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Premium member Presentation Transcript Slide 1: 1Slide 2: It is a medical condition in which the kidneys fail to adequately filter toxins and waste products from the blood. 2Slide 3: The two forms are acute ( acute kidney injury ) and chronic ( chronic kidney disease ); a number of other diseases or health problems may cause either form of renal failure to occur. 3Slide 4: Glomerular Filtration Rate (GFR): = the volume of water filtered from the plasma per unit of time. Gives a rough measure of the number of functioning nephrons Normal GFR: Men: 130 mL/min./1.73m2 Women: 120 mL/min./1.73m2 Cannot be measured directly, so we use creatinine and creatinine clearance to estimate. 4Slide 5: Creatinine: A naturally occurring amino acid, predominately found in skeletal muscle Freely filtered in the glomerulus, excreted by the kidney and readily measured in the plasma As plasma creatinine increases, the GFR exponentially decreases. Limitations to estimate GFR: Patients with decrease in muscle mass, liver disease, malnutrition, advanced age, may have low/normal creatinine despite underlying kidney disease 15-20% of creatinine in the bloodstream is not filtered in glomerulus, but secreted by renal tubules (giving overestimation of GFR) Medications may artificially elevate creatinine: Trimethroprim (Bactrim) Cimetidine 5Slide 6: Creatinine Clearance: Best way to estimate GFR GFR = (creatinine clearance) x (body surface area in m 2 /1.73) Ways to measure: 24-hour urine creatinine: Creatinine clearance = (Ucr x Uvol)/ plasma Cr Cockcroft-Gault Equation: (140 - age) x lean body weight [kg] CrCl (mL/min) = ——————————————— x 0.85 if Cr [mg/dL] x 72 female Limitations: Based on white men with non-diabetes kidney disease Modification of Diet in Renal Disease (MDRD) Equation: GFR (mL/min./1.73m2) = 186 X (SCr) - 1.154 X (Age) - 0.203 X (0.742 if female) X (1.210 if African-American ) ( when >60mL/min/1.73m 2 CKD should not be diagnosed unless other evidence of renal damage (e.g., proteinuria) is present ). 6Slide 7: 1-Prerenal Diseases. 2-Vascular Diseases. 3-Glomerular Diseases. 4-Interstitial/Tubular Diseases. 5-Obstructive Uropathy. 7Slide 8: Reduced renal perfusion due to volume depletion and/or decreased perfusion Caused by: Volume loss (bleeding, Dehydration). Heart failure. Hypotension including Shock. Liver Diseases. Abdominal compartment syndrome. ( IAP > 20 mmHg ) Loss of auto regulation ( NSAIDs, RAAS Blocker ). 8Slide 9: Acute: Vasculitis – Wegener’s granulomatosis. Thromboembolic disease. TTP/HUS ( thrombotic micro angiopathy ). Malignant hypertension. Scleroderma renal crisis. Chronic: Benign hypertensive nephrosclerosis Intimal thickening and luminal narrowing of the large and small renal arteries and the glomerular arterioles usually due to hypertension. Most common in African Americans Treatment: Hypertension control Bilateral renal artery stenosis should be suspected in patients with acute, severe, or refractory hypertension who also have otherwise unexplained renal insufficiency Treatment: Medical therapy, surgery, stents. 9Slide 10: Nephritis: Inflammation seen on histologic exam Active sediment: Red cells, white cells, granular casts, red cell casts Variable degree of proteinuria (< 3g/day) Nephrotic: No inflammation Bland sediment: No cells, fatty casts Nephrotic range proteinuria (>3.5 g/day) Nephrotic syndrome = proteinuria + hyperlipidemia + edema 10Slide 11: Acute: Acute Tubular Necrosis: ( Ischaemic ATN, Toxic ATN ) One of the most causes of acute renal failure in hospitalized patients Causes: Hypotension, Sepsis Toxins: Aminoglycosides, Amphotericin, Cisplatin, Foscarnet, Pentamidine, IV contrast, Uric Acid. Rhabdomyolysis ( heme-pigments are toxins) Urine sediment: muddy brown granular casts. Acute Interstitial Nephritis: Causes: Drugs: Antibiotics ( especially Beta lactam ), Proton-pump inhibitors, NSAIDS , allopurinol Infections: Streptococcal infection, Legionella, Leptospirosis Auto-immune disorders Urine sediment: urine eosinophils (but not always present), white blood cells, red blood cells, white cell casts Cast Nephropathy : – Multiple Myeloma Tubular casts – PAS-negative, and PAS-positive (Tamm- Horsefall mucoprotein) 11Slide 12: Chronic: Polycystic Kidney Disease. Hypercalcemia. Autoimmune disorders: Sarcoidosis. Sj ö gren’s syndrome. 