Renal Physiology and Acute Kidney Injury

Week 6 Announcements ► Fuld, Research Honors, Policy Honors applications are open – check email for more information ► Midterm is next Wednesday during class time and in regular classroom Modules 1-6 Focus on diseases/conditions, risks, causes, pathophysiology, and symptoms...

Week 6 Announcements ► Fuld, Research Honors, Policy Honors applications are open – check email for more information ► Midterm is next Wednesday during class time and in regular classroom Modules 1-6 Focus on diseases/conditions, risks, causes, pathophysiology, and symptoms Know normal enough to help understand abnormal ► We will not have class after the exam ► Post-Renal worksheet due Friday, October 4th. at 11:59pm ► Plenty of office hours availability to discuss current content, study strategies, exam strategies: sign up in Canvas ► Please use the [email protected] email for all course communications ► Exam will be available for download on Monday October 7 th Midterm Information ► 60 questions, 90 minutes ► Case Studies, Multiple choice, SATA, Select “N”, drop downs (fill in the blank) ► Modules 1-6 – questions are mostly equally distributed ► We will stop the exam at the 60 minute point and allow those who have finished to leave the room Please sit in a place that facilitates a quick and quiet dismissal if you are generally a quick test taker Bring a minimum of belongings to facilitate a quick and quiet exit from the room You may not leave the room at any other time ► Grades and Post-exam review: 4:30p, Room TBD Renal Presentation Sarah Allgood with many thanks to Laina Parillo, RN, DNP, PhD Objectives for Today 1. An understanding of normal kidney functioning. Specifically, how the kidney… Filters blood (i.e. the nephron) Concentrates urine Maintains acid/base balance Maintains normal electrolyte levels 2. An understanding of how we monitor kidney function through lab work and clinical presentation 3. An understanding of different types of acute injuries to the kidney 4. An understanding of chronic kidney disease and its presentation Please Note ► Slide 37 in Renal Part 1 incorrectly states the action of ADH ► ADHincreases the permeability of the Distal Convoluted Tubule and Collecting Ducts to water This allows water to move from the urine and back into the blood stream This action creates MORE CONCENTRATED URINE This action also increases blood volume which will increase blood pressure Urine Concentration Case You are taking care of J.D., a 24-year-old diagnosed with diabetes insipidus, a disorder that causes decreased secretion of ADH. What does decreased secretion mean? –Lower levels of ADH being released by the posterior pituitary gland in brain Normally, where does ADH go after being released? –To the distal convoluted tubule and collecting duct What is the expected action of ADH? –Prevents water leaving the body in urine  puts that water back into the blood = more concentrated urine AND expanded Remember, JD is experiencing low ADH production ► What would you expect to see in J.D. in terms of: Urine output? (high, low, or normal) – Why? High output since lack of ADH acting in the distal convoluted tubule and collecting duct is preventing reabsorption of water out of the nephron and back into the bloodstream. All that water is leaving as urine. 7  Urine concentration (high, low, or normal) and color? – Why? Low concentration, very dilute, clear, low colored urine since lack of ADH acting in the distal convoluted tubule and collecting duct is preventing reabsorption of water out of the nephron and back into the bloodstream. All that water is leaving as urine. ► Blood pressure? (high, low, normal) Why? Low blood pressure: blood volume will decrease and blood concentration will increase since the lack of ADH acting on the nephron is allowing water to leave the blood as urine ► Whatother signs/symptoms do you think J.D. will be experiencing as a result of this condition? Tachycardia: the heart will receive signals to increase HR to compensate for low cardiac output (CO=SVxHR, SV = preload, afterload, contractility) Other signs of dehydration Extreme thirst: hypothalamus will respond to decreased blood volume and increased blood concentration (increased plasma osmolality) by triggering thirst ABG’s and Compensation ►A patient on your unit was admitted due to a recent opioid overdose, leading to respiratory depression. You draw an ABG, and it shows the following: pH: 7.25 (normal 7.35-7.45) CO2: 55 mmHg (normal 35-45) HCO3: 22 mEq/L (normal 