Transcript File - Jennifer Smith`s Professional Nursing Portfolio

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
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
The Kidney
Location- relatively high under lower ribs in the retroperitoneal space
Anatomy and Physiology
Average size of adult kidney is 12x6x3 cm
Size variations can occur with age, gender,
BMI, pregnancy, kidney disease, and comorbid conditions
Right kidney smaller
Right kidney lower than left kidney
Renal Anatomy
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
(Greenburg et al, 2009)
pelvis
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)
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)
The Nephron
Blood and Nerve Supply
Renal arteries: branch off of the aorta then further divide to form: segmental
arteries:
1. Lobular arteries
2. Interlobar arteries
3. Arcuate arteries
4. 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)
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)
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)
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)
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
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
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
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
Screening Methods
Chemistries-renal panel, include albumin and MG
Urinalysis
Microalbumin/Cr ratio
Imaging studies
24 hour urine
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
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
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)
Risk Factors
Hypertension
Systemic infections
DM
Low income/education
Minority populations
Autoimmune diseases (vasculitis, connective tissue
disorder)
Obesity
Congenital anomalies
Smoking
Family history of CKD or transplant
Age > 60 years
Kidney stones
Frequent urinary tract infections
Exposure to certain drugs (i.e. NSAID)
Cardiovascular disease
Acute Kidney Injury
Race
Neoplasm
Urinary Tract Obstruction
Hyperlipidemia
(Domino, 2013)
CKD Staging
(Domino, 2013)
Clinical Findings of CKD by Stage
Stage I and II
Stage III
Stage IV
Stage V
• Asymptomatic, BUN/CR slightly elevated or normal, acid-base, fluid, and
electrolyte balance is maintained through compensation of remaining nephrons
• Usually asymptomatic, BUN/CR increased. Erythropoietin decreased and PTH
levels are increased
• Patient may have anemia, acidosis, hypocalcemia, hyperphosphatemia, and
hyperkalemia
• Fatigue, dysgeusia, anorexia, nausea, pruritus, asterixis, uremic breath
Associated Complications
HTN
Anemia
Secondary Hyperparathyroidism (SHPT)
Hyperkalemia
Cardiovascular complications
Bone disease
(Greenburg et al, 2009)
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
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)
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)
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)
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)
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)
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)
Parathyroid Gland
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)
PTH goal based on Stage of CKD
(National Kidney
Foundation, 2010)
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
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
Hyperphosphatemia
Treatment for Hyperphosphatemia
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
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)
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
Nondihydropyridine Calcium Channel Blockers
Optimize control of DM (HGA1C <7.5)
Control dyslipidemia LDL goal <100
Restrict dietary protein
Low phosphorous diet
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)
Drug-Induced Hyperkalemia
Block Sodium Channel in the Distal Nephron
Block Na+, K+-ATPase Activity in the Distal Nephron
Potassium-sparing diuretics: amiloride, triamterene
Cyclosporine
Antibiotics: trimethoprim, pentamidine
Potassium Release from Injured Cells
Block Aldosterone Production
Drug-induced rhabdomyolysis (lovastatin, cocaine)
ACE inhibitors
Drug induced tumor lysis syndrome(chemotherapy
agents in leukemia's, high-grade lymphomas)
ARBs
NSAIDS and COX-2 inhibitors
Heparin
Tacrolimus
Depolarizing paralytic agents (succinylcholine)
Block Aldosterone Receptor
Spironolactone
Eplerenone
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
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
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
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
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
ADPKD
ADPKD
Hepatorenal
Type I
Type II
Usually rapid decline in kidney function
Moderate steady decline in GFR
sCr may double in 2 weeks
Cirrhosis causes decrease in NA and water
excretion, decreased renal perfusion and GFR
Occurs with acute hepatitis, bacterial
infections, major surgery, or massive GI bleed
Decreased ability to excrete NA leads to
ascites
Presence of ascites represents marked
impairment or renal sodium handling
Cardio-Renal
1.
Abrupt worsening of cardiac function leads to AKI
2.
Chronic abnormalities in cardiac function causes progression of CKD
3.
Abrupt worsening of renal function causes acute cardiac dysfunction (heart failure,
arrhythmia, or ischemia)
4.
CKD contributes to decreased cardiac function resulting in hypertrophy and increased risk of
CVD
5.
