AKI, CKD, RRT, Kidney Transplant With Notes Column

Acute Kidney Injury, Chronic Renal Failure, Hemo/Peritoneal Dialysis, Renal Cancer Renal Function • Anatomy • Kidney • Nephrons • Renal vein & renal artery • Ureters • Bladder • Urethra • Normal Renal Function • Fluid balance (absorbs/reabsorbs water) • BP control (renin) • Acid/base hydrogen (H+) and bicarbonate (HCO3) • Electrolyte balance (sodium, potassium, calcium & phosphorus) • Removal of wastes (urea, metabolites, toxins, uric acid) • Erythropoietin (promotes the formation of RBCs in the bone marrow) • Vitamin D (activation) Nephron Anatomy • Functional Unit (FU) • 1-2 million in each kidney • Filtration • Glomerulus within Bowman’s capsule • Amino acids & Glucose • Blood flow • Afferent arteriole –caries blood to the glomerulus • Efferent arteriole – caries blood from the glomerulus • Reabsorption (Reabsorption occurs throughout the entire tubule) • Proximal convoluted tubule • H2O, electrolytes, small molecules, glucose, amino acids, proteins • Loop of Henle • H2 O • Distal convoluted tubule • H2O, some Na+, Urea, other solutes • Ascending loop • Chloride, Na+ • Secretion • Collecting duct • K+, H+ ions, ammonia, uric acid, some drugs, waste products Renal Vasculature • Highly vascular organ: 20%-25% of CO • Renal blood flow (RBF) is about 600 mL/min ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ • Intricate vascular system, capillaries surround all part of nephron • Afferent (arrive) Efferent (exit) at level of glomerulus • Autoregulation – perfusion impaired outside of these pressures • SBP 180-80 mmHg • MAP >65 or 75-85 mmHg (organ perfusion NOTE: • Diastolic Perfusion Pressure (DPP) • Mean Perfusion Pressure (MPP) • Central Venous Pressure (CVP) or MAP-CVP • Are more accurate in preventing/diagnosing AKI. MAP was not. • Perfusion, Perfusion, Perfusion!!!! Renin Angiotensin and Aldosterone System (RAAS) • Endocrine Regulation of the Kidney • Renin • Regulates BP • Produced by the juxtaglomerular cells in the Kidney • ↑ secretion d/t ↓BF and ↓Na+ • Aldosterone • Regulates electrolytes • Produced by the adrenal cortex • ↑secretion d/t ↓BF and ↑serum osmolarity • Antidiuretic hormone (ADH) AKA Vasopressin • Controls Osmolarity by ↑ H2O reabsorption • Osmolarity = 250-900mOsm/kg/24hrs • (50-1200 mOsm/kg random sample) • Produced by the Posterior Pituitary Gland (PPG) • ↑ secretion d/t ↓osmolarity AKA FVD • Sympathetic activity Renal Function • • 2 Labs Blood Urea Nitrogen (BUN) 8-25 mg/dL (≥60 YO: 8-20) • >25 = liver/kidey impairment, dehydration, ↑protein diet, infection, steroid use, GI bleed • <8 = Malnutrition, fluid volume excess, severe hepatic damage Creatinine (Cr) 0.6-1.5 mg/dL (50-110mmol/L) • Male slightly > than female d/t muscle mass ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ >1.5 = CKD, kidney obstruction, intense exercise, low muscle mass, pregnancy, c Bactrim, corticosteroids, vitamin D metabolites, salicylates, phenacemide, pyrim BUN/Cr ratio 10:1 -20:1 • >20:1 = Dehydration (FVD) or ↓renal perfusion and function • <10:1 = Fluid volume excess or malnutrition GFR 100-125ml/min • Starting @ 35-40 YO annual ↓of 1ml/min • 90-60: Early-stage kidney disease • 59-15: Kidney disease • <15: Kidney Failure Specific gravity 1.002-1.035 • >1.030 = FVD • <1.005 = FVE • Fixed @ 1.010 = kidney disease • • • • Glomerular Filtration Rate (GFR)100-125ml/min • • • • • • GFR AKA Creatinine Clearance (CrCl) Decreases by 1 mL/min annually after age 40 Abrupt ↓in GFR will show an ↑in Creatinine (Cr) Gradual ↓in GFR & renal blood flow (RBF) with aging will show little change in Cr 40% of people with ↓GFR have a serum creatinine within normal range Potassium regulation is compromised in acute and chronic kidney disease, with a glomer Urinalysis • • • • • • • • • • • • Color: Clarity Sediment Specific gravity (1.002-1.035) book says →1.010-1.025 pH (4.5 -8.0) Bacteria & leukocytes Protein Ketones Glucose Nitrites Bilirubin/urobilinogen Toxins Effects of • • • • • • • • • • • • Aging on the Renal system The loss of skeletal muscle mass is in proportion to the loss of GFR so the serum Cr does Loss of renal mass RBF decreases by 10%/10 years >40 years (most profound in the renal cortex) Nephrons Decreased renin, aldosterone