【持续性肾脏替代治疗crrt英文精品课件】 to “pee” or not to “pee”—the kidney in health and disease

To “Pee” or not to “Pee”the KIDNEY in health and disease,Barb Bancroft, RN, MSN, PNP CPP Associates, Inc. Chicago IL (BB),Renal diseases are responsible for a great deal of morbidity but are not major causes of mortality. Approximately 35,000 deaths are attributed to renal disease per year (as compared to 750,000 deaths due to heart disease, 400,000 due to cancer, and 200,000 due to stroke). Millions of persons are affected annually by nonfatal kidney diseases, most notably infections of the kidney or lower urinary tract, kidney stones, and renal obstruction. Twenty percent of all women have a urinary tract infection or kidney infection at some time in their lives, and at least 1% of the U.S. population develops kidney stones. Dialysis and renal transplantation keep many people alive who would formerly have died of renal failure, adding to the pool of renal morbidity.,The kidney as an innocent bystander,In addition to primary kidney disease, the kidney is involved in many systemic diseases and conditions The deadly duo-“Sugar” diabetes and hypertension HF (Heart failure) Septic shock, hypovolemic shock DIC (Disseminated intravascular coagulation),The kidney as an innocent bystander,Autoimmune diseaseslupus, autoimmune glomerulonephritis, Goodpastures disease, Wegeners granulomatosis, sarcoidosis Toxic effects of drugsaminoglycosides, radiocontrast agents, amphotericin, cisplatinum, acetaminophen Cancermalignant infiltration, multiple myeloma,Lets start at the very beginning,How much embryology did you get in nursing school? The sperm meets the egg and then,Embryologythe development of the kidney,The kidneys and the ears from the same mesenchymal tissue The otorenal axis Nephrotoxic drugs and ototoxc drugs,Time to refresh your memory with a little “gross” anatomy,Kidneys located in the retroperitoneal space between T12 and L3 Right lower than the left,The kidneyretroperitoneal space,CVA tenderness Acute pyelonephritis Glomerulonephritis Palpation? Can you palpate the kidney in an adult? Not unless the kidney is HUGE(tumor) Polycystic kidney disease (PKD),Polycystic kidney disease,Autosomal dominant polycystic kidney disease (ADPKD) 1/1000; CAA; 4-10% of patients w/ kidney failure on dialysis or needing transplant 50% by age 50 have renal failure Kidneys can be the size of a football,Gross anatomy,Renal capsule Renal cortex (glomeruli) Renal medulla (tubules) renal papillae the renal interstitium (columns) renal pelvis (pyelo)/calyces Pyelonephritis vs. glomerulonephritis Plus the associated structures (ureters, bladder, urethra, prostate),Gross Anatomyblood supply,Aortarenal arterybranches into arcuate,Blood supply to and from the glomerulus,Afferent arteriole delivers blood to the Glomerulusa tuft of capillaries Blood exits via the efferent arteriole,Gross Anatomyblood supply,renal vein inferior vena cava right atrium,What can go wrong with the blood supply into and out of the kidney?,Atherosclerosis of the renal artery or aorta Hypertension with decreased blood flow Diabetes with hypertension and atherosclerosis Clamping the aorta above the renal artery (AAA surgery) Sudden cessation with a renal artery embolus,What can go wrong with the blood supply to and from the kidney?,Decreased blood pressure with acute blood loss and hypovolemic shock, heart failure, dehydration, septic shock Renal artery vasoconstriction with NSAIDs; efferent arteriole vasodilation with ACE inhibitors Microthrombosis of glomeruliDIC (disseminated intravascular coagulation) Immune complex deposition in the glomerulus triggering the inflammatory response (lupus nephritis),Atherosclerosis of the aorta and renal artery,Fatty plaques in the renal artery-chronic decreased blood flow to the kidney Renal atrophy/increased release of reninangiotensin aldosterone (RAA) Hypertension CKD (chronic kidney disease) Which comes first? Whos at risk?,Whos at risk?,All of the above are proatherosclerotic and proinflammatory Inflammation (and oxidation) damage endothelial cells LDL cholesterol is deposited in the blood vessel and starts to form atherosclerotic plaques Smoking and hypertension are also vasoconstrictive, decreasing blood flow to the kidney PREVENTION,Prevention,Stop smoking,Lower BP w/DASH diet,Anti-inflammatory diet,Decrease trans and saturated fats Increase fresh fruits and vegetables (high ORAC numberthe Bs) Omega-3 fatty acids