11. study guide - renal.docx

Renal Function Functions of the kidneys Excretory functions: excrete substances that are not needed to maintain normal body fluid composition, or that are in excess Excrete metabolic wastes: -Urea: waste product from protein metabolism -Uric Acid: Waste product from nucleic acid breakdown from consu...

Renal Function Functions of the kidneys Excretory functions: excrete substances that are not needed to maintain normal body fluid composition, or that are in excess Excrete metabolic wastes: -Urea: waste product from protein metabolism -Uric Acid: Waste product from nucleic acid breakdown from consumed meat. -Creatine: muscle metabolism when muscles break down creatine phosphate for energy -Drugs: Kidneys also breakdown drugs so that they don’t build up to toxic levels in the blood Regulate Fluid Volume: (BP) Gets rid of extra fluid that we don’t need, and this also affects BP Regulate Electrolyte Balance: Gets rid of extra electrolytes Regulate Acid-Base Balance: Kidneys are the main way to get rid of extra acids/bicarb from the body Endocrine functions: produce chemical mediators that travel through blood to exert actions at distant sites Produce Renin: (Blood Volume & BP) RAAS system: When blood flow to the kidneys is low, they produce renin, which catalyzes the formation of Angiotensin I, which then is converted to Angiotensin II in the lungs. Angiotensin II tells the adrenal cortex to make Aldosterone, which makes you retain Na+ and lose K+ and retain water. Angiotensin II regulates volume, BP, Na+ and K+ levels. It is also a vasoconstrictor to control BP. Produce Erythropoietin: Stimulated by hypoxia, the kidneys produce erythropoietin that tells the bone marrow to make more red cells. Activates Vitamin D: (w/ the liver); We get vitamin D from the skin and food and it is activated first in the liver, and step 2 takes place in the kidneys. -Vitamin D is important for helping to absorb calcium. Structure of kidneys Functional unit of kidney: nephron; Each kidney has more than 1 million nephrons. There are two components in each nephron: Glomerulus: filters blood; the vascular component which filters blood through the nephrons to be cleaned. System of tubules: selectively reabsorbs or secretes substances into urine; Collects filtrate that eventually becomes urine. Gross structure of kidney Outer cortex: contains glomeruli, and portions of tubules Inner medulla: mostly the tubular portions of nephrons Renal calyces and renal pelvis: collect the urine that empties from tubules, and funnel it to ureter Normal physiology: Renal system Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Nephron – structure/function -Each kidney is supplied w/ blood from the renal artery that branches off the aorta. -When the renal artery enters the kidney, it further divides into smaller and smaller arteries and each nephron has its own set of arterioles. Vascular component afferent arteriole: receives blood from branches of renal artery, supplies blood to glomerulus glomerulus: capillary bed from which fluid and substances from the blood are filtered to form urine filtrate (which collects in Bowman’s capsule). Content of filtrate determined mostly by integrity of glomerular basement membrane -Glomerulus has 3 layers: The important one is the middle layer: Basement Membrane: It’s what determines what will pass into the urine and what won’t. The size of the spaces between the fibers determine the what will pass; it’s like a screen that determine what’s too big to pass to the urine; Usually RBCs and plasma proteins are too big to pass to the urine. -Once the blood goes through the glomerulus anything that doesn’t get pushed out into the tubular component then travels to efferent arteriole. efferent arteriole: along with afferent arteriole, selectively constricts/dilates to regulate blood flow/pressure within glomerulus, which, along with arterial BP, determines GFR (normally around 125 ml filtrate formed per minute) How much filtrate gets pushed out of the glomeruli per minute and is pushed out through the tube and goes on its way to become urine. -Afferent and efferent control how much filtrate is made by constricting or dilating to adjust the pressure in the glomerulus. -The higher the pressure in the glomerulus, the more filtrate you make. peritubular capillary network: surrounds tubule, allowing for movement of water and solutes between blood and urine filtrate -Surrounds the tubular component of the nephron -Allow for reabsorption into capillary network or getting rid of more substances -Allow us to change the composition of the filtrate as it moves through the nephron vasa recta: long, looping capillaries near kidney medulla, important in concentrating urine. From here, blood then enters venous circulation, via renal veins Tubular component -Composition changes as it moves through tubules to fine tune the urine to get rid of what we don’t want and keep what we do want -Of the 125 mL of filtrate, only 1 mL is actually excreted as urine; most of the filtrate gets reabsorbed somewhere along the way. You make 1mL per minute, so about 60mL or urine per hour. -If Urine output is below 30-40mL/hour we worry that person is going into renal failure proximal convoluted tubule: extends from Bowman’s capsule reabsorbs nutritionally important substances like glucose, amino acids, water soluble vitamins, etc. Things like glucose have a limit as to how much can be absorbed at once. If the amount in filtrate is greater, not all of it will get reabsorbed, so that is why there is glucose in urine like people with diabetes. So much glucose in the blood, so a lot of the glucose appears in the filtrate because the nephron can only reabsorb so much, so if there is glucose in the urine, that means that the blood glucose is very high and not being controlled. reabsorbs large amounts of electrolytes; 65-85 % of the electrolytes get reabsorbed here. If you reabsorb a lot of Na+ or Cl-, water will follow, so a lot of water is reabsorbed here as well. water passively follows loop of Henle descending limb – permeable to both water and solutes ascending limb – permeable to solutes only Result: produces dilute urine filtrate, plus generates a high osmolarity gradient in medulla for fine-tuning of water reabsorption from collecting tubules distal convoluted tubule -By the time the filtrate gets here, it is very dilute; as dilute as it will get. diluting segment: further dilutes filtrate late distal tubule: site of aldosterone’s action (fine-tunes sodium and potassium concentration of urine); also involved in fine-tuning of acid-base balance -Aldosterone makes you retain Na+ and lose K+, and retain water, so depending on how much aldosterone is present, you will retain Na+ and lose K+. This happens at the end of the distal tubule and the beginning of the collecting tubule. -Where we also regulate acid-base balance; this is where the kidney gets rid of acid or bicarb. collecting tubule: empties into renal calyces/pelvis cortical collecting tubule: same as late distal tubule inner medullary collecting tubule: site of ADH’s action (fine-tunes concentration of urine by influencing how much water gets reabsorbed) -At the end of the collecting tubule is where ADH is working; Comes from the posterior pituitary and it makes you save water so there is less water. Result: about 1 of the 125 ml of filtrate formed each minute is excreted as urine (the rest is reabsorbed) Pathological change: Renal artery stenosis/occlusion w/ a clot or stenosis from atherosclerosis Pathological change: altered permeability of basement membrane due to damage Pathological change: damage to tubules due to ischemia Pathological change: abnormal levels of aldosterone or ADH -Diuretics act on certain parts of the tubules. The earlier in the tubule that the diuretic acts, the more powerful that diuretic is. -One of the most powerful are looped diuretics; work in loop of Henle to block reabsorption of water so you lose more water in the urine. -Thiazide diuretics are not as powerful and work in the distal tubule. -Collecting duct is where the K+ sparing diuretic works Nursing problem: Blood Flow to kidney drops from stenosis or occlusion, so it cannot make urine; If there is a problem with the renal artery, it cannot make urine and may go into renal failure. Nursing problem: If there is a disease like nephrotic syndrome, membrane gets damaged and things will leak into urine that don’t belong or substances lost in urine like RBCs and we can develop anemia; if we lose antibodies, we will have immunity problems, or if we lose clotting factors, we will have problems with bleeding; if albumin gets lost, that tells us that there is kidney damage and we will see edema because if we lose albumin, we lose colloidal osmotic pressure so fluid starts leaking out of the capillaries. Nursing problem: Acute tubular necrosis due to ischemia; this will change permeability of tubular component and may cause acid-base imbalance, electrolyte imbalance. Nursing problem: The nephron may be working fine, but if there is abnormal aldosterone and ADH, we may still see fluid and electrolyte imbalances Normal physiology: Renal system Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Regulation of renal blood flow – 3 mechanisms that control constriction and dilation