ADH and hypertonicity Decrease fluid intake Decreased CO & HTN Glomerular sclerotic changes Cystocele in women, estrogen protects & slows progression of CKD BPH in men, androgen deprivation slows progression of CKD Bladder tone • Incontinence • Retention 3 Types of Declining Renal Function • Slow decline is on a continuum • The minimum amount of urine needed to rid the body of metabolic waste of normal metabolic waste products is 400ml/24hr or 0.5ml/kg/hr. • Renal insufficiency (RI) • Functions continue, nephrons compensate, but not as well and toxins accumulate • S/Sx: Nocturia, polyuria, anorexia, N/V, weakness, fatigue, ↑BUN, Cr <2, ↓GFR, mild anemia • Toxins accumulation and kidneys can fail without intervention • Acute Kidney Injury (AKI) • 3 types (pre, intra, post) • Treatable if treated early • If left untreated can lead to permanent loss of function • Chronic Renal Failure/Chronic Kidney Disease (CRF or CKD) • Kidney disease is divided into 5 stages, based on filtration • Manifestations of impaired kidney function are not often seen until GFR is < 50% • Body demands not met, increase in quantity (early) NOT quality • ↑BUN with Cr >5, GFR continues to decrease • S/Sx: Oliguria to anuria, volume retention, HTN • Azotemia, acidosis, anemia, elevation in K+, Na+, PO4; low Ca+ • End Stage Renal Disease (ESRD) • Kidney function fails (permanent), need dialysis or transplant to sustain life • Systemic impairments (uremic syndrome) • Severe elevation in BUN, Cr >10 GFR <15, high K+, Na+, PO4; low Ca+; acidosis Kidney Disease and GFR 4 ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ Acute Kidney Injury (AKI) Characterized by an abrupt ↓in renal function Time limited response. Eventual ischemia and infarction of nephrons CKD, DM, HF, HTN, and cirrhosis can lead to acute tubular necrosis (ATN) If BP continue to ↓, ATN may develop → death of nephrons Criteria for AKI: • ≥ 50% ↑in serum creatinine above baseline • Normal creatinine is less than 1 mg/dL • Nonoliguria (> 800 mL/day), Oliguria (< 0.5 mL/kg/hr), or Anuria (< 50 mL/day) • Causes are divided by located: prerenal, intrarenal, postrenal • Systemic hypoperfusion (↓BF or ↓BV), increases vascular tone (HTN) • Renin, angiotensin, antidiuretic hormone systems are activated • Most common cause: Prerenal volume depletion from loss of body fluids • AKI with Renal Replacement Therapy (RRT) mortality→ 50% • • • • • Manifestations • Fluid & electrolyte imbalances: ↑SG or fixed • Usually critically ill & lethargic; Drowsiness, headache, muscle twitching, N&V, seizures • Acid-base imbalance Metabolic acidosis • pH depends on number of functioning nephrons • Skin and mucus membranes dry, and oliguria • Marked Azotemia (↑in BUN & Cr) & ↓GFR • Anemia, HTN and CHF, Pruritus Categories of AKI Prerenal: BV loss or impaired BF, resulting in renal hypoperfusion and ischemia • Filtration pressure declines in the face of reduced renal blood flow • Glomerular filtration pressures also fall • Structural damage has not yet occurred, and the condition is reversible. • Volume depletion (↓ECF): • Vena cava obstruction, renal artery stenosis/thrombosis • Gastrointestinal losses (dehydration, vomiting, diarrhea, NG suction) • Diuretic agents, osmotic diuresis, 3rd spacing • Cardiac efficiency impaired (↓CO): • Hypotension, AAA, Hemorrhage • Tension pneumothorax, Dysrhythmias • HF , MI, Cardiogenic shock, Pump failure, Tamponade, Valve dysfunction, • Vasodilation: Trauma: Crush injury • Anaphylaxis, Sepsis, Shock, anaphylaxis, anesthetics, Drug OD • ACE inhibitors & angiotensin receptor blockers in pts with ↓volume • Arteriolar vasoconstriction d/t hypercalcemia, amphotericin Intrarenal (Intrinsic): involves renal tissue (parenchyma) • ATN = Acute Tubular Necrosis • Very important to note clinical events and predisposing factors • Prolonged ischemia resulting from: • Acute Tubular Necrosis (ATN) most common cause • Hemoglobinuria (transfusion reaction, hemolytic anemia) • Rhabdomyolysis/myoglobinuria (trauma, crush injuries, burns) • Pigment nephropathy (associated with the breakdown of blood cells containing pigments that in turn occlude kidney structures) • DIC, SLE, HIV nephropathy, DM • Nephrotoxic agents such as: • Aminoglycoside ABX (gentamicin, tobramycin) • “It’s