Olive oil Nuts,How about the Cardiologists diet?,“If it tastes good, spit it out!”,Preventionsay YES to drugs!,Lowering blood pressure and protecting the kidneys ACE inhibitors (“prils”) and/or ARBs (“sartans”) (ACE=angiotensin converting enzyme and ARB=angiotensin receptor blockers) Obviously “angie” is a problem if all we want to do is inhibit “her”,“prils” and “sartans” to the rescue (ACE inhibitors and angiotensin receptor blockers or ARBS)protect kidneys,Captopril (Capoten) Enalapril (Vasotec) Lisinopril (Prinivil, Zestril) Perindopril (Aceon) Moxepril (Univasc) Benazepril (Lotensin) Quinapril (Accupril) Trandolapril (Mavik) Ramipril (Altace) Is there a #1 “pril”?,losartan (Cozaar), valsartan (Diovan), candesartan (Atacand), telmisartan (Micardis) irbesartanAvapro olmesartan(Benicar),“PRILS”The ACE inhibitors,Who is “ACE” and why do we want to inhibit him? Angiotensin Converting Enzyme (ACE) inhibits the conversion of AT1 to AT2 What are the functions of angiotensin 2?,ALDOSTERONE,ACE-,What does angiotensin 2 do?,“Tenses” your “angios”vasoconstricts Triggers release of “AL”aldosterone (from the adrenal cortex to save Na+ & H2O and excrete K+) The above 2 are normal compensatory mechanisms in heart failure If you block them, the heart gets a breather What else does angiotensin-2 do? Increases inflammation in the arteries Prothrombotic Increases tissue resistance to insulin Potent growth factor,“Angie” and the healthy kidney,Afferent arteriole (vasodilated via (prostaglandins) Blood entering glomerulus Glomerulusfilter Efferent arteriole (vasoconstricted via (angiotensin 2) Blood exiting glomerulus,PG,AT2,Toilet,filter,The pressure difference between the afferent and the efferent arterioles sets up the glomerular filtration pressure and determines the rate at which the kidney filters urine (the GFR) The afferent arteriole is in a constant vasodilated statepartially due to prostaglandin synthesis The efferent arteriole is in a constant vasoconstricted statedue to angiotensin 2,The Diabetic Kidneyhyperglycemia/HTN (the deadly duo),Afferent arteriole ( vasodilation by ( prostaglandins) Blood entering glomerulus Glomerulusfilter Efferent arteriole ( vasoconstriction via ( angiotensin 2) Blood exiting glomerulus,Microalbuminuria (between 30 mg300 mg of alb/g creatinine10-fold risk of RD & CKD),Why is microalbuminuria a “bad” thing?,There is a 4-fold increase in acute coronary syndromes in Type 1 DM greater than 35 years old; When microalbuminuria is present the risk is increased by a factor of 140! The presence of albuminuria suggests that large vessel walls are more permeable to lipoproteins or damage from the local release of growth factors Aggressive treatment of dyslipidemia demonstrates beneficial effects not only on macrovascular disease but on microvascular disease as well (retinopathy and nephropathy),What do the “prils” and “sartans” do in the diabetic kidney?,Vasodilate the efferent arteriole Decreases intraglomerular hypertension Reduce filtration pressure Decrease microalbuminuria Decreases destruction of the glomerulus (Once you lose a glomerulus, thats it) Prevent the progression of nephropathy PRILS and SARTANS can decrease the decline by 50% or MORE in the diabetic kidney If the HbA1C is greater than 6.2, the risk for CV disease and renal disease starts to increase!,Side effects,Hypotension Hyperkalemia (excreting sodium and water and retaining potassium) Hypoglycemia Cough Angioedema (“Does my voice sound funny to you?”),What is the mechanism of the ACE inhibitor-induced angioedema?,ACE inhibitors inhibit the breakdown of bradykinin Accumulation of bradykinins have 3 results: 1) vasodilation 2) increased permeability 3) increased hereditary, acquired, and ACE inhibitor-induced angioedema High-risk patientspatients with a C1 esterase inhibitor deficiency; African Americans (4.5x ) Side effect has been shown to occur up to 1 year after starting ACE inhibitors,Side effectsRx of hyperkalemia,Hyperkalemia- Add a thiazide diuretic to the “pril” and voil! Capozide (captopril + thiazide) Vaseretic (enalapril +thiazide) Prinizide (lisinopril + thiazide) Zestorectic (as above) Lotensin HCT (benazepril + hydrochlorothiazide) Decrease foods containing potassium especially when the ACE inhibitors are combined with spironolactone (Aldactone) or the newest potassium-sparing agenteplerenone (Inspra),Adding drugs that block aldosteronespironolactone (Aldactone) and eprelrenone (Inspra),Be