of afferent and efferent arterioles: -The goal of all of the mechanisms is to keep GFR at a constant rate Neural control mechanism – through sympathetic nervous system. Helps regulate constriction/dilation of afferent and efferent arterioles 🡪 adjusts blood flow to keep GFR relatively constant helps 🡫 UO and maintain BP during shock states Humoral control mechanism – through substances that cause constriction or dilation of renal vessels (ex: angiotensin II, dopamine, prostaglandins, etc.) -Hormones that are in the blood that make the arterioles constrict or dilate to maintain GFR at a constant rate Autoregulation – through specialized cells in kidney called the juxtaglomerular complex. Regulates synthesis/release of renin based on feedback re: blood pressure in afferent arteriole, etc. -Mechanisms through which the kidney regulates its own blood flow -The primary autoregulation is juxtaglomerular apparatus; they monito BP in afferent an composition of filtrate in distal tubule and give feedback to kidney to decide how much renin should be released Pathological change: abnormalities in function of these mechanisms Nursing problems: Change in blood flow to kidney can change composition of urine, how much urine is made, and this can lead to fluid/electrolyte imbalances and BP problems Normal physiology: Renal system Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Urinary tract defenses (to keep urinary tract sterile and free from infection) “Washout phenomenon” – bacteria flushed from bladder/urethra during voiding = peeing -When the bladder empties, it flushes out any organisms that may have entered through the urethra Protective mucin layer = bladder lining -Protects from infection/invasion by pathogens -Prevents urine from getting reabsorbed in the bladder -Secretory IgA in the mucus layer-antibodies to defend bladder against pathogens Peristaltic movements of ureters facilitate urine flow, prevent urinary stasis Local immune responses (presence of phagocytes, secretory IgA) Pathological change: Infection PF: UTI altered urinary tract defenses immunosuppression urinary obstruction = urinary stasis -Scar tissue, kidney stones, benign prostatic hyperplasia urinary retention = pooling of urine in bladder, ischemia of bladder wall -Urinary retention causes loss of washout phenomenon and urine is pooling in the bladder and it’s a good medium for bacterial growth -Retention could be due to smooth muscle issues or voluntary retention -Immobility: patients use bedpans in hospitals so it’s hard to completely empty the bladder -As the bladder gets full, the bladder wall starts to distend and as it stretches, it compresses the blood vessels in the bladder wall, so the it gets a little ischemic which makes it more susceptible to infection urinary reflux -Urine going the opposite way- UT is most sterile at kidney end and least sterile at urethra end, so if urine is going backward, it increases chances of infection gender -Women get UTI’s more due to shorter urethra and it’s closer to GI tract and vagina so it’s easier to contaminate age -Due to decreased immune system -The older the person is, the less efficient the immune system is -Older people also tend to have more chronic diseases that cause immobility; more likely to have diseases that increase risk like older men who have benign prostatic hyperplasia where urethra is pinched off due to enlarged prostate -Also, older people are more likely to have diabetes and blood sugar gets high and is lost in the urine and jmakes the urine a better medium for bacterial growth instrumentation Invasive procedures like catheters even if there is sterile technique because organisms can climb up and cause infection Nursing problem: UTI: A general term that refers to an infection somewhere in the urinary tract -Urinary tract is supposed to be sterile, so if pathogens get in, this could cause infection -Some infections could be mild and just cause mild discomfort and not interfere with normal kidney functions -Some infections can become severe or chronic at which point they might produce scar tissue that could cause permanent damage which could affect kidney function -The goal is to identify the problem early before they cause severe problems -In most cases, UTIs cause discomfort and inflammation but usually don’t interfere with normal kidney functions Example of disorder: Cystitis -Cystitis is a general term for bladder infection Assessment findings: -Pain or burning when urinating = dysuria; caused by irritation from infection and inflammation in bladder and irritation in the urethra -Blood in urine -Frequency- urinating often; irritation gives a sensation that you