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Introduction to Nephrology

Introduction to Nephrology. Jennifer Smith, FNP-S. Objectives. Provide an overview of basic renal anatomy and physiology Discuss the growing epidemic of chronic kidney disease due to increased incidence of obesity, hypertension, and diabetes

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Introduction to Nephrology

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  1. Introduction to Nephrology Jennifer Smith, FNP-S

  2. Objectives • Provide an overview of basic renal anatomy and physiology • Discuss the growing epidemic of chronic kidney disease due to increased incidence of obesity, hypertension, and diabetes • Define the stages of chronic kidney diseases and discuss associated complications such as: anemia of chronic kidney disease, secondary hyperparathyroidism, hypertension, cardiovascular disease, hyperkalemia, hyperphostphatemia, and bone disease • Discuss management of chronic kidney disease • Discuss other common kidney disorders that may lead to end-stage renal disease

  3. The Kidney • Location- relatively high under lower ribs in the retroperitoneal space

  4. Anatomy and Physiology • Average size of adult kidney is 12x6x3 cm • Size variations can occur with age, gender, BMI, pregnancy, kidney disease, and co-morbid conditions • Right kidney smaller • Right kidney lower than left kidney

  5. Renal Anatomy

  6. Structure of Kidney • Cortex-the outer layer of the kidney comprising the glomeruli, most of the proximal tubules, and some of the distal tubules • Medulla-formed by 7-9 cone shape pyramids which extend into the renal pelvis • Renal Pelvis-flat funnel-like tube continuous with ureter as it leaves the hilus • Calyces- subdivided into major and minor calyces • Major calyces-2 or 3 branches off of renal pelvis • Minor calyces- cup-shaped areas that enclose the papillae of the pyramids. Continuously collect urine draining from papillae, emptying it into the renal pelvis (Greenburg et al, 2009)

  7. The Nephron • Functional unit of kidney • Consisting of glomerulus and long tubule • Approximately 1 million nephrons in each kidney • Filters plasma->reabsorption and secretion->forms filtrate free of protein->regulates the filtrate to maintain fluid volume, electrolytes, and pH (Greenburg et al, 2009)

  8. The Nephron • Glomerulus-tuft of capillaries surrounded by Bowman’s capsule. Together form the renal corpuscle. • Tubules- segmented into proximal tubule, loop of Henle, distal tubule, and collecting tubules • Tubular Transport: • Proximal Tubule- active reabsorption of sodium • Loop of Henle and distal tubule- concentration or dilution of urine • Collecting Tubules- run through medullary pyramids (give them their striped appearance) (Greenburg et al, 2009)

  9. The Nephron

  10. Blood and Nerve Supply • Renal arteries: branch off of the aorta then further divide to form: segmental arteries: • Lobular arteries • Interlobararteries • Arcuate arteries • Interlobular arteries • More than ¼ of the cardiac output is delivered to the kidneys each minute (1200ml/min) • More than 90% of blood entering kidney perfuses the cortex (Greenburg et al, 2009)

  11. Blood and Nerve Supply • Renal Veins-trace pathway of arterial blood supply in reverse • Empty into the inferior vena cava • Left renal vein is about 2x longer in order to extend to IVC in its position to right of vertebral column • Renal Plexus-network of autonomic nerve fibers and ganglia. Supplied by sympathetic fibers from thoracic and lumbar splanchnic nerves • Sympathetic fibers-vasomotor fibers that control renal blood flow by adjusting arteriolar diameters (Greenburg et al, 2009)

  12. Functions of Kidney • Maintenance of body fluids composition (fluid volume, osmolarity, electrolyte, and acid/base balance. • Excretion of metabolic end products and foreign substances (i.e. urea, toxins, drugs). • Production/secretion of enzymes and hormones (Greenburg et al, 2009)

  13. Functions of Kidney • Renal Hormones and Enzymes • Renin- produced in juxtaglomerular apparatus. Catalyzes production of angiotensin which is important for sodium balance and blood pressure regulation • Erythropoietin- stimulates maturation of RBC’s in bone marrow • 1,25-Dihydroxyvitamin D3- most active form of Vitamin D3, steroid hormone that helps the body regulate calcium/phosphorus balance (Greenburg et al, 2009)

