To Pee or not to Pee the KIDNEY in wellbeing and malady - PowerPoint PPT Presentation

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To Pee or not to Pee the KIDNEY in wellbeing and malady PowerPoint Presentation
To Pee or not to Pee the KIDNEY in wellbeing and malady

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To Pee or not to Pee the KIDNEY in wellbeing and malady

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  1. To “Pee” or not to “Pee”—the KIDNEY in health and disease Barb Bancroft, RN, MSN, PNP CPP Associates, Inc. Chicago IL (

  2. 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.

  3. 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)

  4. The kidney as an innocent bystander… • Autoimmune diseases—lupus, autoimmune glomerulonephritis, Goodpasture’s disease, Wegener’s granulomatosis, sarcoidosis • Toxic effects of drugs—aminoglycosides, radiocontrast agents, amphotericin, cisplatinum, acetaminophen • Cancer—malignant infiltration, multiple myeloma

  5. How much embryology did you get in nursing school? The sperm meets the egg and then… Let’s start at the very beginning…

  6. Embryology—the development of the kidney • The kidneys and the ears from the same mesenchymal tissue • The otorenal axis • Nephrotoxic drugs and ototoxc drugs

  7. 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

  8. The kidney…retroperitoneal 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)

  9. Polycystic kidney disease • Autosomal dominant polycystic kidney disease (ADPKD) • 1/1000; C>AA; 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

  10. 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)

  11. Gross Anatomy—blood supply • Aorta→renal artery→branches into arcuate→

  12. Blood supply to and from the glomerulus • Afferent arteriole delivers blood to the • Glomerulus—a tuft of capillaries • Blood exits via the efferent arteriole

  13. Gross Anatomy—blood supply • renal vein → inferior vena cava → right atrium

  14. 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

  15. 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 glomeruli—DIC (disseminated intravascular coagulation) • Immune complex deposition in the glomerulus triggering the inflammatory response (lupus nephritis)

  16. 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 renin→angiotensin→ aldosterone (RAA) • Hypertension • CKD (chronic kidney disease) • Which comes first? • Who’s at risk?

  17. Who’s 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

  18. Stop smoking Lower BP w/DASH diet Prevention…

  19. Anti-inflammatory diet • Decrease trans and saturated fats • Increase fresh fruits and vegetables (high ORAC number—the B’s) • Omega-3 fatty acids • Olive oil • Nuts

  20. “If it tastes good, spit it out!” How about the Cardiologist’s diet?

  21. Prevention—say 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”

  22. 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) irbesartan—Avapro olmesartan—(Benicar) “prils” and “sartans” to the rescue (ACE inhibitors and angiotensin receptor blockers or ARBS)—protect kidneys

  23. “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--

  24. 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

  25. “Angie” and the healthy kidney… • Afferent arteriole (vasodilated via (prostaglandins) • Blood entering glomerulus • Glomerulus→filter • Efferent arteriole (vasoconstricted via (angiotensin 2) • Blood exiting glomerulus PG filter AT2 Toilet

  26. 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 state—partially due to prostaglandin synthesis • The efferent arteriole is in a constant vasoconstricted state—due to angiotensin 2

  27. The Diabetic Kidney…hyperglycemia/HTN (the deadly duo) • Afferent arteriole (  vasodilation by (  prostaglandins) • Blood entering glomerulus • Glomerulus→filter • Efferent arteriole (  vasoconstriction via (  angiotensin 2) • Blood exiting glomerulus Microalbuminuria (between 30 mg—300 mg of alb/g creatinine—10-fold > risk of RD & CKD)

  28. 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)

  29. 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, that’s 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!!

  30. Side effects… • Hypotension • Hyperkalemia (excreting sodium and water and retaining potassium) • Hypoglycemia • Cough • Angioedema (“Does my voice sound funny to you?”)

  31. 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 patients—patients 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

  32. Side effects…Rx of hyperkalemia Hyperkalemia-- Add a thiazide diuretic to the “pril” and voilá! • Capozide (captopril + thiazide) • Vaseretic (enalapril +thiazide) • Prinizide (lisinopril + thiazide) • Zestorectic (as above) • Lotensin HCT (benazepril + hydrochlorothiazide) • Decrease foods containing potassiumespecially when the ACE inhibitors are combined with spironolactone (Aldactone) or the newest potassium-sparing agent—eplerenone (Inspra)…

  33. Adding drugs that block aldosterone—spironolactone (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 • BUT…For 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

  34. 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 • for K+ content of 1,200 foods

  35. 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)

  36. Prevention • The “statin” drugs should also be prescribed—decrease 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

  37. “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?

  38. 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 ½ as likely to develop albuminuria (Diabetes Care January 06)

  39. 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

  40. The anatomy of a nephron—greater detail • The basic functioning unit of the kidney • The nephron—1.5 million per kidney in normal birth weight individuals** • Afferent arteriole → glomerulus → basement membrane → Bowman’s capsule → tubular system (proximal convoluted tubule (PCT), Loop of Henle, distal convoluted tubule (DCT), collecting duct)

  41. 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

  42. Premature babies/LBW babies • Average number of nephrons in people w/ HBP was fewer than ½ that of people w/ normal BP • Couldn’t find damaged nephrons or nephrons that had dropped out—suggesting inherited # of nephrons • Good prenatal nutrition and the # of nephrons—restricting proteins ↓ # of developing nephrons • (N Engl J Med 9 Jan 2003)

  43. 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 nephrons—if remaining kidney has fewer #’s due to LBW, this increases the risk of hypertension in the donor—overworked and underpaid triggering the release of renin-angiotensin-aldosterone

  44. The filtration membrane • The filtration membrane—3 layers 1) the endothelial cells of the glomerulus 2) the basement membrane between the glomerulus and the, 3) epithelial cells of Bowman’s capsule • Diseases—1) Lupus nephritis 2) sugar diabetes 3) nephrotic syndrome

  45. The glomerular capillary wall (endothelial cells) The basement membrane (a glycoprotein layer) The fenestrated wall (epithelial) cells of Bowman’s 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 The glomerular filtration membrane 3 2 3 1

  46. A note on the tubules of the kidney… • The tubules (like Bowman’s capsule and the PCT—proximal 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)

  47. 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

  48. 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 water—edema, weight gain, HTN Retention of urea, creatinine (most sensitive) Retention of sodium, potassium resulting in hypertension, hyperkalemia, Retention of H+ ions—metabolic acidosis MAJOR FUNCTIONS OF THE KIDNEY

  49. 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 calcium—secondary hyperparathyroidism • Osteomalacia and chronic renal failure • Phosphate binders in patients with renal failure

  50. 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? • Food—fatty fish, cod liver oil, and egg yolks • Fortified foods—milk, breakfast cereals, margarine, butter, certain brands of OJ and yogurt