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Acute Renal Failure PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Acute Renal Failure” by Syed Rizwan, MD.

This medical PowerPoint presentation is about acute renal failure, also known as acute kidney injury (AKI). Acute renal failure is a sudden loss of kidney function that occurs over a period of hours to days. This condition is characterized by a rapid increase in serum creatinine levels and a decrease in urine output.

There are several causes of acute renal failure, including decreased blood flow to the kidneys, direct damage to the kidneys, and obstruction of urine flow. Common causes include dehydration, sepsis, medication toxicity, and kidney stones.

Symptoms of acute renal failure may include decreased urine output, swelling in the legs and ankles, fatigue, nausea, confusion, and shortness of breath. Diagnosis is typically made through blood and urine tests, as well as imaging studies such as an ultrasound or CT scan.

Treatment for acute renal failure depends on the underlying cause and may include addressing any underlying medical conditions, stopping any medications that may be contributing to the problem, and providing supportive care such as intravenous fluids and electrolyte replacement. In severe cases, dialysis may be necessary to help remove waste products from the body.

It is important to seek prompt medical attention if you experience symptoms of acute renal failure, as early diagnosis and treatment can help prevent long-term complications and improve outcomes.

Tags : Acute Renal Failure, acute kidney injury, loss of kidney function, Nephrology, Nephrology PowerPoint presentation

Published on : Jun 07, 2023 | Views : 845 | Downloads : 2

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Slide 1-

1 Acute Renal Failure Syed Rizwan, MD
Slide 2-

2 Acute Renal Failure Comprises a family of syndromes Abrupt decrease in GFR(over hours to days)
Slide 3-

3 MANIFFESTATIONS of ARF Increase in BUN Increase in creatinine Oligouria(< 400 –500 cc)
Slide 4-

4 DEFINITION No consensus Multiple Relative rise in Serum Creatinine > 0.5mg/dl if baseline creatinine is normal > 1 mg/dl if baseline serum creatinine is high
Slide 5-

5 Creatinine and GFR Creatinine produced in muscles Creatinine excretion depends on, Glomerular filtration Proximal tubular excretion Change in Serum Creatinine with no change in GFR Muscle wasting or amputation lowers creatinine Medications(Trimethoprim, Cimetidine) increase creatinine by deceasing tubular excretion
Slide 6-

6 Blood Urea and GFR Increase BUN with no change in GFR GI Bleed Hyper catabolic states Protein loading Glucocorticoids Tetracycline Decrease BUN with no change in GFR Protein Malnutrition Severe Liver disease
Slide 7-

7 ARF and Biomarker Lack of sensitivity of BUN and creatinine Need for Biomarkers Kidney Injury Molecules-1(KIM-1) increased in Patients with Acute Tubular Necrosis None available for cliniical utility yet
Slide 8-

8 Epidemiology of ARF Incidence, etiology and outcome varied depending on Population studied and Definition used Mostly in-Patient than out –Patient 5-7% of hospital admissions Mortality varies between 20%-85% depending on cause
Slide 9-

9 ARF Classification Prerenal Renal Postrenal
Slide 10-

10 Prerenal ARF Hemodynamically mediated reduction in GFR in absence on Renal Parenchymal injury. ARF resolves if hemodynamic insult is reversed If hemodynamic insult is sustained, can result in overt renal injury
Slide 11-

11 Renal ARF Renal Parenchymal injury
Slide 12-

12 Postrenal ARF Acute obstruction to the Urinary Tract
Slide 13-

13 Prerenal Azotemia Decreased Glomerular perfusion(no renal injury) True Volume Depletion e.g. Diarrhea Effective Volume Depletion, cirrhosis Altered Intrarenal Hemodynamics e.g. ACEI Affenet dilatation Efferent vasoconstriction
Slide 14-

14 Prerenal Azotemia True or Effective Volume depletion, Neurohumoral vasoconstrictor Increased catecholamine Renin-angiotensin system activation Increased vasopressin release
Slide 15-

15 Renal Autoregulation Maintains Glomerular Blood Flow and thus GFR Afferent Vasodialtaion, Prostaglandins Kallikrein-kinin Myogenic influence Nitiric oxide Efferent vasoconstriction Angiotension 11
Slide 16-

16 Prerenal Azotemia Prerenal ARF presents with Oligouria Low Urine Na from Na retention Increased BUN :creatinine ratio >20:1 FENa < 1% Existing Renal Insufficiency or Diuretic can alter this picture
Slide 17-