  14. Functions of Kidney • Alterations in body fluid composition and fluid volume can impact: • Cardiac Output and Blood Pressure- dependent on optimal plasma volume • Enzyme Function- most function best in narrow range of pH and ion concentrations • Cell Membrane Potential- depends on potassium concentrations • Membrane excitability- depends on calcium ion concentrations

  15. Evaluation of Renal Function • Glomerular Filtration Rate (GFR) • Serum Creatinine, Blood Urea Nitrogen • MAU/CR ratio • 30-300 mg/dl microalbuminemia • >/= 300mg/dl- macroalbuminemia • 24 hour urine collection

  16. Glomerular Filtration Rate (GFR) • GFR- amount of fluid filtered from blood into glomerular capsule each minute • GFR- 180 L/day • GFR controlled by: • Auto-regulation (tubuloglomerular feedback) • Neural regulation • Hormonal regulation- renal aldosterone angiotensin system

  17. Screening • DM-largest single cause of CKD in the U.S. • Initial screening 5 years after diagnosis of Type I DM • AT DIAGNOSIS of type II DM • Annually thereafter • HTN • Family history of CKD • Autoimmune disorders

  18. Screening Methods • Chemistries-renal panel, include albumin and MG • Urinalysis • Microalbumin/Cr ratio • Imaging studies • 24 hour urine

  19. Abnormalities on Imaging Studies • Renal cysts-often incidental findings and usually benign. Ultrasound is preferred method to differentiate between cystic and solid lesions. (If complex cyst or indeterminate lesions follow up with MRI) • Nephrolithiasis- non-contrast CT is gold-standard • Hydronephrosis

  20. Chronic Kidney Disease • CKD is defined as: • Kidney damage for 3 months or longer to include either structural or functional abnormalities With or without a decrease in GFR (as seen by pathology abnormalities, markers of kidney damage in blood or urine, or abnormalities on imaging studies). • GFR of less than 60 ml/min for at least 3 months

  21. Prevalence • 31 million in U.S. (16% of population) and rising • 1 in 10 adults have some level of CKD • Majority of people with CKD are in Stage 1-3 • Incidence is increasing rapidly in those >65 • ESRD expected to reach 2.2 million by 2030 • ESRD males > females • Most people with CKD die before they are diagnoses, primarily of cardiovascular complications • African Americans are 4 times more likely to develop CKD than Caucasians. (Domino, 2013)

  22. Risk Factors • Hypertension • DM • Autoimmune diseases (vasculitis, connective tissue disorder) • Congenital anomalies • Family history of CKD or transplant • Kidney stones • Frequent urinary tract infections • Exposure to certain drugs (i.e. NSAID) • Cardiovascular disease • Acute Kidney Injury • Systemic infections • Low income/education • Minority populations • Obesity • Smoking • Age > 60 years • Race • Neoplasm • Urinary Tract Obstruction • Hyperlipidemia (Domino, 2013)

  23. CKD Staging (Domino, 2013)

  24. Clinical Findings of CKD by Stage

  25. Associated Complications • HTN • Anemia • Secondary Hyperparathyroidism (SHPT) • Hyperkalemia • Cardiovascular complications • Bone disease (Greenburg et al, 2009)

  26. Hypertension • Can be cause or effect • Inappropriate sodium reabsorption leading to increased fluid volume is primary cause of HTN in CKD • RAAS stimulation • Renal Artery Stenosis • Vascular Calcifications

  27. Managing HTN in CKD • Goal is BP < 130/80 mm/Hg • Many patients will require multiple drug classifications to control BP due to increased vascular resistance and increased fluid volume • Uncontrolled HTN is key risk for progression of CKD • An increase in BP of 20/10mmHg doubles risk for cardiovascular disease (Greenburg et al, 2009)