a SIN to give mySIN” • ACE inhibitors • Heavy metals (lead, mercury) • Nonsteroidal anti-inflammatory drugs (NSAIDs) • Radiopaque contrast agents “Contrast Kills” • GERD meds: Cimetidine (Tagamet), Ranitidine HCl (Zantac) • Solvents and chemicals (ethylene glycol, carbon tetrachloride, arsenic) • Infectious processes such as: • Acute glomerulonephritis • Acute pyelonephritis, Hepatorenal syndrome, Malignancies, Vasculitis Postrenal: Obstruction of urine from the kidneys. Can be mechanical or functional • BPH, Blood clots, Calculi (stones), Strictures Tumors • Bilateral ureteric obstruction • Urethral obstruction • Obstruction of single functioning kidney Compare and contrast AKI Categories Characteristic Prerenal Intrarenal Postrenal ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ 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___________________________________ ___________________________________ ___________________________________ ___________________________________ Etiology Hypoperfusion Excessive fluid loss, ↑vascular capacity, Vascular obstruction, Drugs that alter renal hemodynamics Ischemia Rhabdomyolysis Intratubular obstruction Nephrotoxicity Mechanical: blood clots, calculi, tumors, BPH, prostate cancer, urethral strictures Functional: Diabetic neuropathy, neurogenic bladder, drugs BUN ↑(out of normal 20:1 ratio to creatinine) ↑ ↑ Creatinine ↑ ↑ ↑ UO ↓ Varies, often ↓ Varies, may be ↓, or sudden anuria Sodium (urine) ↓to <20mEq/L ↑ to >40 mEq/L Varies, often ↓ to ≤20 mEq/L Urine Sediment Normal, few hyaline casts Abnormal casts and debris Usually normal Urine Osmolarity ↑ to 500 mOsm ~350 mOsm, similar to serum Varies, ↑ or equal to serum Urine SG ↑ Low normal Varies Contrast Induced AKI (CI-AKI)or Contrast Inducted Nephrop • Occurs 24-48 hours post administration • Creatinine peaks in 3-4 days (34% mortality) • Can minimize risk with pre-contrast prophylaxis • Hydration with NS, hemofiltration, bicarbonate • N-acetyl cysteine (mucolytic) 2016 meta-analysis determines oral administration w • Contrast material types • Ionic, high molecular weight (greater risk) • Non-ionic, low molecular weight • Variables • Patient hydration and hemodynamic status, underlying kidney disease or comprom • Volume of contrast administered • Repeated does within 48 hours • Patients on vasopressors Causes of Renal Hypoperfusion • Hypovolemia • GI: vomiting, diarrhea, GU: diuretics, Burns, Hemorrhage • Cardiac • CHF, tamponade, valvular disease, pump failure, MI • Reduced PVR • Sepsis, drug OD, antihypertensives, hepatorenal syndrome (see chart→) • Local renal hypoperfusion • Renal artery stenosis malignant HTN Factors Affecting Renal Excretion • Blood flow to the kidney • Urine flow rate • Urine pH and pKa (protein kinase attaches phosphate to protein) • The lower the pKa the stronger the acid • Controls renal fluid secretion • Physicochemical properties • Distribution and binding • Drug interactions • Biological factors & Disease states Phases of AKI Initial may last up to a week • Begins with the initial insult and ends when oliguria develops Oliguric may last 10-14 days • Occurs within 1-7 days after injury • ↑ in urea, creatinine, uric acid, organic acids, potassium and magnesium • Uremic symptoms and life threating conditions (hyperkalemia) appear • Hyponatremia • Fatigue/Malaise 6 ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ • Metabolic acidosis • Urinalysis: casts, RBCs, WBCs, SG fixed @ 1.010 • Urine output: <400ml/day Diuresis • Gradual ↑in urine output, d/t glomerular filtration recovery • Laboratory values stabilize and eventually ↓ • Urinary output may be normal or elevate • Renal function may still be markedly abnormal • Observe for dehydration: if dehydration occurs, uremic symptoms likely to ↑ • Urine output: 1-3L/day up to 3-5L Recovery • May take 3-12 months • Laboratory values return to the patient’s normal level • Although a permanent 1-3% ↓ in GFR may occur, not clinically significant. RIFLE Classification System for Acute Kidney Injury GFR Criteria Urinary Criteria R (Risk) ↑ Cr (1.5 x baseline) or GFR ↓ > 25% UO < 0.5 mL/kg for 6 hours I (Injury) ↑ Cr (2 x baseline) or GFR ↓ > 50% UO < 0.5 mL/kg for 12 hours F (Failure) ↑ Cr (3 x baseline) or GRF ↓ 75% or