A systemic condition results in both cardiac and renal dysfuction
Aging and Renal Function
Natural decline in GFR is 8ml/min for every decade after 40 despite normal creatinine
Renal blood flow declines by 10% per decade
Renal mass decreased from 400g to 300g by age 90
All the above accelerated by: HTN, DM, lead exposure, smoking, atherosclerotic vascular
disease, and male gender
Acute Kidney Injury
Incidence increasing with the number of hospitalizations with AKI diagnosis rose from 3,942 in
1996 to 23,052 in 2008
5% to 30% of hospital ICU admissions
25% of people develop while in the hospital
50% of cases are iatrogenic
Pre-renal- response to hypoperfusion->volume depetion, sepsis, heart failure, cirrhosis
Intra-renal- conditions that affect parenchyma->acute tubular necrosis, acute interstitial
nephritis, nephrotoxic medications
Post-renal-obstruction of urinary outflow->BPH, renal calculi
(Domino, 2013)
Nephrotic Syndrome
Clinical syndrome characterized by massive proteinuria (>3g/24hrs)
Associated with many types of kidney diseases such as minimal change disease, membranous
glomerulopathy, diabetes, and amyloidosis
Hypoalbuminemia
Edema
Hyperlipidemia
Lipiduria
May have fatigue, weight gain, anorexia, foamy urine
Treatment involves addressing underlying cause and complications
May need a kidney biopsy
May require long-term immunosuppressant therapy
(Domino, 2013)
End-Stage Renal Disease (ESRD)
Cardiovascular disorders are leading cause of death for ESRD patients
More than 50% of dialysis patients die from cardiovascular complications
Risk of CV death is 50% higher in this population if patient also has DM
Screen patients annually for CV disease with electrocardiogram, stress test
Refer to cardiologist
Signs and Symptoms of ESRD
Head-headaches, fatigue, and difficulty thinking
Mouth- food may taste bad or like metal, foul smelling breath (like urine)
Lungs-dyspnea caused by fluid or anemia
Stomach- loss of appetite, nausea and vomiting
Bladder- less or no urine. Some people still make urine but it is just fluid no waste products are
removed
Hands and feet- swelling
Skin-build up of uremic wastes causes itching
Blood vessels- high blood pressure failing kidneys can no longer keep pressure under control
(Greenburg, 2009)
Hemodialysis
Done through a vascular access (fistula, graft, or permacath)
Usually requires four hour sessions three days a week
Special considerations
•Some antibiotics require dose adjustment/timing adjustment to avoid removal of medication
through dialysis
Peritoneal Dialysis
Advantages
Disadvantages
Convenient done at home
High Risk for peritonitis
Daily treatments more closely match natural
renal functions
Requires compliance with aseptic technique
Patients have less fluid/dietary restrictions
Patients with history of multiple abdominal
surgeries or hernia may not be candidates
Renal Transplant
Evaluation process can start when GFR is <20
Many options are available such living relative, non-related living, and cadaver
Requires extensive workup to be placed on list
Compliance
Requires immunosuppressant therapy
Caution when prescribing/adjusting transplant patient’s medication
Burden of ESRD
Economic costs
Total Medicare costs for ESRD care in 2005 were $19.3 billion
Decreased quality of life
Increased morbidity and mortality
Complications associated with dialysis
Referral
Electrolyte abnormalities
Persistent proteinuria
Uncontrolled HTN
Elevated serum CR/decreased GFR –guidelines CR 1.5 female, 2.0 male
Patient with known CKD that are likely to progress
Don’t wait to refer to nephrologist when the patient needs dialysis
Patients need to have dialysis access, education, and preparation
Collaboration
CKD requires collaboration and coordination among many health care providers
CKD stages I-III usually managed by PCP
Nephrologist usually consulted when CKD III or other kidney disorder
Dietician
Cardiologist
Vascular Surgeons
Endocrinologist
Social workers
Educational Resources
National Kidney Foundation www.kidney.org
American Nephrology Nurse’s Association http://ww.annanurse.org
Internet School of Nephrology http://www.Ukidney.com
International Society of Nephrology http://www.theisn.org
American Society of Nephrology http://www.asn-online.org/
Questions
 The number one cause of death in patients with ESRD:
A. Complications from DM
B. Septicemia
D. Cardiovascular Disease
E. Cancer
 The functions of the kidney are:
A. Production and secretion of enzymes and hormones
B. Excretion of metabolic end products and foreign substances
C. Maintenance of body fluid composition
D. Both A & B
E. All of the above
 The best antibiotic choice for a 69 y/o female with a urinary tract infection
A. Cipro 250mg BID
B. Bactrim DS 1 tablet BID
C. Do not provide antibiotics wait for urine culture
References
Claudio, R., Haapio, M., House, A., Anavekar, N., & Bellomi, R. (2008, November). Cardiorenal
syndrome. Journal of American College of Cardiology, 52(19), 1527-1539.
Collins, T. (2012). Twelve things hospitalists need to know about nephrology. The Hospitalist.
Retrieved February 7, 2014 from http://the-hospitalist.org/details/article/3782901/12
Things Hospitalists Need to Know About Nephrology.html
Deja Review Internal Medicine (2011). Mobasser, S., McGraw Hill Medical, New York
Dunphy, L., Winland Brown, J., Porter, B., & Thomas, D. (2011). Primary Care: The art and science of advanced practice nursing. 3 rd Edition.
Philadelphia: F.A. Davis. ISBN 978-0-8036-2255-5.
Domino, F. (2013). Griffith’s 5 Minute Clinical Consult. 19th Ed. Lippincott Williams & Wilkins.
Fibromuscular Dysplasia (n.d.). Retrieved February 7, 2014 from http://www.mayoclinic.com/
health/fibromuscular-dysplasia/DSO1101.
Greenburg, A., Cheung, A.K., Coffman, T.M., Falk, R. J., Jennette, J.C. (2009). Primer on kidney diseases. (5th ed.), Philadelphia, Saunders Elsevier
National Kidney Foundation (2010). Nephrology essentials: chronic kidney disease. Retrieved
February 8,2014 from http://www.kidney.org/professionals/CAP/nephEssentials.cfm
References
National Kidney Foundation (2012). Clinical Practice Guidelines for Chronic Kidney Disease
Evaluation, Classification, and Stratification.
National Kidney and Urologic Diseases Information Clearinghouse (2012). Retrieved February
10, 2014 from http://www.nih.gov/kudiseases/pubs/kustats/#top
Niels-Peter, B., Farhat, A., Syed, R., Biyabani, Q., Masood, A., Imtiaz, R.(2012) Ultrasonographic
renal size in individuals without known renal disease. Journal of Pakistan Medical Association.