really careful to check K+ levels within the first week after adding Aldactone or Inspra RALES (1999) (Random Aldactone Evaluation Study)adding Aldactone postpones or prevents 200 deaths/1000 people w/CHF BUTFor every 1000 new spironolactone RX in heart failure patients, there are 50 more hospitalizations for hyperkalemia Dose 12.5-25 mg per day of spironolactone,Decrease the intake of foods with high potassium,Banana (1 m) 422 mg Potatoes (with skin) 540 mg French fries (1 med) 924 mg Halibut (3 oz) 490 mg Spinach (1c) 839 mg Pasta sauce (1c) 940 mg Oranges 1 m 237 mg Prunes (elderly) 10 615 mg H/heartextra for K+ content of 1,200 foods,Other potential K+ boosters,Stop taking any K+ supplements including salt substitutes such as K+ iodide Go easy on the NSAIDS (decrease GFR) with retention of fluids and electrolytes (including K+) Herbal or natural remedies with hefty doses of potassium include noni juice, Siberian ginseng, and hawthorn berries (Harvard Heart Letter, December 2004),Prevention,The “statin” drugs should also be prescribeddecrease total cholesterol, Decrease LDL-cholesterol Shrink plaques including plaques in the renal artery Prevent the formation of new plaques, and, Decrease inflammation in the vessels,“Statins” to the rescue to decrease hyperlipidemia,Hyperlipidemia is a disease-promoting factor thought to perpetuate previous glomerular injury. Both epithelial cells and mesangial cells have receptors for LDL and oxidized LDL and the statins have been shown to inhibit mesangial proliferation Who are the statin sisters?,Who are the statins?,Lovastatin (Mevacor) Pravastatin (Pravachol) Fluvastatin (Lescol) Rosuvastatin (Crestor)* Atorvastatin (Lipitor) * Higher HDLs=better kidneys (107 patients w/ T1DM; 42 w/ albuminuria; 65 without; the average HDL in patients w/ albuminuria was 55 mg/dL vs. 66 mg/dL; for every 21-mg/dL increase in HDL, people are as likely to develop albuminuria (Diabetes Care January 06),How about the use of NSAIDS and ACE inhibitors at the same time in a patient with renal insufficiency?,ACE inhibitors and ARBs vasodilate the efferent arteriole by inhibiting the function of angiotensin 2 NSAIDS vasoconstrict the afferent arteriole by blocking prostaglandin synthesis Front door closes, back door opens THIS can and does, lead to acute renal failure in patients with renal insufficiency,The anatomy of a nephrongreater detail,The basic functioning unit of the kidney The nephron1.5 million per kidney in normal birth weight individuals* Afferent arteriole glomerulus basement membrane Bowmans capsule tubular system (proximal convoluted tubule (PCT), Loop of Henle, distal convoluted tubule (DCT), collecting duct),Premature babies/LBW babies,Is your risk of hypertension related to the number of nephrons you were born with? LBW babies are much more likely to develop hypertension later on in life and it may be due to the fact that they had less nephrons to start with Autopsies on patients between 35-59 10 kidneys w/ known hypertension; 10 w/ normal BP,Premature babies/LBW babies,Average number of nephrons in people w/ HBP was fewer than that of people w/ normal BP Couldnt find damaged nephrons or nephrons that had dropped outsuggesting inherited # of nephrons Good prenatal nutrition and the # of nephronsrestricting proteins # of developing nephrons (N Engl J Med 9 Jan 2003),Premature babies/LBW babies,Another implication Screening kidney donors for LBW may be important when deciding who might be a candidate as an appropriate donor The donor loses 50% of nephronsif remaining kidney has fewer #s due to LBW, this increases the risk of hypertension in the donoroverworked and underpaid triggering the release of renin-angiotensin-aldosterone,The filtration membrane,The filtration membrane3 layers 1) the endothelial cells of the glomerulus 2) the basement membrane between the glomerulus and the, 3) epithelial cells of Bowmans capsule Diseases1) Lupus nephritis 2) sugar diabetes 3) nephrotic syndrome,The glomerular filtration membrane,The glomerular capillary wall (endothelial cells) The basement membrane (a glycoprotein layer) The fenestrated wall (epithelial) cells of Bowmans capsule into the first part of the tubule (the proximal tubule)(epithelial cells) 1) Lupus nephritis/glomeruloneprhitis 2) diabetic nephropathy 3) nephrotic syndrome (90% of kids with IgE mediated disease),Glom BM BC PCT,1,2,3,3,A note on the tubules of the kidney,The tubules (like Bowmans