12Slide 13: Obstruction of the urinary flow anywhere from the renal pelvis to the urethra. Common causes includes Prostatic enlargement , bilateral kidney stone , or malignancy . Can be acute or chronic. Need to have bilateral obstruction in order to have renal insufficiency or unilateral in solitary Kidney . 13Slide 14: Acute kidney injury (AKI) , previously called acute renal failure (ARF), is a rapidly progressive loss of renal function ( An abruptly increase in serum creatinine ≥ 0.3 mg / dl with in 48 hrs , few weeks, months ) , generally characterized by oliguria (decreased urine production, quantified as less than 400 mL per day in adults, and fluid and electrolyte imbalance . AKI can result from a variety of causes, generally classified as prerenal , intrinsic , and postrenal . An underlying cause must be identified and treated to arrest the progress, and dialysis may be necessary to bridge the time gap required for treating these fundamental causes . 14Slide 15: Frequently have: Metabolic acidosis. Hyperkalemia. Disturbance in body fluid homeostasis. Secondary effects on other organ systems. 15Slide 16: Most community acquired acute renal failure (70%) is prerenal Most hospital acquired acute renal failure (60%) is due to ischemia or nephrotoxic tubular epithelial injury ( acute tubular necrosis ). Mortality rate 50-70% 16Slide 17: Advanced age. Preexisting renal parenchymal disease. Diabetes mellitus. Underlying cardiac or liver disease. Genetic predisposition: The APOL1 gene has been proposed as a major genetic risk locus for a spectrum of nondiabetic renal failure in individuals of African origin, these include HIV-associated nephropathy (HIVAN) , primary nonmonogenic forms of focal segmental glomerulosclerosis , and hypertension affiliated chronic kidney disease not attributed to other etiologies . Two western Africans variants in APOL1 have been shown to associate with end stage kidney disease in African Americans and Hispanic Americans. 17Slide 18: Oliguria: = daily urine output < 400 mL When present in acute renal failure, associated with a mortality rate of 75% ( versus 25% mortality rate in non-oliguric patients) Most deaths are associated with the underlying disease process and infectious complications. Anuria: No urine production. probably time for dialysis. 18Slide 19: Cancer? Recent Infections? Blood in urine? Change in urine output? Flank Pain? Recent bleeding? Dehydration? Diarrhea? Nausea? Vomiting? Blurred vision? Elevated BP at home? Elevated sugars? 19Slide 20: Family History: Cancers? Polycystic kidney disease? Medications: Any non-compliance with diabetic or hypertensive meds? Any recent antibiotic use? Any NSAID use? 20Slide 21: Vital Signs: Elevated BP: Concern for malignant hypertension Low BP: Concern for hypotension/ hypoperfusion ( acute tubular necrosis ). HEENT: Dry mucus membranes: Concern for dehydration ( pre-renal ) Extremity: Edema: Concern for nephrotic syndrome Abdominal: Ascites: Concern for liver disease ( hepatorenal syndrome ), or nephrotic syndrome CNS: Confusion: hypercalcemia , uremia, malignant hypertension, infection, malignancy Skin: Tight skin, sclerodactyly – Sclerodermal renal crisis Malar rash - Lupus 21Slide 22: Fractional excretion of sodium: (Urine Na+ x Plasma Creatinine ) FE Na = ______________________ x 100 (Plasma Na+ x Urine Creatinine ) FE Na < 1% → Prerenal , renal hypoperfusion with intact tubular function. FE Na > 2% → Epithelial tubular injury ( acute tubular necrosis), obstructive uropathy. If patient receiving diuretics, can check FE of urea. A value of less than 35% suggest a pre renal process. 