22-29) ► What acid/base imbalance does this represent? Respiratory acidosis ► How do you think the nephron can help compensate (re-establish homeostasis) this imbalance? PCT (proximal convoluted tubules) and DCT (distal convoluted tubules) will reabsorb (put back into the blood) bicarb DCT will secrete (remove from blood and put into urine) hydrogen ions These two things will help to re-balance the blood pH Knowledge Check ► D.W.has hypertension and was prescribed the diuretic furosemide (Lasix) to decrease their BP. How do diuretics in general decrease blood pressure? – Help increase urine production  lowers blood volume  lowers blood pressure and/or reduces free fluid build-up in the body ► Furosemide (Lasix) acts at the ascending loop of Henle. Why is this important to know? – Loop diuretics can cause electrolyte imbalances (hypokalemia, hypocalcemia, and hyponatremia) because they block the active transport channels found there Knowledge Check ► Youcheck D.W.’s electrolyte levels a week later and note that they have a potassium level of 2.5 mmol/L (very low). What clinical manifestations would occur due to low potassium (Module 1)? Spastic paralysis, fatigue, cramps, cardiac issues including arrhythmias Acute Kidney Injury ►An acute/sudden decline in kidney function. Decrease in GFR Decrease in urine output Build up of waste products – Increased BUN & Cr levels BUN, Creatinine, and GFR ► What is BUN? Blood urea nitrogen Waste product from liver – liver produces ammonia which contains a lot of nitrogen. Nitrogen forms urea which is the filtered by kidney out of the blood ► What is creatinine? Waste product from muscle metabolism ► What is GFR? Glomerular filtration rate. Creatinine is used in a formula to estimate GFR ► We use BUN, creatinine and eGFR to assess kidney Tests of Renal Function ► Glomerular filtration rate: Rate that the nephron is filtering blood Adult Normal ► Creatinine (from plasma) Creatinine: Most common surrogate for GFR 0.7 – 1.0 mg/dl If creatinine doubles, the GFR has probably Adult Normal BUN: reduced filtration by 50% 8-21 mg/dl Takes 7-10 days to stabilize ► BUN (blood urea nitrogen) Indicates how efficient kidneys are at removing urea nitrogen, a waste product Levels increase as GFR decreases Tests of Renal Function: Urine Dipstick 18 Acute Kidney Injury Acute Kidney Injury (AKI) Pre-Renal Renal (Acute Tubular Necrosis [from Post-Renal (Hypoperfusion caused by ischemia or nephrotoxic agent], (Bilateral urinary tract hypotension, hypovolemia, acute glomerulonephritis, obstruction [ex. BPH, neurogenic sepsis, CHF, renal artery interstitial disease (ex. tumor bladder, renal calculi]) stenosis) growth) Mini Unfolding Case ► You are working as a nurse on a postpartum unit. Your patient just delivered baby Quinn. You are looking through a note from the patient’s OBGYN. It states that they found a congenital disease on the prenatal screening that causes an obstruction of the urethra, preventing the outflow of urine. What type of acute kidney injury are you worried about in this newborn? Post-renal injury/obstruction. The obstruction will block urine flow and cause a back-flow of urine up into the ureters and kidney. Mini Unfolding Case ► What is the term for a build-up of urine in the kidneys? Hydronephrosis. 21 Post-Renal Obstruction ► Blockedurine flow for any reason can lead to backpressure of urine from bladder back up into kidneys potentially causing issues Pregnancy Stenosis of ureters Stones ► Hydronephrosis Increased intra-renal pressure can cause: – Renal pyramid infarcts – Kidney cortex atrophies – Tubulointerstitial fibrosis: scar tissue in kidneys Mini Unfolding Case ► Quinn had surgery to correct the obstruction and it was very successful! You are about to discharge Quinn and family, but first the parent has a question about caring for their newborn. They say they heard that babies cannot have ibuprofen (an NSAID) until they are 6 months old. They want to know why this is because they take ibuprofen all the time. ► You are a very smart nurse and reply that ibuprofen is nephrotoxic and can be damaging to a baby’s kidney under 6 months old. What type of acute kidney injury would we worry about if a newborn was given an NSAID medication? Intra-renal/Renal injury. NSAIDs can cause acute tubular necrosis, as they are nephrotoxic agents. Intra-Renal Injury/Obstruction ► Intrarenal: intrinsic kidney injury, often from prolonged or severe renal hypoperfusion ► Common causes: Prolonged pre-renal injury, radiographic contrast