capsule and the PCTproximal convuluted tubule) are lined with epithelial cells The epithelial cells are extremely vulnerable to hypoxia Without oxygen, the epithelial cells become necrotic and slough into the tubule; clogging the works resulting in Acute tubular necrosis (ATN),Ethylene glycol nephrosis,Dogs and cats love the sweet taste of antifreeze Crystals precipitate in the tubular lumen resulting in intrarenal obstruction, degeneration and necrosis of the lining of the tubular epithelium Irreversible renal failure,MAJOR FUNCTIONS OF THE KIDNEY,Regulation of water, solutes, electrolytes, and acid-base balance 1) urea, creatinine 2) sodium, potassium, calcium, phosphorus 3) hydrogen and bicarbonate,If the kidney FAILS Retention of wateredema, weight gain, HTN Retention of urea, creatinine (most sensitive) Retention of sodium, potassium resulting in hypertension, hyperkalemia, Retention of H+ ionsmetabolic acidosis,Aids in Vitamin D metabolism,Vitamin D is necessary for the absorption of calcium from the GI tract With increased phosphate retention or decreased calcium absorption the parathyroids increase their production of PTH PTH breaks down bone to replace the calciumsecondary hyperparathyroidism Osteomalacia and chronic renal failure Phosphate binders in patients with renal failure,Some notes on Vitamin D,10-15 minutes of exposure to sunlight on face, hands, and arms 2-3 days per week is required to synthesize sufficient amounts of vitamin D (in shorts and a t-shirt, people can soak up enough UV-B rays to produce 12,000 U of vitamin D within 20 minutes) Sunscreen? SPF-8? Foodfatty fish, cod liver oil, and egg yolks Fortified foodsmilk, breakfast cereals, margarine, butter, certain brands of OJ and yogurt,Secretes renin from the juxtaglomerular apparatus,Renin (kidney)angiotensin 1 (liver) angiotensin 2 (tissues)aldosterone (primarily from the adrenal cortex; some tissue aldosterone production as well),Major functions of the kidney,Direct renin inhibitornew anti-hypertensive drug known as TEKTURNA Reninangiotensinaldosterone with increased blood pressure Drugs to block the systemACE inhibitors (“prils”), angiotensin receptor blockers (“sartans”), and aldosterone antagonists (spironolactone/Aldactone and eplerenone (Inspra),Major functions of the kidney,Secretes erythropoietin to stimulate the bone marrow to produce RBCsthe failing kidney does not secrete erythropoietin One of the earliest signs of declining renal function is the presence of anemia 8 million of the 20 million have stage 3 CKD, and almost half are anemic (Stage 3is characterized by a GFR of 30-60 mL/min/1.73 m) Anemia has been independently associated with an increased risk of left ventricular dilation, left ventricular hypertrophy, coronary artery disease, heart failure,Anemia and CKD,The link between heart failure, CKD, and renal failure is known as cardiorenal anemia syndrome Synthetic erythropoietin ESAs (erythropoiesis stimulating agents) have been available since 1989 Epoetin alfa (1989) and darbopoetin alfa (2001) BUTfully restoring hemoglobin (greater than 13 g/dL) in patients with CKD increases their risk of all-cause mortality, poorly controlled BP, and AV access thrombosisso partial restoration of Hb is advised. Target Hb of 11-12 g/dL; Monitor Hb at least monthly when on ESAs (each 1 gm causes LV dilation by 42%)(50% lower survival rates with LVH),Major functions of the kidney,Conservation of free water (ADH receptors on the distal tubule and collecting duct) Diurnal rhythmkicks in around midnight with water conservation and reduced urination at night Early a.m. specimen is concentrated One of the earliest signs of renal insufficiency is the inability to concentrate urine at night ORbeer and ETOH inhibit ADHurinating all night And morphine increases ADH as well as tightens the urinary sphincter (urinary retentionproblem after surgery),Nocturia-what are the causes?,Inability of the kidney to respond to ADHimmaturity? Enuresis in kids? (DDAVP); Nephrogenic diabetes insipidusgenetic lack of receptors Booze before bedtimealcohol inhibits ADH “sugar” diabetesglucose is an osmotic diuretic Enlarged “prostrate” UTI CHF Pregnancy Diuretics at bedtimelasix Morphine increases ADH and tightens urinary sphincter resulting in urinary retention,Now that you know what the kidney is supposed to do,Accurate intake and output Daily weights Lab tests Blood pressure Check for signs of fluid retention,Check volume statuspe