Cr ≥ 4 mg/dl UO < 0.3 mL/kg or anuria (< 50 mL/day) for 12hrs L (Loss) Complete loss of renal function for ≥ 4 weeks E (ESKD) Need RRT for > 3 months Focused Renal Assessment of AKI • Identify risk factors for the development of AKI→ • Physical Assessment • Neurologic: Irritability, drowsiness, confusion, ALOC, seizures • Cardiac: Tachycardia, HTN or HYPTN, arrhythmias (AFib) or peaked T waves d/t hyperkalemia, ↓MAP, ↓PVR, ↓SVR, ↓Pre/Afterload, ↓CO, ↓EF, CAD, MI • Ocular: Retinopathy, keratitis, iritis, uveitis • Pulmonary: bibasilar moist crackles • GI: Uremic breath, N, V, diarrhea, constipation, appetite calories, protein sufficient, 3Ps, sodium, bleeding) Oliguria/Anuria (<0.5ml/kg/hr for >6hrs) ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ Hematologic & immune system Integumentary: Bleeding abnormalities, ecchymoses, purpura, dry, pruritic skin, mac and pretibial areas • Musculoskeletal: Myoclonus • Laboratory • BUN, Cr, GFR • Osmolality • Electrolyte imbalances • Metabolic Acidosis • S/Sx: Headache, ↓BP, hyperkalemia, muscle twitching, warm flushed skin, n respirations • D/T: DKA, severe diarrhea, renal failure, or shock • Remember all the reasons for an altered urine output including decreased oral fluid int • • Pharmacological Treatment of AKI • Oliguric phase • Diuretics-Furosemide (Lasix): Assists fluid balance and correction of fluid volume ove acid (Edecrin) may be given to initiate diuresis. • Inotropes-Dopamine hydrochloride: in small does (1-5 mcgs/kg) causes selective dila therefore urine flow • Vasodilators-Fenoldopam (Corlopam): is a selective dopamine receptor agonist that effects. Indicated for those with severe HTN including patients with renal compromis • Sodium bicarbonate: treatment of acidosis • Hypertonic glucose-and-insulin infusions (sorbitol), sodium bicarbonate, & sodium hyperkalemia • Diuretic phase • IV fluids: based on pt stage (fluids limited during oliguric phase) • N-acetylcysteine: prevention of contrast nephropathy • Mannitol (Osmitrol): 2nd line agent to prevent AKI in pts experiencing rhabdomyolysis. M • Tamsulosin HCl: alpha-adrenergic blocker for bladder outlet obstruction secondary to BP • CCB- Nifedipine relaxes smooth muscle and produces vasodilation which in turn improve mediated through vasodilation and are used to enhance the function of transplanted kidn Medical Treatment of AKI • • • • • Treat the underlying cause Maintain fluid balance: Daily weights, serial measurements of CVP, serum and urine conc Maintain renal blood flow: IV fluids or transfusions of blood products Avoid fluid excess: Mannitol (Osmitrol), furosemide (Lasix), or ethacrynic acid (Edecrin) m Renal replacement therapy (PRN): hemodialysis, peritoneal dialysis, or a variety of contin Chronic Renal Insufficiency (CRI) • • • • • • 8 Reduction of blood flow to the kidneys Often caused by renal artery disease (HTN, diabetes) Defined as decline in renal function to approximately 25% of normal Risks factors: Older age, gender, family history, race or ethnicity, genetic factors, hyperlipi Stages Usually symptomatic when <50% “kidney function” is left. Renal Diet Limit the 3 P’s and Sodium Protein: Protein needs and restriction based on body weight and dialysis (protein is lost during dialysis) Mildly ill: 0.8-1.2g/kg/day. Critically ill: 1.2-1.5g/kg/day Potassium: Limit or avoid organ meats, fish, dried fruits, beef, chicken, pork, milk, dark green leafy vegetables, salt substitutes Phosphorus: Limit or avoid milk, cheese, yogurt, collard greens, dried beans, coffee Sodium: Limit or avoid processed foods, fast foods, prepackaged meats, potato chips, pretzels, pickles, ham, bacon, sausage • Sodium and fluid restrictions (urine output plus 200ml/day) • High-carb diet (has protein sparing effect) • During the recovery phase pt is placed on a high-protein, high-calorie diet and encouraged to resume activities gradually Chronic Kidney Disease (CKD) Overview • Defined as either the presence of kidney damage or a sustained GFR <60 mL/minute/1.73m2 for 3 months • Progressive loss of RF→↓GFR, azotemia, and interrupted regulation of extracellular fluid volume and electrolytes • S/Sx: minimal until > 75% of glomerular filtration lost; worsen as kidney function declines • Fatal unless