material, aminoglycosides, nonsteroidal anti- inflammatory drugs (NSAIDs), or other nephrotoxic substances), glomerulonephritis (GN), This Photo by Unknown Author is licensed under CC BY-NC-ND etc. 24 Mini Unfolding Case ► Quinn and family are discharged home and are happy and healthy! ► When Quinn turned 8 months old, their parent enrolled them in daycare. At daycare, there was an outbreak of viral gastroenteritis (the “stomach flu”). Quinn caught it and is very dehydrated from GI losses (diarrhea/vomiting). What type of acute kidney injury would we worry about with prolonged dehydration? Pre-renal. Dehydration can lead to hypo-perfusion of the kidneys. ► What are some other hemorrhage, causes of thisdiuretics, type of acute kidney injury? Hypotension, excessive sweating, heart failure 25 Pre-Renal Injury/Obstruction ► Pre-renal (reduced renal perfusion, typically reversible) Hypotension, volume depletion (GI losses, excessive sweating, diuretics, hemorrhage), reduced CO Decreased renal perfusion (often due to hypovolemia) leads to a decrease in GFR, which if prolonged or severe can progress to an acute kidney injury and progress to an intrarenal condition such as acute tubule necrosis 26 Case Study ► You are a nurse in the emergency department caring for 32yo who tells you their urine has been abnormally dark – almost the color of coffee. ► They also tells you they have noticed a red, patchy rash on their face and that they've been having muscle and joint pain. 27 Case Study ► On your physical exam, they are awake, alert, and oriented. Not pale or jaundiced, however you note a “butterfly rash” on their face. They have bilateral pedal edema 2+, but no edema noted elsewhere. Vitals are as follows: Temp: 37°C (98.6°F). BP:145/97 HR: 122 beats/min RR: 18 breaths/min ► What is abnormal about this person’s vitals and/or physical exam? ► What additional information/lab-work would you need? Case Study Continued… ► Youdecide to perform a urine dipstick and send off a CMP and CBC. The urine dips shows the following: Protein: +1 Blood: +3 Image from: Roberts, 2007 29 Case Study Continued… ► Their CBC and CMP come back with the following abnormal values: Albumin: 3.0 g/dL –Normal is 3.5-5.5 Creatinine: 3.0 mg/dL –Normal is 0.7-1.0 BUN: 30 –Normal is 8-21 mg/dL 30 Case Study Continued… With this information, what might be going on with this person? 31 Case Study Continued… This patient was diagnosed with Lupus, and their symptoms are associated with a nephritic syndrome 32 Nephritic Syndrome Clinical Manifestations  Nephritic syndrome is not a disease by itself. It is a combination of symptoms and laboratory findings: Hematuria –Urine contains massive amounts of blood and varying degrees of protein, which is NOT usually severe (300mg to 3g/day) and lipids and either a microscopic amount of blood or no blood at all. 46 Nephrotic Syndrome ►Nephrotic syndrome is not a disease by itself. It is a combination of symptoms and laboratory findings: Generalized swelling (swelling is most common around the eyes, in the legs and the scrotum in boys) Low albumin level in the blood Large amounts of protein in the urine Elevated cholesterol 47 Case Study 2 Continued… ► What changes to Starlings forces may contribute to the edema seen in this case? Hint: in nephrotic syndromes we see decreased levels of albumin in the blood Decreased capillary oncotic pressure, leading to decreased re- absorption of fluid from the interstitial space back into the capillaries. 48 Case Study 2 Continued… ►A year later, you assigned as the nurse for M.J. on a renal medical surgical unit. M.J.’s kidney function has declined to less than 25% of normal and is classified has having chronic kidney disease (CKD). ► What were M.J.’s risk factors of developing CKD? Diabetes, hypertension, intrinsic kidney injury. 49 Case Study 2 Continued… ►What physical findings do you expect to see on your patient assessment? ►What lab values do you expect to see in the chart? 50 Case Study 2 Continued… Clinical Manifestations Labs ► Hypertension ► Anemia RAAS: renin will be activated Lack of EPO because of decreased renal ► perfusion Hypocalcemia and Vitamin D Deficiency ► ► Hyperphosphatemia Edema From loss of protein and high blood ► Hypoglycemia pressure (fluid overload) ► Accumulation of metabolites ► Other S/S: ► Azotemia and uremia Anorexia, nausea, vomiting, diarrhea or constipation, malnutrition and weight loss, pruritus, edema, neurologic and cardiovascular disease, and skeletal changes 51 Time for Your Questions – Any and All Modules on Exam 52