  28. Pharmacologic Management HTN in CKD • ACE/ARB • “Reno protective” • Lowers intra-glomerular pressure and reduces proteinuria, slowing the progression of CKD • May see initial increase in sCr (less than 30% that returns to baseline within 2 months if acceptable) • Monitor K level • Contraindicated in renal artery stenosis, uncontrolled hyperkalemia, pregnancy, history of angioedema • Not unusual to see patients with CKD on several different classifications of medications (Collins, 2012)

  29. Pharmacologic Management HTN • Calcium Channel Blocker: • Dihydropyrodines-Amlodipine, Valsaartan • Increase intraglomerular pressure causing worsening of proteinuria if not used in combination with a ACE/ARB • Non-Dihydropyrodines (Diltiazem, Verapamil) • If failing on ACE/ARB therapy, have been shown to reduce proteinuria • Vasodilators (Hydralazine, Isosorbide) • May be useful in patients with known renal artery stenosis (Collins, 2012)

  30. Pharmacology Continued • Diuretics • Diuretic resistance may be due to high sodium diet • Loop Diuretics • Best dosed BID for CKD III or higher • May take second dose 6 hours after 1st dose • Monitor serum K+ levels, may need replacement • Thiazide Diuretics • Effective in patients with GFR>30 • Monitor uric acid level as may cause gout • Monitor serum K+ levels (Collins, 2009)

  31. Diuretics • Most CKD patients require diuretics • Enhances antihypertensive therapy • Reduces tubular sodium reabsorption which in turn increases sodium excretion and lowers ECF volume, lowering BP • Choice of diuretic depends on CKD stage, volume of fluid overload, and other individual patient factors • Use potassium sparing diuretics with caution if GFR is less than 30, or if concomitant use of ACEI/ARB • Don’t decrease diuretics due to increase BUN/Cr. BUN/Cr will fluctuate with fluid volume • Don’t treat the lab, treat the patient! (Collins, 2009)

  32. CKD in Pregnancy • Renal function in CKD may deteriorate during pregnancy • CR >1.5 and hypertension are major risk factors of worsening renal function • Increased risk of premature labor, preeclampsia, and/or fetal loss • ACE inhibitors and ARBs are contraindicated • Use diuretics with caution (Domino, 2009)

  33. Parathyroid Gland

  34. Secondary Hyperparathyroidism (SHPT) • The parathyroid glands main function is to control calcium within the blood and bones • Parathyroid glands atrophy due to constant stimuli in CKD (either hypocalcemia or hyperphosphatemia). • Atrophied glands secrete PTH, causing serum levels to rise • PTH stimulates conversion of active Vitamin D to increase calcium absorption from the GI tract • Over time, elevated PTH leads to bone disease, vascular and soft tissue calcifications, decreased quality of life, amputations, and increased mortality (Greenberg et al, 2009)

  35. PTH goal based on Stage of CKD (National Kidney Foundation, 2010)

  36. SHPT • Monitoring • Intact PTH levels • Ca and Phosphorus levels • Vitamin D 1,25 level • Treatment • Oral Calcitriol, Zemplar, Hectoral, Sensipar • May need Vitamin D replacement • Treat hyperphosphatemia- if you control phosphorus you will control the parathyroid • May need parathyroidextomy

  37. Hyperphosphatemia • Increases cardiovascular risk factors • Calcifications develop may result in bone deformities and amputations • High levels of phosphorous cause Calcium to be pulled from bone • Osteoporosis • Bone pain • Fractures

  38. Hyperphosphatemia

  39. Treatment for Hyperphosphatemia

  40. Cardiovascular Complications in CKD • Patients with CKD more likely to die from CVD • Survival rate of MI patients with CKD are 53% compared to 36% • Vascular calcifications common in patients with hyperphosphatemia and SHPT • Cardio-renal syndrome • Patients with CKD should have annual EKG, stress test on file