treated • Ninth leading cause of death in the United States • AKA chronic renal failure (CRF) ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ Lab Results • BUN↑; Cr↑ (serum). Na, K, P, and ammonia levels are all ↑ • ABG analysis shows ↓ pH & ↓bicarbonate • Hct & Hbg↓, RBC survival time ↓ • Serum albumin level may be ↓; albumin excretion is > 30 mg/24 hours • Mild thrombocytopenia & platelet defects appear • Aldosterone↑ • BG↑ & ↑triglyceride • HDL↓ • UA: proteinuria, glycosuria, RBCs, leukocytes, casts, and crystals Causes • HTN • Endocrine disease, DM • Glomerular disease (primary or secondary) • Congenital anomalies, such as polycystic kidney disease • Kidney damage • Vascular disease • Cystic kidney disease • Acute kidney injury Diagnostic procedures • Kidney biopsy identifies the underlying pathology • Electroencephalography shows changes suggesting metabolic encephalopathy Stages Stage 1: GFR normal or ↑(> 90 mL/minute/1.73 m2) but at an ↑risk of KD Stage 2: GFR mildly ↓(60-89 mL/minute/1.73 m2) & signs of mild KD Stage 3a: GFR mod. ↓(45-59 mL/minute/1.73 m2) & signs of moderate CRI Stage 3b: GFR mod. ↓(30-44 mL/minute/1.73 m2) & signs of moderate CRI Stage 4: GFR severely ↓(15-29 mL/minute/1.73 m2) & signs of severe CRI Stage 5: GFR indicates RF (<15 mL/minute/1.73 m2) and signs of ESKD With stages 1 and 2, the diagnosis is better established with one or more of Treatment • Treatment of underlying cause the following conditions present: • Avoidance of factors that may increase progression • Albuminuria (greater than 30 mg in 24 hours) • Control of HTN and diabetes • Urine sediment abnormalities • Smoking cessation • Electrolyte imbalances • Weight reduction in patients who are overweight or obese • Histologic abnormalities • Venous thromboembolism (VTE) prophylaxis if the patient is • Structural abnormalities hospitalized • History of kidney transplant Risk Factors Assessment Diet • Renal Diet except with History Physical Findings • Family history • Usually no /Sx until stage 4 • ↓urine output peritoneal dialysis, ↑-protein • Chronic infections, such as • Sodium and fluid restrictions • History of underlying disease • HYPTN or HTN chronic pyelonephritis • Protein restriction for stage 5 • Dry mouth • Altered level of consciousness • Collagen diseases, such as disease based on serum • Fatigue • Peripheral edema systemic lupus erythematosus • Nausea, vomiting • Cardiac arrhythmias protein and albumin levels and scleroderma Activity • Anorexia • Bibasilar crackles • Nephrotoxic agents • Rest periods when fatigued • Hiccups • Pleural friction rub • Obstructive processes, such as Meds • Muscle cramps, weakness • Gum ulceration and bleeding calculi • ACE/ARBs • Fasciculations, twitching • Signs of malnutrition • Vascular diseases, such as • proteinuria • Pruritus • Loss of lean body mass endocarditis • Antidiabetics • Infertility, decreased libido • Uremic fetor • Heart disease • Calcium Carbonate/Acetate • Amenorrhea • Abdominal pain on palpation • Elevated cholesterol levels • hyperphosphatemia • Erectile dysfunction • Poor skin turgor • Obesity • Epoetin/Darbepoetin alfa • Pathologic fractures • Pale, yellowish bronze skin • Smoking • anemia • Sleep problems • Renal artery stenosis • Ferrous Sulfate • Use of illicit drugs, such as • Change in urine output • proteinuria • Shortness of breath; reduced heroin • Statins • Black heritage exercise capacity • Diuretic • Older than age 65 • Chest pain • Cinacalcet hydrochloride • Peripheral edema • ↓PTH • New-onset heart failure • Sevelamer carbonate • Bleeding tendency; ecchymosis • ↓phosphate • Analgesics Medical Complications and Treatment of ESKD Sodium & Water • Edema, HF, HTN • Hypovolemia & Hypotension ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ • Treatment: daily weights, fluid allowance per day is 500 to 600 mL more than th Metabolic Acidosis • D/T ↓ ability to excrete ↑ loads of acid • Treatment: if symptomatic →sodium bicarbonate supplements or dialysis Calcium & Phosphate • D/T: ↑P → ↓Ca → ↑PTH → bone demineralization (renal osteodystrophy) • Bone Disease & Metastatic & Vascular Calcifications • R/T: ↑ phosphorus, ↓ Calcium, abnormal Vit D metabolism, ↑ albumin • Treatment: Calcium and Phosphate Binders *Avoid Magnesium