have to urinate more often -Urgency due to irritation- have to go in that moment -Lower abdominal/lower back discomfort and cramping occurs sometimes -Mild fever and malaise -Cloudy urine is very common (white blood cells and bacteria in urine) Example of disorder: Acute Pyelonephritis -Pyelonephritis is a general term for kidney infection, more severe than bladder Assessment findings: -By the time the kidneys get infected, the person will be sicker than with cystitis -Higher fever, chills, and more malaise -Cloudy urine, but likely to see blood in the urine; really bad smell -Flank pain on the side of the infected kidney -Sometimes we see symptoms of both cystitis and pyelonephritis because a lot of the time it starts as a cystitis and the organisms travel from the bladder up the ureter, and to the kidneys so now the person will have both infections, but not all people get kidney infections because of cystitis -If pathogens didn’t enter from bladder and traveled up to the kidneys, then they probably entered from the blood; all the blood in the body circulates through the kidneys, so if organisms are in the blood, they can make their way to the kidney and start an infection, so a person can just have signs of the kidney infection without the bladder infection. -If we catch these infections before they become severe or chronic, the kidneys should still be able to carry out normal functions Antibiotics: Depending on whether its kidney or bladder, we use either oral AB or through IV -Kidney infections are treated more aggressively to prevent permanent kidney damage (renal failure) -Bladder: a few days of oral antibiotics -Kidney: a few days of IV antibiotics followed by a couple of weeks of oral antibiotics to make sure that the infection goes away so that it doesn’t become chronic and cause permanent damage -Push fluid to flush organisms out of urinary tract with washout phenomenon -Correct any PF that may have caused it like retention or reflux to prevent future UTIs vnb Normal physiology: Renal system Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Urinary tract components and urine flow Kidneys – urine drains from collecting tubules into renal calyces/pelvis Ureters (urine flow facilitated by peristaltic movements) Urinary bladder Urethra Pathological change: obstruction of urine flow PF: urinary calculi -Most common cause of UT obstruction benign prostatic hyperplasia -Where prostate enlarges and pinches off the urethra congenital defects scar tissue r/t infections or inflammation -Scar tissue that causes obstructions in the ureter or in the renal calyx tumors pregnancy Nursing problem: Obstructive Disorders: -Things that lead to obstruction of the flow of urine out of the urinary tract; any obstruction in the pathway from the kidneys to the bladder to the ureter to the urethra to the outside; not obstruction in blood flow, but obstruction of urine. -If the obstruction is not too severe, the worst that would probably happen is urine stasis, UTI, etc. -If obstruction is more severe, we may develop a hydroureter or hydronephrosis. -Urine is backing up behind the obstruction (like kidney stone) and as the urine collects, the ureter starts to get distended = Hydroureter -The ureter can only distend so much and if urine continues to collect, eventually, the pressure will cause kidney distention =Hydronephrosis -The kidney can only distend so much and overtime, the pressure will start to compress the blood vessels in the kidney and it can cause ischemia and cause acute renal failure (Worst case scenario) -Highest priority concern when we have a UT obstruction is to assess if they’re going into acute renal failure and to intervene before that happens Example of disorder: Renal Calculi/Nephrolithiasis/Urolithiasis (Kidney Stones/name depends on location) Pathophysiology involves one or more of the following factors: Most likely to cause kidney stones to develop supersaturation of urine with stone components (ex: calcium oxalate, calcium phosphate, struvite, uric acid, cystine) -Saturation of urine with a certain substance that the stones are made of -Stones are most commonly made from calcium; They can be calcium oxalate or calcium phosphate (75-85% of stones are calcium-based) -Saturation is usually caused by increase of the substance like calcium and like from bone disease where calcium is leaving the bones or due to immobility and is excreted in the urine or more commonly, the way that the urine becomes supersaturate is dehydration because when you’re dehydrated, you excrete less fluid in the urine, so whatever is in the urine gets super concentrated even if there is a normal amount of calcium, but