22Slide 23: Diagnosis BUN : Cr FE Na (%) Urine Osmolality (mOsm /Kg Urine Na Urine Specific Gravity Sediments Prerenal Azotemia >20:1 <1% >500 <20 >1.020 Bland Oliguric ATN <20:1 >1% <350 >40 Variable Granular Cast 23Urinalysis:: Urinalysis: Hematuria: Non-glomerular: Urinary sediment: intact red blood cells Causes: Infection Cancer Obstructive Uropathy Rhabdomyolysis myoglobinuria Glomerular: Urine sediment: dysmorphic red blood cells, red cell casts Causes: Glomerulonephritis Vasculitis Atheroembolic disease TTP/HUS (thombotic microangiopathy) 24Urinalysis (cont.):: Urinalysis (cont.): Protein-Urea: Need microscopic urinalysis to see microabluminemia Can check 24-hour urine protein collection Nephrotic syndrome - ≥ 3.5 g protein in 24 hours Albuminuria Glomerulonephritis Atheroembolic disease (TTP/HUS) Thrombotic microangiopathy Nephrotic syndrome Tubular proteinuria Tubular epithelial injury (acute tubular necrosis) Interstitial nephritis 25Urinary Casts:: Urinary Casts: Red cell casts Glomerulonephritis Vasculitis White Cell casts Acute Interstitial nephritis Fatty casts Nephrotic syndrome, Minimal change disease Muddy Brown casts Acute tubular necrosis 26Slide 27: Renal Ultrasound Intravenous urography Radionuclide scanning Magnetic resonance imaging Computed tomography 27Slide 28: when the glomerular process is suspected, it may be useful to check : ESR. ANA. Anti-GBM. ANCA. SPEP. ASO titer. Viral serology. Complement levels ( C3, C4). 28Slide 29: If unable to discover cause of renal disease, renal biopsy may be warranted. Renal biopsy frequently performed in patient’s with history of renal transplant with worsening renal function. 29Slide 30: Treat underlying cause Blood pressure. Infections. Stop inciting medications. Nephrostomy tubes/ureteral stents if obstruction. Treat scleroderma renal crisis with ACE inhibitor. Hydration Diuresis (Lasix) Dialysis Renal Transplant 30Slide 31: Refractory fluid overload Hyperkalemia (plasma potassium concentration >6.5 meq/L) or rapidly rising potassium levels Metabolic acidosis (pH less than 7.1) Azotemia (BUN greater than 80 to 100 mg/dL [29 to 36 mmol/L]) Signs of uremia , such as pericarditis, neuropathy, or an otherwise unexplained decline in mental status Severe dysnatremias (sodium concentration greater than 155 meq/L or less than 120 meq/L) Overdose with a dialyzable drug/toxin 31Slide 32: Chronic kidney disease (CKD) can develop slowly and, initially, show few symptoms. CKD can be the long term consequence of irreversible acute disease or part of a disease progression. 32Slide 33: = a GFR of < 60 for 3 months or more. Most common causes: Diabetes Mellitus Hypertension Management: Blood pressure control! Diabetic control! Smoking cessation Dietary protein restriction Phosphorus lowering drugs/ Calcium replacement Most patients have some degree of hyperparathyroidism Erythropoietin replacement Start when Hb < 10 g/dL Bicarbonate therapy for acidosis Dialysis? 33Slide 34: Stage Description GFR (mL/min/1.73 m2) 1 Kidney damage with normal or increased GFR ≥ 90 2 Kidney damage with mildly decreased GFR 60-89 3 Moderately decreased GFR 30-59 4 Severely decreased GFR 15-29 5 Kidney Failure < 15 34Slide 35: Acute kidney injuries can be present on top of chronic kidney disease, a condition called acute-on-chronic renal failure ( AoCRF ). The acute part of AoCRF may be reversible, and the goal of treatment, as with AKI, is to return the patient to baseline renal function, typically measured by serum creatinine. Like AKI, AoCRF can be difficult to distinguish from chronic kidney disease if the patient has not been monitored by a physician and no baseline (i.e., past) blood work is available for comparison. 35Slide 36: 36-It indicated when conservative medical management is un able to control the metabolic demand of the kidney disease . -This applies to the acute and chronic setting. -Indicated Acutely in: 1-Hyperkalemia. 2-Metabolic Acidosis. 3-Volume Overload. 4-Uremic encephalopathy or Pericarditis. 5-Certain drugs intoxication (e.g., methanol, ethylene glycol, salicylates ). -In chronic setting, it typically begun when creatinine clearance fall below 10 ml/min in non diabetic or 15 ml/min in diabetic. -Deteriorating nutritional status in advanced CKD is also an indication to start dialytic therapy.: -It indicated when conservative medical management is un able to control the metabolic demand of the kidney disease . -This applies to the acute and chronic setting. -Indicated Acutely in: 1-Hyperkalemia. 2-Metabolic Acidosis. 