Antacids • calcium carbonate (Os-Cal) or calcium acetate (PhosLo) • If ↑Ca or the calcium–phosphorus product > 55 mg/dL, polymeric phosphate bin • ↑hypercalcemia • sevelamer hydrochloride (Renagel) • 1-4 tablets with food HTN • D/T: Na & H2O retention and malfunction of the RAA system • Treatment: Antihypertensives, fluid restriction, low-sodium diets, diuretic agents, inotr dialysis Neurologic (Seizures) • IV diazepam (Valium) or phenytoin to control seizures. Raise & pad side rails Anemia • D/T: ↓ erythropoietin production, ↓ RBC lifespan, GI bleeding, Blood loss during hemod • Treatment: erythrocyte-stimulating agents (recombinant human erythropoietin) • Epoetin alfa IV or subcutaneously 3x per week • may take 2-6 weeks for hematocrit to increase • A/E: HTN (especially during early stages of treatment), ↑clotting of vascular acce stores (iron sucrose (Venofer), iron dextran (INFeD or Dexferrum), and ferric gl Hyperkalemia (acute) • Notify Provider if Hyperkalemia is >5.5 S/Sx ECG changes • Treatment: Cation-Exchange Resins, via PO or retention Enema • sodium polystyrene sulfonate (Kayexalate) • Sorbitol can be added for a diarrhea effect • PO • Enema: via rectal catheter. Pt should retain the Kayexalate for at least 30 to removal. Post treatment a cleansing enema is given. • FEN • Restrict fluids • Hyperphosphatemia and hypocalcemia • Hyperkalemia • Limit protein, K+, Na+, phosphorous • Increase calories (fat, CHO) K+ & Ca+ Imbalances and Effects on ECG Hemodialysis (HD) • Works through osmosis and diffusion • Requires large vascular access • Most efficient and effective clearance • Complications • Disequilibrium syndrome, muscle cramps, hemorrhage, air embolus, hemodynamic flux (hypotension, dysrhythmias, anemia) • Components include • Access • Dialyzer • Filter 10 ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ • Dialysate How HD Works Indications • Refractory hyperkalemia • Refractory acidosis • Volume overload • Elevated BUN with symptoms of complications • Pericarditis • Encephalopathy (hepatorenal syndrome/AMS, ALOC • Pulmonary edema Mnemonic = HAVEPEE Inpatient • Dialysis Center • Set schedule/time slot • Night-time option Home hemodialysis • • • Flexible schedule, less nausea, more energy, better sleep Decreases risk of complications/problems • Painful muscle cramps, HTN, HA, stroke, hypotension, high phosphate, puiritis Treatments last between 2-10 hours • Standard home hemodialysis - 3x/week • Short daily hemodialysis - 5-7 days/week • Nightly home hemodialysis – 3-6x/week Continuous Renal Replacement Therapy (CRRT) Primarily used for clients in critical care who are hemodynamically unstable • More gradual and continuous • 5 methods • SCUF works by convection to pull off fluid • CAVH works by convection to pull off fluid and waste using patients blood pre • CAVH-D with dialysate • CVVH works by diffusion like a “slow” hemodialysis • CVVH-D with dialysate by diffusion and convection • Indications • MODS, sepsis, ARF, inability to tolerate hemo/ peritoneal dialysis • Complications • Fluid imbalance, hemorrhage, hemofilter occlusion, infection, thrombus, vascular occlusion Indications for CRRT Acute management of life-threatening complications A: Metabolic acidosis (pH <7.1) E: Electrolytes –Hyperkalemia (K > 6.5 or rapidly rising), hypermagnesemia I: Ingestion –Certain alcohol and drug intoxications • Salicylates, lithium, methanol, ethylene glycol, theophylline, phenobarbital O: Refractory fluid overload (postoperative) U: Uremia –high catabolism of ARF (pericarditis, neuropathy, decline in mental status • Renal support: RRT even before any of the complications of AKI Temporary Dialysis Vascular Access • • • • Do not use for routine access or blood draw HD team use only Use only the 3rd port if present during an emergency Flush lock with sodium citrate (4%)versus heparin ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ • Aspirate and disguard Arterial Venous (AV) Fistula HD Standards of Care • Pretreatment • Medications,, nutrition, fluids • VS, weight, labs,, symptoms • Post treatment • Handoff –VS, Labs, fluids in/out, weight changes, blood glucose • Labs • Fluid and electrolyte shifts • Site observations • Medications, nutrition, rest • Discharge, support services (transportation, groups) • Complications and Stressors • Fluid limitations, muscle cramps, fatigue, food limitations, limitation of activity, slee social isolation, puiritis, long dialysis treatment times Case Study -Dialysis • The patient is a 67-year-old male, who is 3 days postoperative after a CABG x 3 operatio ESRD, which is treated with hemodialysis 3x/week. The patient has a left AV shunt. He is taking the following medications: Sevelamer (Renegel) 2 capsules with each meal Vitamin D, B12 and iron supplements with each meal Calcium carbonate (OS-Cal): 3 tablets with each meal Procrit (epoetin alfa): 100U/kg dose subcutaneously every M, W, & F on dialysis days 70/30 NPH and regular insulin 30U twice daily and finger stick blood glucose taken before meals and at bedtime and regular insulin given as per CHO intake as per sliding scale • Coreg (carvedilol 12.5 mg twice daily • Lanoxin 0.125 mg every other day (on even days) • Acetaminophen with Codeine No.3 1-2 tabs every 6 hours PRN for pain • Diphenhydramine hydrochloride 25 mg every 8 hours PRN for itching ___________________________________ • DSS (Colace)100 mg twice daily • The patient is ordered to have daily dialysis. What is the rationale for this? ___________________________________ • The patient is going to hemodialysis at 0900 on an odd day. Which medication(s) ___________________________________ should the nurse hold before sending the patient? Why? • What nursing management considerations should be made for this patient? ___________________________________ • • • • • • Case Study Answers • The increased metabolic rate increases metabolic wastes, therefore wastes accumulate faster in those with ESKD –uremia develops, and they need daily dialysis to get rid of wastes. • Hold the beta blocker/antihypertensive • Sign for restrictive extremity,; assess AV fistula, assess VS for hypotension, Check IVF for rate, K+ & Mg++, assess for FVE (weight, etc), lung sounds, heart sounds, monitor for complications: pericarditis, pleural effusions, PNA, electrolytes, monitor diet, appetite, check pre/albumin. Check skin/skin care, wound healing, blood glucose, saturation, pain control. Peritoneal dialysis (PD) • • • • • 12 Peritoneal cavity is used as a semipermeable membrane Depends on both osmosis and diffusion Prescribed volume, dialysate (solution), dwell time 2-2.5 L, warmed, infused/drained by gravity Diet needs ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ • Complications • Peritonitis (abd pain, cloudy effluent is 1st sign), anorexia, hernia, LBP, altered body ima • Continuous or intermittent • CAPD (Continuous ambulatory peritoneal dialysis) • 4 x/day 7days a week • CCPD (Continuous cycling peritoneal dialysis) • “automated” • NIPD (Niight time intermittent peritoneal dialysis) • Cycles a night • • • • • • Easy access via intraabdominal catheter Less effective than HD Various solution gradients (low to high) Solution weight difference informs water loss/gain Various cycles (instill, dwell, drain) Labs denotes clearance of wastes PD Nursing Responsibilities • Assessment • Verify orders (solution, dwell time, cycles) • Assess VS, weight, breath sounds, signs of peritonitis, labs • Peritonitis rigid abdomen, pain, distension, increased WBC, check for sepsis) • Assess abdominal insertion site • Redness, swelling, drainage, pain, catheter stabilization, dressing, • Perform site care • Check lines, tubing, caps • Assess for mechanical complications • Confirm phase of therapy (infusion, dwell or capped) • Assess solution (before and after) • Evaluate efficacy of therapy • Evaluate patient self care knowledge & technique 13 Kidney Transplantation Preoperative • Basic preoperative care and checklist and focused transplant and renal assessments • Continue RRT as needed • Administer immunosuppressive drugs to prevent immediate graft rejection • Evaluations and diagnostics Postoperative • VS and hemodynamic monitoring • Measure UO every 30-60 minutes to determine transplant function • Diuretics • Indwelling urinary catheter care • Replace fluid mL for mL • Monitor electrolytes and renal function tests • Postoperative education include medications, S&S of rejection, VS, fluids, diet, prevent infection, support because there is no guarantee Kidney