17 ARF and ACEI &ARB ACEI & ARB have greatest benefits in Patients with high risk of ARF Old age Diabetics Cardiomyopathy CHF with higher dose oh Diuretic Renal Vascular disease Chronic Kidney disease
Slide 18-

18 Prerenal ARF with ACEI &ARB Efferent Vasodilatation deceases GFRmedications Lower GFR raises serum creatinie but usually less than 30% Must monitor serum creatinine and electrolytes before and after starting or changing dose of these medications Stop if ARF Correct volume status W/u for renal Artery Stenosios Can reintroduce cautiously if reversible factors corrected
Slide 19-

19 Prerenal ARF & NSAIDs Both COX1/Cox!! Inhibitors cause lower Prostaglandins synthesis Impairs Afferent vasodilatation decrease Glomerular perfusion Effect greatest in high risk population CHF Cirrhosis CKD Vascular disease elderly
Slide 20-

20 Abdominal Compartment Syndrome Unusual cause of ARF Associated with increased intra-abdominal pressure Manifestations, Respiratory compromise Decreased cardiac output Intestinal ischemia Hepatic Dysfunction Oliguric ARF Increased renal venous pressure Recovery with decreased intraabdominal pressure
Slide 21-

21 Post-Renal ARF Obstruction – complete or Partial Anuria or variable urine output Recovery depends on duration of obstruction Conditions Sonogram may not show obstruction, Retroperitoneal fibrosis Tumors Adenopathy Encasing ureter prevent dilatation
Slide 22-

22 ARF- Renal Useful to categorize according to Anatomical injury. Primary sites, Glomerulus- Acute Glomerulonephritis Tubules- Acute Tubular Necrosis Interstitium- Acute Interstial Nephritis Vascular- Atheroembolism ATN- most common U/A-Protein, RBC,Casts,pigments
Slide 23-

23 Acute Tubular Necrosis Ischemic vs Nephrotoxic Most frequently multi-factorial Medical vs Surgical Ischemic- Hypotension,shock Nephrotoxic- Dye induced, Rhabdomyolysis
Slide 24-

24 Acute Tubular Necrosis Initiation, maintenance, recovery Phases Mortality from very low to very high Potentially Preventable Long –term outcome in survivors very good
Slide 25-

25 ATN- Specific Syndromes Radiocontrast Nephropathy Rhabdomyolysis Aminoglycoside Related Amphotericin B associated
Slide 26-

26 Radiocontrast Nephropathy 10% of Hospital acquired ATN Mild and Transient in Majority Risk factors, Amount of Dye(> 100cc) Volume Depletion Renal Insufficiency DM Old Age CHF ACEI or NSAIDs
Slide 27-

27 Radiocontrast Nephropathy Risks higher with higher creatinine Normal- negligible risks Mild- Moderate RI(Creatinine< 2)– 5-10% risks Mild- Moderate RI with DM- 10-40% risks Advanced Renal Disease- >50%
Slide 28-

28 Radiocontrast Nephropathy Pathogenesis incompletely understood Severe Renal vasoconstriction within seconds of contrast administration Direct Renal Tubular injury FENa < 1%
Slide 29-

29 Radiocontrast Nephropathy Independent risk factor of death Prevention in high risk Patients Consider Alternate imaging.g. MRI Volume repletion with Saline Minimize amount of Dye Low Osmolality contrast media? N-Acetylcysteine(Mucomyst)? Fenoldopam-Selective Dopamine agonist? Lasix, Mannitol, Dopamine –not helpful, may be risky Prophylactic Hemodialysis- not helpful
Slide 30-

30 Radiocontrast Nephropathy N-Acetylcysteine – reducing agent, scavenge reactive oxygen species(ROS) No good large randomized trial to prove its efficacy Impact on morbidity and mortality unknown Used commonly in practice b/o potential benefits and lack of Toxicity
Slide 31-

31 Aminoglycoside Nephrotoxicity Usually after 7-10 days Depends on dose and frequency Direct Proximal Tubular injury Once a day dosing may be less Nephrotoxic K. Ca. MG wasting Risk factors- age, Renal insufficiency, Dose,Volume depletion
Slide 32-

32 ARF from Rhabdomyolysis Muscle injury leading to ARF Most cases subclinical Myoglobinuria cause, Renal vasoconstriction Proximal tubular damage Intratubular cast (Obstruction) Hypovolemia(Third Spacing) Metabolic Acidosis, Electrolyte Imbalance(K,Ca,P)
Slide 33-