low fluid makes the urine saturated -Parathyroid disease can also cause supersaturation of urine with calcium because parathyroid regulates calcium balance and if it doesn’t function, you may have more calcium in the blood and urine deficiency of endogenous inhibitors of stone formation -Kidneys makes inhibitors that prevent substances from precipitating out of the urine and forming stones triggering substance -Substances that serve as nucleus for substances to collect around to make a stone, like blood in the urine, pus, dead tissue, a foreign substance like a catheter in the UT urinary stasis -If urine is supersaturated with a substance, that substance is more likely to precipitate out and form a stone easier if the urine is stagnant urinary pH conducive to stone formation -Depending on substance that urine is saturated with will depend on how easily they precipitate out -There are also struvite stones, uric acid stones, cystine stones, etc. -Struvite is magnesium, ammonium, and phosphate combined -If we know what the stone is made of, we can alter pH, change diet, or give meds to try to keep the substance out of the urine to prevent a second stone and to educate the patient -To find out what type of stone it is, we have patient strain their urine and we send to lab to analyze what the stone is made of Assessment findings: -Pain is the primary symptom; usually in the flank depending on the side of the kidney, can radiate to the upper-outer quadrant of the abdomen and head towards the groin because it follows path of ureter; usually a colicky pain (renal colick) a cramping or spasmodic pain that comes and goes in waves because if the stone is stuck in the ureter, the ureter generates peristaltic waves to try to pass the stone down -Pain is severe and triggers nausea, vomiting, tachycardia, pale clammy skin due to SNS activation -How intense the pain is not necessarily related to degree of distention itself, but how quickly the distention develops -Blood in the urine = Hematuria; Usually happens when the stone is passed down the ureter, it may scrape the sides of the ureter walls and cause bleeding -Primary issue with kidney stones is the pain unless the hydroureter and hydronephrosis occur, then there is risk for renal failure. Pain Medication: -Usually narcotics or opioid analgesics like morphine -Toradol-injectable NSAID so more powerful Fluid: -If the stone is small, we chose the “push fluid and ambulate method” to flush stone out by patient drinking and walking around to flush it out Other: -If bigger stone, pt. cannot pass on their own, we do ESWL (extra-corporal shock wave lithotripsy) and use shock waves that we focus on the stone to try to shatter the stone into smaller pieces, so they can pass the stone in the urine Surgery: -If stone is bigger or there are many and we can’t shatter, we can do percutaneous removal and go in surgically with nephroscopy tube to remove the stone through the kidney by sucking the stone out or lasering them. Also a cystoscopy can go through urethra and ureter and into the kidney to get it out -If the stone is very big (staghorn calculus), it would have to be removed by open surgery - need to find out what the stone is made of in order to educate best. We try to educate the patient on how to prevent future stones -Meds to change urine pH based on the substance of the stone -Correct any PF that may have contributed or caused -Important to drink water to keep the urine dilute Normal physiology: Renal system Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Kidneys Excretory functions: excretes substances not needed by body, or that are in excess Metabolic wastes Fluid Electrolytes Hydrogen/bicarbonate ions (acids/bases) Endocrine functions: produces chemical mediators that exert actions at distant sites Renin (part of renin-angiotensin-aldosterone mechanism) – helps regulate BP and blood volume Erythropoietin – stimulates RBC production by bone marrow Activates vitamin D – helps regulate calcium balance Pathological change: failure of kidneys to perform normal functions PF: (for AKI) -Not time-related, but location- related classifications; refer to where the problem is Prerenal failure: -Means that the cause of the failure happened before it got to the kidney(Kidney tissue is not damaged) in terms of urine production. So, the only thing that happens is that blood has to flow to the kidney. If the kidney doesn’t get any blood to filter, it can’t make urine r/t impaired renal blood flow to kidney without ischemic injury/damage yet (ex: severe bleeding, hypovolemia, atherosclerosis in renal artery, clot, shock, low CO, etc.) Intrarenal/intrinsic renal