Transplant Complications • ATN • Electrolyte imbalances • Hemorrhage • Surgical emergency • Urethral anastomosis failure • Renal artery thrombus • Abrupt onset of HTN and reduced GFR • Infection • Immediate and ongoing risk due to patient’s immunosuppression • Monitor urine, surgical sites, LOC • Rejection Kidney Transplant Rejection • Hyperacute (humoral, B-lymphs) • Minutes to hours after transplant • Microcoagulation leads to ischemia causes necrosis • Acute (cell-mediated by T-lymphs) • Days to months after transplant • Antibody-mediated vasculitis (not clot) • Chronic • Chronic inflammatory response • Functional tissues, fibrotic scarring • Vessels damaged, progressive ischemia Kidney Transplant Rejection Symptoms • • • • • • • Elevated BUN/creatinine & K+ Decreased creatinine clearance Decreased urine output Graft tenderness Graft enlargement Low-grade temperature Elevated blood pressure Pharmacological management • • Rejection: cell-mediated immunity response Drugs target cell mediated immune response • Induction (started perioperative) • Maintenance (low dose) • Rescue (high dose more drugs)-immunosuppressants • Side effects • Secondary infection, hepatotoxicity, nephrotoxicity, delayed wound healing, hyperglycemia, fevers , itching, fluid overload Renal Cancer • Types: Benign and Malignant • Pathophysiology • Obstruction of flow and invasion of functioning tissues and lymph • Risk factors • Smoking, overuse of pain killers, chemical exposure, genetics • S & Sx • Hematuria, dysuria, frequency, urgency, fever, HTN, abdominal mass or lump, flank pain, persistent fatigue, rapid/unexplained weight loss, edema in LE • Treatment • Radical/partial nephrectomy, radiation, chemotherapy • Cystectomy • Nephron sparing treatment, gene therapy, biological or immunotherapy Case Study Renal Cancer 14 ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ 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___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ • Your patient, a 42-year-old factory worker made an appointment with his PCP because h blood in his urine. • During the admission assessment he stated that he is a 2-pack-per-day smoker and just money problems (his twins just started college). He also stated that he worked, for 30 y contamination. • Upon physical assessment the patient c/o pain when you percuss his flank area but den • A CT and ultrasound are ordered, and both reveal a mass in the renal pelvis. • What risk factors for renal cancer does this patient demonstrate? List. • The diagnosis of renal cancer is made. What are the classic symptoms of this disease pr • Upon further evaluation, metastatic renal carcinoma is diagnosed, and the patient is sch this procedure? • The patient develops postinfarction syndrome. What clinical manifestations does the nu managed? Case Study Answers • Gender, tobacco, asbestos • Classic triad = hematuria, pain, and mass in the flank. Painless hematuria is the first sy • Renal artery embolism is performed to impede blood flow to the tumor. • Stimulates immune response • May also reduce the number of tumor cells entering the venous system during surg • S/Sx: pain localized to the flank and abdomen, elevated temp, GI symptoms • Treat pain with parenteral analgesics; acetaminophen for fever; antiemetics, restri Renal Surgery • Nephrouterectomy • Nephrectomy • Open, Laparoscopic, Robotic assisted: daVinci Surgical System Glomerulonephritis • Pathophysiology • Inflammatory reaction in the glomerulus. • Main cause is streptococcus • IgAN (glomerulonephropathy) • S/Sx • Sore throat, malaise, HA, increased BUN & creatinine, FVE, flank pain, increased BP anemia • Proteinuria, RBC casts, hematuria • Treatment • Get rid of strep • Dialysis • Diet (decrease Na++ and increase carbs) • BR • I & O and daily weights • Teach S & S of renal failure Nephrotic Syndrome • Pathophysiology • Inflammatory response in the glomerulus • Think inflammation for causes of nephrotic syndrome • S/Sx • Anasarca, hypoalbuminemia, proteinuria • Treatment • BR • Diuretics • Prednisone • Diet (decreased Na++ and increased protein) • Dialysis Common rule: Limit protein with kidney problems except with nephrotic syndrome 15 Notes _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ 16