (grey zone) in all these indices. The so-called renal failure index [RFI = UNa/(U/P)Cr] and the more commonly employed fractional excretion of Na [FENa= 100(UNa X PCr) / (PNa X UCr)], which combine different single indices, provide better discrimination. Recent data have demonstrated that the fractional excretion of sodium (FENa) , which expresses the fraction of filtered sodium that escapes reabsorption and eventually appears in the urine, is a more discriminating test to distinguish between pre-renal azotemia and oliguric ATN. FENa > 1 % strongly suggests ATN while FENa < 1 % suggests pre-renal azotemia. However, the FENa is not infallible, and there are a number of exceptions where pre-renal azotemia can be associated with FENa values greater than 1 % - e.g., recent diuretic use or pre-renal azotemia superimposed on chronic renal insufficiency. In a similar manner, many instances of ATN will have FENa < 1 % - e.g., early phase of contrast-induced ATN, rhabdomyolysis or septic ATN. Thus, the clinician should utilize the FENa in conjunction with the overall clinical picture and other lab tests and should not be wedded to a particular FENa result when other data suggest a different cause for ARF. As discussed, the main differential in the oliguric patient with acute renal failure is between pre-renal azotemia (PR) and acute tubular necrosis (ATN). Although a careful history and physical examination coupled with a careful urinalysis will often distinguish between these two conditions, the use of urinary electrolytes provides further information. The basis of the urinary electrolytes is the different tubular responses to salt and water conservation. Tubular function with pre-renal azotemia is normal allowing maximum tubular sodium and water reabsorption resulting in a concentrated urine that is low in sodium. In acute tubular necrosis, tubular dysfunction leads to sodium wasting and an inability to concentrate the urine. The ratio of urine to plasma creatinine concentrations (U/P)Cr has also been proposed as a discriminating marker. In pre-renal ARF, UCr is high due to water reabsorption without Cr reabsorption and PCr is usually only mildly increased resulting in a high (U/P)Cr ratio. In ATN, the UCr is lower due to an inbility to concentrate the urine and the PCr is increased in prpoprtion to the degree of renal failure so the U/P cr is generally lower than that seen in pre-renal azotemia. Unfortunately, as shown in the slide, there is considerable overlap (grey zone) in all these indices. The so-called renal failure index [RFI = UNa/(U/P)Cr] and the more commonly employed fractional excretion of Na [FENa= 100(UNa X PCr) / (PNa X UCr)], which combine different single indices, provide better discrimination. Recent data have demonstrated that the fractional excretion of sodium (FENa) , which expresses the fraction of filtered sodium that escapes reabsorption and eventually appears in the urine, is a more discriminating test to distinguish between pre-renal azotemia and oliguric ATN. FENa > 1 % strongly suggests ATN while FENa < 1 % suggests pre-renal azotemia. However, the FENa is not infallible, and there are a number of exceptions where pre-renal azotemia can be associated with FENa values greater than 1 % - e.g., recent diuretic use or pre-renal azotemia superimposed on chronic renal insufficiency. In a similar manner, many instances of ATN will have FENa < 1 % - e.g., early phase of contrast-induced ATN, rhabdomyolysis or septic ATN. Thus, the clinician should utilize the FENa in conjunction with the overall clinical picture and other lab tests and should not be wedded to a particular FENa result when other data suggest a different cause for ARF.

    82. Treatment Duretics Fluids Dialysys Mode Intensity Timing

    83. Thank you