3-Volume Overload. 4-Uremic encephalopathy or Pericarditis. 5-Certain drugs intoxication (e.g., methanol, ethylene glycol, salicylates ). -In chronic setting, it typically begun when creatinine clearance fall below 10 ml/min in non diabetic or 15 ml/min in diabetic. -Deteriorating nutritional status in advanced CKD is also an indication to start dialytic therapy. 37Slide 38: 38- The most commonly used form of renal replacement therapy. - Modalities: Intermittent haemodialysis ( IHD ): -Run for 3-4 hours/ session. -Used in ESRD & AKI. -In chronic setting performed 3 times/ Week. Continuous renal replacement therapy ( CRRT ): -Used when the patient is hemodynamicly un stable and cannot tolerate the rapid fluid shift of IHD. -Take 24 hours. -Due to slow blood flow it is necessary to anti coagulate the blood with systemic heparin or regional citrate. -Require specialized nursing & an intensive care setting. -The most employed form is continuous veno-venous hemodiafilteration ( CVVHDF ) when the blood is slowly pumped to a dialysis solution (Diffusion) & replacement fluid infused into the circuit to balance most of the ultrafilterate (Convection).: - The most commonly used form of renal replacement therapy. - Modalities: Intermittent haemodialysis ( IHD ): -Run for 3-4 hours/ session. -Used in ESRD & AKI. -In chronic setting performed 3 times/ Week . Continuous renal replacement therapy ( CRRT ): -Used when the patient is hemodynamicly un stable and cannot tolerate the rapid fluid shift of IHD. -Take 24 hours. -Due to slow blood flow it is necessary to anti coagulate the blood with systemic heparin or regional citrate. -Require specialized nursing & an intensive care setting. -The most employed form is continuous veno-venous hemodiafilteration ( CVVHDF ) when the blood is slowly pumped to a dialysis solution (Diffusion) & replacement fluid infused into the circuit to balance most of the ultrafilterate (Convection). 39 -Sustained low efficiency dialysis ( SLED ): -Is hybrid form of IHD & CRRT. -The intermediate blood flow reduce the risk of clotting and the intermediate long duration of the session ( 8-10 hours ) allow adequate clearance.: -Sustained low efficiency dialysis ( SLED ): -Is hybrid form of IHD & CRRT. -The intermediate blood flow reduce the risk of clotting and the intermediate long duration of the session ( 8-10 hours ) allow adequate clearance. 40 Complications Of Hemodialysis: 1. Infections. 2. Bleeding. 3. Pneumothorax. 4. Thrombosis of A-V fistula or graft. 5. Intradialytic hypotension from IV fluid depletion from rapid ultra filtration. 6. Dialysis disequilibrium syndrome: cerebral edema (nausea, emesis, headache, confusion, seizures). : Complications Of Hemodialysis: 1. Infections. 2. Bleeding. 3. Pneumothorax. 4. Thrombosis of A-V fistula or graft. 5. Intradialytic hypotension from IV fluid depletion from rapid ultra filtration. 6. Dialysis disequilibrium syndrome: cerebral edema (nausea, emesis, headache, confusion, seizures). 41Slide 42: 42 - Used in treatment of ESRD. - Not used if the patient has recent abdominal surgery or multiple peritoneal adhesions. - Modalities: - Manual Exchanges: - Also called Continuous ambulating peritoneal dialysis ( CAPD ). - Patient instill dialysis fluid into the peritoneum after a period of time dialysate is drained & replaced by another dwell. - Automated modality: - Also called Continuous cycling peritoneal dialysis ( CCPD ). - Typically operate over night where machine run while patient is sleeping.: - Used in treatment of ESRD. - Not used if the patient has recent abdominal surgery or multiple peritoneal adhesions. - Modalities: - Manual Exchanges: - Also called Continuous ambulating peritoneal dialysis ( CAPD ). - Patient instill dialysis fluid into the peritoneum after a period of time dialysate is drained & replaced by another dwell. - Automated modality: - Also called Continuous cycling peritoneal dialysis ( CCPD ). - Typically operate over night where machine run while patient is sleeping. 43Slide 44: 44 Complications of peritoneal dialysis: 1. Peritonitis. 2. Tunnel or exit site infection. 3. Out flow failure. 4. Sclerosing encapsulating peritonitis. 