33 ARF from Rhabdomyolysis Subclinical causes more common Drugs PVD Seizure FENa < 1% U/A- Heme/+vie but no RBC Aggressive Volume replacement Urinary Alkalization?, Mannitol?
Slide 34-

34 Amphotericin B Nephrotoxiciy Very high incidence of ARF Binds to sterol in cell membrane Multiple sites in Nephrons Distal Tubular Acidosis Mg and K wasting Dose dependent Liposomal Amphotercin formulation less toxic Saline loading helpful
Slide 35-

35 Postoperative ARF ARF after vascular,cardiac and major abdominal surgery. Very high mortality Multifactorial 1-5% after CABG. Risk factors, Renal disease, cardiogenic shock,emergent surgery, Left main disease etc,
Slide 36-

36 Acute Interstitial Nephritis Classical triad(fever rash & eosinophilia) not usually seen Mostly Drug related e.g. Cipro Infection : Strept., Staph, CMV, EB virus, Hantaan virus etc Systemic Diseases : SLE, Sarcoidosis. Eosinophiluria may be absent Dx by renal Biopsy. Rx supportive, Hold Drug, Steroids ?
Slide 37-

37 Atheroembolic ARF Require high degree of suspicion Cholesterol emboli Renal failure – acute or subacute Multisystem disorder Lived reticularis Digital Ischemia(Blue Toe Syndrome) GI bleed, TIA, Rahbdomyolysis
Slide 38-

38 Atheroembolic ARF ARF after vascular procedure ARF can be abrupt needing dialysis within few days. Can be subacute occurring in staggered steps separated by stable renal function. Patients on Anticoagulants are at high risk Eosinphilia, eosinphiluria, low complement. High mortality
Slide 39-

39 Hepatorenal Syndrome Profound renal vasoconstriction Resemble Pre-renal Azotemia Volume Expansion fail to improve renal function. Pathogenesis incompletely understood Oligiuric ARF, FENa low Diagnosis of exclusion
Slide 40-

40 Hepatorenal Syndrome Two Types Type 1 HRS: rapid ARF, hospitalized Pt.,>90% mortality Type 11 HRS : insidious onset, slow progression of RI, refractory ascites, better prognosis. ATN vs HRS Low FENa I n ATN casts in Bilirubinemia with HRS
Slide 41-

41 Hepatorenal Syndrome Rx difficult Volume expansion with Albumin Terlipressin(vasopressin analogue) Midodrine (selective alpha 1 adrenergic agonist)+ octreotide(a somstoastatin analogue) TIPS, Liver Transplantation Dialysis in selective Patients
Slide 42-

42 ARF in HIV/AIDS Prerenal Azotemia Renal salt wasting from Adrenal Insufficiency. HIV Nephropathy High risk for ATN Drug side effects e.g. Pentamidine.Crystal nephropathy(indinavir) TTP(prognosis worse ) Rhabomyolysis
Slide 43-

43 ARF from RPGN Less common Rapidly Progressive Glomerulonephritis include vasculitis, SLE, Wagner's Active Urinary sediments(RBC cast diagnostic) Higher degree of Proteinuria Serology helpful(ANCA, ANA,IgMantibodyetc0 Renal Biopsy usually required. Early diagnosis essential to prevent ESRD Rx with Steroids and Cytoxan
Slide 44-

44 Rx of ARF No proven Drugs Many cause preventable Volume expansion Withdrawal of Drugs Diuretics help in management but not curative Dopamine potentially harmful
Slide 45-

45 RRT in ARF Renal Replacement Therapy usually the only option in severe ARF. Indication of RRT HYPERKALEMIA METABOLIC Acidosis Uremic Symptoms Fluid Load “Prophylactic” RRT Intermittent Hemodialysis CVVHD Extended Daily Dialysis(6-12h) Peritoneal Dialysis- not favored
Slide 46-

46 CVVHD vs Hemodialysis HD – more stable Pt, SBP >90, no heparin, allows larger amount of fluid removal in3-4 hours CVVHD Unstable Pt., low BP with high dose Pressers, allows gradual removal of fluids 24h EDD Allows no heparin dialysis, gradual removal of fluids, but expensive b/o Nursing Support
Slide 47-

47 RRT- how to improve outcome? Lot of Questions to answer Frequency of Dialysis Quantification of Dialysis Type of Membrane of Dialysis Synthetic vs. Cellulose Does Erythropoietin improves outcome? Faster fluid removal vs. slow fluid removal?