failure: -An issue with the kidney itself injury to nephron (ex: toxic agents, immune mechanisms, ischemic injury, etc.) -things that actually damage the kidney like AI disease or infection that damaged the kidney, or a nephrotoxic drug (certain classes of antibiotics, antivirals, dye for diagnostic tests) that can cause kidney damage -If kidney is not getting blood flow and causes ISCHEMIC damage to kidney tissue (only if damage is caused) Postrenal failure: -The initial cause happened somewhere after the kidney in the UT r/t obstruction to urinary outflow (ex: renal calculi, etc.) Kidney did it’s job but urine not escaping 0 -Problem is in the UT after the kidney like hydronephrosis (initial problem is the stone that got stuck in the ureter and caused back pressure and damaged the kidney) PF: (for CKD) severe/chronic infection glomerular disorders systemic diseases such as diabetes, lupus, etc. urinary obstruction uncontrolled HTN - stress on blood vessels from high pressure can damage the vascular component of the nephrons Nursing problem: Renal Failure: A state where kidneys are unable to remove metabolic waste and not able regulate fluid, electrolyte, and acid-base balance -If kidneys cannot remove waste products, there will be a lot of waste in the blood -If kidneys cannot regulate electrolytes and acid-base, we will see imbalances which will affect almost every system in the body Example of disorder: Acute Kidney Injury (AKI)/Acute Renal Failure (ARF) -Comes on more suddenly -Can be reversed if caught on time before permanent damage occurs and can progress into chronic renal failure -Can reverse all 3 of the classifications if caught in time before damage or before it’s too severe where you can’t repair -More due to chronic conditions like hypertension Assessment findings: Example of disorder: Chronic Kidney Disease (CKD) -More due to chronic conditions like chronic hypertension high pressure can damage arterioles in nephron or Diabetes where high sugar concentration damages blood vessels in kidney -Occurs more gradually, but is not reversible once it occurs Stages in progression: (older terminology) diminished renal reserve: GFR 50% of normal, no s/s yet renal insufficiency: GFR 20-50% of normal -> isosthenuria (pt. is putting out large amounts of dilute urine due to kidney still making urine but can’t appropriately concentrate it) , azotemia: high level of nitrogenous waste product in the blood urine like urea, creatinine, uric acid, etc. (first 2 symptoms that we see when GFR drops) Then we move from azotemia to uremia where nitrogenous waste products are high enough that they are causing the symptoms (symptoms: brain function is decreased (uremic encephalopathy), can lead to coma, RBC and WBC disfunctions, may be at an increased risk of infection) renal failure: GFR <20% of normal -> uremia end-stage renal disease (ESRD) GFR <5% of normal -> requires dialysis or transplantation for survival -as GFR drops and pt. starts to develop symptoms, the first 2 that we may see are: Isosthenuria: patient is putting out large amounts of dilute urine due to kidney still making urine but can’t appropriately concentrate it. (Polyuria) An early stage of kidney failure so kidney can still make urine. Can lead to dehydration. Azotemia: high level of nitrogenous waste product in the blood urine like urea, creatinine, and uric acid etc. Then progresses to uremia. Uremia: where nitrogenous waste products are high enough that they are causing the symptoms Stages from National Kidney Foundation Practice Guidelines (newer) Stage 1 – kidney damage with normal or increased GFR (≥ 90 ml/min/1.73 m2) Stage 2 – kidney damage with mild decrease in GFR (60-89) Stage 3 – moderate decrease in GFR (30-59) Stage 4 – severe decrease in GFR (15-29) Stage 5 – kidney failure (<15, or on dialysis) -Labels are different, but the progression in stages is similar Assessment findings: -Seen in both Chronic and Acute: Due to Waste Build-Up: (all due to uremia) -If not getting rid of waste products, we will have azotemia and uremia where levels of waste products go up in the blood -BUN (Blood urea nitrogen) tells level of urea in the blood; urea is waste product from protein -Creatinine is a waste product from skeletal muscles breaking down creatine phosphate for energy -Uric Acid is a waste product that you get when you break down nucleic acids when you eat meat. -Creatinine is a more definitive test to evaluate kidney function because not much else causes creatinine build-up in the blood other than impaired kidney function. -BUN we look at in conjunction with creatinine, but a lot of other things can affect BUN, like a high protein