5. Hyperglycemia. 6. Hyperkalemia. 7. Protein loss. : Complications of peritoneal dialysis: 1. Peritonitis. 2. Tunnel or exit site infection. 3. Out flow failure. 4. Sclerosing encapsulating peritonitis. 5. Hyperglycemia. 6. Hyperkalemia. 7. Protein loss. 45Slide 46: 46Slide 47: A 82-year old female with a history of Alzheimer’s dementia presents from her nursing home with diarrhea for three days. Per nursing home documents, there have been multiple recent outbreaks of C. difficile colitis among their residents. 47Slide 48: PMH: Alzheimer’s Dementia Osteoarthritis Allergies: PCN Meds: Aricept. Ibuprofen PRN. 48Slide 49: Physical Exam: Temp: 36.1, 82/46, 96, 16, 98% on RA Gen.: Slightly lethargic, oriented to self only; in NAD HEENT: very dry mucous membranes CV: RRR; no murmurs Abd.: soft, nontender, NABS Ext.: No LE edema 49Slide 50: Labs: WBC: 19.2 Hgb.: 11 Hct: 32.8 Platelets: 202 Sodium: 132 Potassium: 5.6 Chloride: 103 Bicarbonate: 18 BUN: 32 Cr.: 1.8 Glucose: 79 Urine dipstick: Protein: none Ketones: trace Blood: none Leuk est: none 50Slide 51: What further information would be helpful in evaluating this patient? What are some possible diagnoses in this patient? What further studies would you like to do? What might you see in urinary sediment? 51Slide 52: Urine sodium = 40 mg/dL Urine creatinine = 140 mg/dL Renal ultrasound: no sign of hydronephrosis 52Slide 53: What kind of renal failure do you think this patient has? How would you treat this patient? 53Slide 54: A 75-year old woman is admitted to the hospital for confusion. The patient is oriented to person but not time or place. She has a history of cervical cancer, treated with total hysterectomy and radiation 18 months ago. Previous evaluation in her private physician’s office 3 months ago showed her serum creatinine concentration was 1.0 mg/dL. 54Slide 55: Physical examination shows a temperature of 36.2 ° C, a regular pulse rate of 98/min., a regular respiration rate of 20/min., and a blood pressure of 110/60 mmHg. There is no orthostasis. There is no neck vein distention at 45 degrees, and the chest is clear. S1 and S2 are normal, without gallop or murmur. Liver span is 18 cm, and the edge is three finger breadths below the right costal margin. The spleen tip is palpable before the left costal margin. There is shifting dullness and bowel sounds are present. There is 2+ pedal edema. Cranial nerves and reflexes are normal, and the neurologic examination did not elicit focal findings . 55Slide 56: Labs: Hct: 30.7 WBC: 7.3 Sodium: 131 Potassium: 5.7 Chloride: 98 Bicarbonate: 15 Calcium: 7.2 Phosphorus: 6.8 BUN: 64 Creatinine: 7.3 Urinalysis: Specific gravity: 1.011 Glucose: negative Protein: trace Blood: negative Ketones: negative Microscopic: 0 to 1 RBC per high-power field 0 to 1 WBC /hpf No cellular casts Sodium: 28 mEq /L FENa: 4.1% Osmolality: 168 mosm /kg 4-hour urine volume: 40 mL 56Slide 57: The most appropriate initial step in the clinical management of this patient is: Renal ultrasound Renal Biopsy A trial of normal saline at 300 mL/hr for 2 hours Continuous arteriovenous hemofiltration Renal scintigraphy 57Slide 58: A 45-year old male with a history of metastatic colon cancer is admitted to the hospital for pain control. Patient has known metastases to the spine and pelvis, and has had worsening pain over the last several weeks. Palliative care is consulted and helps with pain control. However, his hospitalization is complicated by nosocomial pneumonia. He underwent a staging CT on Hospital #6, which showed a mild increase in size of spinal, pelvic mets. On hospital day #8, his daily chemistry shows an increase in his creatinine from 1.0 the day before to 1.9. 58Slide 59: PMH: Colon cancer (diagnosed 4 years ago, s/p partial colectomy, chemo., radiation; known mets to liver, lungs, spine/pelvis) GERD Allergies: PCN Current Meds: Ciprofloxacin Vancomycin Amikacin Dilaudid PCA Pericolace Nexium 59Slide 60: What are some possible causes of renal failure in this patient? What would you do the urine sediment shows muddy brown casts? What would you suspect if urine eosinophils are seen? 60Slide 61: 61 You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.