  41. Hyperkalemia • Decreased Renal Excretion • Acute or chronic renal failure • Aldosterone deficiency (frequently associated with diabetic nephropathy, chronic interstitial nephritis, or obstructive uropathy) • Adrenal Insufficiency (Addison’s disease) • Kidney diseased that impair distal tubule function (Sickle cell, Systemic Lupus Erythematosus) • Abnormal Potassium Distribution • Insulin deficiency • B-Blockers • Metabolic and Respiratory Acidosis • Abnormal Potassium Release from Cells • Rhabdomyolysis • Tumor lysis syndrome (Greenburg et al, 2009)

  42. Treatment Goals to Slow Progression of CKD • Control blood pressure <130/80 or <140/80 in renal artery stenosis • Low NA diet • ACE/ARB therapy • Diuretics • NondihydropyridineCalcium Channel Blockers • Optimize control of DM (HGA1C <7.5) • Control dyslipidemia LDL goal <100 • Restrict dietary protein • Low phosphorous diet

  43. Prescribing Considerations in CKD • Dose adjust medications based on GFR (Metformin, Allopurinol, many antibiotics, etc) • Avoid use of nephrotoxic drugs (NSAIDS, contrast dye, Bactrim) • When treating DM with CKD less insulin may be required due to decreased gluconeogenesis • Best to avoid 1st generation sulfonylureas as they have increased risk for hypoglycemia due to decreased renal clearance • Second generation sulfonylureas are preferred (Glipizide) • As always start low and go slow! (Greenburg et al, 2009)

  44. Drug-Induced Hyperkalemia • Block Sodium Channel in the Distal Nephron • Potassium-sparing diuretics: amiloride, triamterene • Antibiotics: trimethoprim, pentamidine • Block Aldosterone Production • ACE inhibitors • ARBs • NSAIDS and COX-2 inhibitors • Heparin • Tacrolimus • Block Na+, K+-ATPase Activity in the Distal Nephron • Cyclosporine • Potassium Release from Injured Cells • Drug-induced rhabdomyolysis (lovastatin, cocaine) • Drug induced tumor lysis syndrome(chemotherapy agents in leukemia's, high-grade lymphomas) • Depolarizing paralytic agents (succinylcholine) • Block Aldosterone Receptor • Spironolactone • Eplerenone

  45. NSAID’s • Major cause of CKD • Block Aldosterone Production • Widespread use of these drugs are leading to increased cases of NSAID-induced nephropathy • Not a problem if no renal impairment • Avoid in CKD and transplant patients

  46. Diabetic Nephropathy • About 35% of patients with DM (Type I and Type II) will develop nephropathy after about 25 to 30 years • Approximately 45% of dialysis patients have diabetic nephropathy as cause of ESRD • However many type II patients die from CV disease before they reach ESRD • May not be able to tell patient has kidney disease based on GFR • Need to have a micro albumin urine test to determine level of proteinuria • Need to be on ACE/ARB for renal protection

  47. Renal Artery Stenosis • Classic findings: • Uncontrolled HTN despite multiple medications • Causes: • Usually atherosclerosis • Fibro muscular dysplasia • Diagnosis: • Nuclear renal scan, renal arteriogram, MRA, or Doppler ultrasound • Treatment: • Angioplasty or surgery

  48. Obstructive Uropathy • Obstruction can occur anywhere along urinary tract causing hydonephrosis • Renal calculi • BPH • Colon, cervical, or uterine cancer • Neurogenic bladder • Can be unilateral or bilateral • Treatment • Resolve obstruction- may need stents • Treat BPH • Foley catheter or nephrostomy tubes

  49. Autosomal Dominant Polycystic Kidney Disease • Most common inherited kidney disease • Affects 1 in 1000 people • Systemic disease causing kidney, liver, pancreas, thyroid, and subarachnoid cysts and intracranial aneurysm • Clinical hallmark sign is gradual and massive cystic enlargement of kidneys resulting in kidney failure • May be present in childhood with symptoms usually beginning in middle age • Symptoms can include abdominal pain, hematuria, nocturia, flank pain, and fatigue • Diagnosis usually made by ultrasound • Presence of enlarged kidneys with multiple cysts required for diagnosis

  50. ADPKD

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