diet or if starving person. They will breakdown protein in the body for fuel; GI bleed due to ulcer and cells get digested (cells have protein); dehydration can make BUN go up -If BUN and creatinine are high, then we worry about the kidney function -Uremic Encephalopathy- brain is not functioning as well as it should be due to the build-up of waste products in the blood; lethargy, confusion, or late stages can fall into a coma due to build-up of waste products -Bleeding like bruising, nose bleeds (epistaxis), GI bleeds due to platelets and clotting factors not functioning properly in the waste product build-up -Immune system may be impaired and cause increase risk for infection because WBCs have trouble functioning in the waste -Peripheral neuropathy: restless leg syndrome, burning sensation of the feet, paresthesia -Anorexia, nausea, vomiting due to high levels of waste -Pruritis (Itching) due to increased waste and because body tries to get rid of waste through skin and we see uremic frost: urea and phosphate crystals that were excreted through the sweat and crystalized -> causes the itching -Can’t get rid of drug waste products so we will see drug toxicity Due to Fluid Imbalance: -Dehydration due to ithostenuria and large amounts of urine in early stages of chronic failure -In acute renal failure, we tend to see ithostenuria when pt. is recovering -Fluid overload (Oliguria) - due to not being able to get rid of the urine: pulmonary and peripheral edema -Increased BP -Weight gain -Neck vein distention -Signs of R and L heart failure due to overworking of the heart. -BP and weight will increase which can predispose to heart failure due to increased blood volume. - high K, high Phosphorus, low Calcium- since not urinating as they should. With high K, worried about cardiac dysrhythmias since K helps with action potentials and the heart uses them. With phosphorous, think of the calcium phosphorous balance they have an inverse relationship. When phosphorus goes up, calcium goes down, because vitamin D is lacking leads to no absorption of calcium from food we eat. Parathyroid starts to make more CA by stealing it from bones, leads to renal osteodystrophy (CKD-mineral bone disorder) Due to Electrolyte Imbalance: - Common is increase in potassium; When we eat K+ in food, one of the normal ways to get rid of the extras is through the urine. If kidney is not making urine to get rid of extra potassium, you see a build-up and we have concerns for cardiac dysrhythmias -Phosphorus levels go up too and calcium will go down due to reciprocal relationship of calcium and phosphorus. To keep phosphorus levels normal, you must excrete an equal amount in urine of what you consumed in the diet. -Kidney helps activate Vitamin D, which helps absorb Calcium and if kidney fails it cannot activate vitamin D and calcium levels will drop. - Hypocalcemia: may not see CATS because if calcium drops, parathyroid will make PTH to make sure that calcium doesn’t drop and if it does, we can take calcium from the bones, so we see weak bones: Renal Osteodystrophy or CKD mineral bone disorder and can cause pathological fractures with minimal impact that shouldn’t normally fracture the bone. Acid-Base Balance: -Patient will go into Acidosis because cells are always making acid and only carbonic acid is gotten rid of in lungs and kidneys do the rest so if kidneys fail and not making urine to get rid of the acid, pH will drop and become acidic; acids accumulate faster than the bases because cells always make acids as part of metabolism, not bases. Endocrine Functions: -Kidneys make erythropoietin and tells bone marrow to make red cells; If they fail then -> Anemia due to not enough red cells being made -3 more likely seen in chronic: -Renal osteodystrophy because this takes time and you won’t see in acute -Anemia because you have to wait for current red cells to die off and not get replaced -Uremic Frost because it takes time for body to try to get rid of waste products in sweat Acute: ID cause & correct it and give kidney time to recover. In the mean time we treat symptoms like high BP, electrolyte imbalance Chronic: Can’t reverse but ID cause and get rid of cause to slow down the progression -Treat symptoms like high BP with meds; if anemic, we can give synthetic erythropoietin; calcium + vitamin D supplement to prevent weakened bones Renal Diet- -Low protein- because they have a lot of urea so there will be high waste products -Low K+ because they already have a lot -Low Na+ because they already have fluid overload -High calorie because if they don’t have enough calories, they will start to break down own body protein and create urea