Download Nephrology.GRS9 - Geriatrics Care Online

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NEPHROLOGY
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OBJECTIVES
Know and understand:
• How age-related anatomic, hemodynamic, and hormonal
changes affect kidney function
• The most practical method of monitoring kidney function
in older adults
• How to recognize and manage the kidney diseases and
disorders that are most common in older adults
• At what point patients with chronic kidney disease need
referral to a nephrologist and renal dietician
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TOPICS COVERED
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Declines in Kidney Function with Aging
Kidney Assessment
Metabolic and Volume Disorders
Secondary Hypertension and Renal Artery Disease
Hematuria and Nephrolithiasis
Acute Kidney Injury
Intrinsic Renal Disease
Nephrotic Syndrome
Chronic Kidney Disease
End-Stage Renal Disease
DECLINES IN KIDNEY FUNCTION
WITH AGING (1 of 2)
Function
Mechanisms
Clinical significance
↓ GFR
Advanced glycation end
products
Comorbidities
Medication use
Chronic kidney disease
↑ risk of acute kidney
injury
↓ diluting
capacity
↑ ADH secretion
Comorbidities (CHF, liver, renal
disease)
Medications (thiazide diuretics)
↑ risk of hyponatremia
↓ concent↓ sensitivity of kidney to ADH
rating ability ↓ tonicity of renal medulla
↓ ADH at night in nocturnal
polyuria syndrome
↑ risk of hypernatremia
Poor compensation for
volume depletion
Nocturia
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DECLINES IN KIDNEY FUNCTION
WITH AGING (2 of 2)
Function
Mechanisms
Clinical significance
↓ sodium
↓ sodium reabsorption
Volume depletion
conservation ↓ plasma renin activity
Osmotic diuresis
↓ production of aldosterone Nocturia
↑ atrial natriuretic hormone
↓ sodium
excretion
↓ suppression of plasma
renin activity with sodium
loading
Salt sensitive
hypertension
Edema
↓ ammonium ↓ plasma renin activity
Metabolic acidosis
production
↓ production of aldosterone
and
↓ GFR
generation of
bicarbonate
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KIDNEY ASSESSMENT
• Serum creatinine can be misleading
 Decline in muscle mass parallels decline in kidney function,
can lead to stable serum creatinine despite declining GFR
• The GFR is the most important indicator of kidney
function in older adults
• Direct measurement of GFR is not practical in clinical
settings, so estimation formulas are used:
 Cockcroft-Gault
 Modified Diet in Renal Disease (MDRD)
 CKD-Epi
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MEASURES OF KIDNEY FUNCTION
• Many clinical laboratories now provide an
estimated GFR usually based on the CKD-Epi
formula
• Valid only when serum creatinine is stable
• Maybe in unreliable in patients with more or less
muscle mass than average patients their age:
 Very obese patients
 Those with cachexia
 Amputees
MEASURES OF URINARY PROTEIN
EXCRETION
• Standard urine dipstick is a simple screening test
 Insensitive for low levels of proteinuria
 Reacts with negative charged proteins like albumin,
but not positive charged proteins like light chains
• Urine microalbumin/creatinine ratio
 Best screening test for low levels of albuminuria in
high-risk individuals
 Microalbuminuria: 30-300 mg/g creatinine
 Frank albuminuria >300 mg/g creatinine
• Urine albumin/creatinine ratio provides an estimate of
24-hour albumin excretion
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CHANGES IN ANTIDIURETIC HORMONE
(ADH) WITH AGING
• ADH regulates water balance
• Leads to reabsorption of water through water
channels, resulting in concentrated urine
• Normally suppressed in hyponatremia,
increased in severe volume depletion
• ADH system is altered in older adults
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HYPONATREMIA
• Occurs in 11.3% of hospitalized geriatric patients
and up to 22.5% of older adults in long-term
care facilities
• Older adults have diminished ability to excrete a
free water load
• Many medications and common medical
comorbidities in older adults also contribute to
hyponatremia
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RECOGNIZING HYPONATREMIA
• Overt symptoms most likely to develop when serum
sodium concentration acutely falls below 125 mEq/L
• Brain edema can lead to apathy, disorientation,
lethargy, muscle cramps, anorexia, nausea,
agitation, headache, seizures, and coma
• Even when mild and apparently asymptomatic,
hyponatremia is associated with deficits in gait and
attention, falls, and increased fracture risk
• The only manifestations of chronic hyponatremia
may be lethargy, confusion, and malaise
DETERMINING UNDERLYING CAUSE OF
HYPONATREMIA
• Obtain serum osmolality
– Most hyponatremia is hypotonic, with low
serum osmolality
• Next determine the patient’s volume status
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HYPONATREMIA WITH VOLUME DEPLETION
• Older adults are prone to volume depletion (due to
comorbidities, meds such as diuretics, decreased
aldosterone secretion, exaggerated atrial natriuretic
hormone release)
• Significant volume depletion leads to release of
ADH, which stimulates the kidneys to concentrate
the urine
• Urine sodium concentration <10 mEq/L
• Serum sodium drops when patient takes in free
water
• Treatment: replete intravascular volume with
isotonic fluid
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HYPONATREMIA WITH VOLUME OVERLOAD
• Common conditions: heart failure, cirrhosis,
nephrotic syndrome
• Decrease in effective arterial volume stimulates the
renin-angiotensin-aldosterone system (RAAS)
promoting salt retention and edema, and stimulates
ADH release
• Urine sodium concentration <10 mEq/L
• Patients are edematous and thirsty
• Treatment: fluid restriction and loop diuretics
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HYPONATREMIA WITH NORMAL
EXTRACELLULAR FLUID VOLUME
• Causes include kidney disease, thiazide diuretics,
hypothyroidism, adrenal insufficiency, SIADH, reset
osmostat
• SIADH
– Usually urine sodium >40 mEq/L
– May be caused by pulmonary and brain pathology,
medications, agents that potentiate ADH
– Treatment: discontinuation of offending medications, fluid
restriction, loop diuretics, occasionally demeclocycline,
lithium, or tolvaptan
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TREATMENT OF SEVERE OR
SYMPTOMATIC HYPONATREMIA
• Urgent/emergent treatment indicated when
hyponatremia is severe (<120 mEq/L) or
symptomatic
• Treat with IV hypertonic saline
 Monitor volume status and sodium levels
frequently
 Avoid overly rapid correction of chronic
hyponatremia, which can result in central pontine
myelinolysis
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HYPERNATREMIA
• Major risk factors: Impaired thirst, immobility,
depressed level of consciousness, systemic
illnesses, infections, fever, dementia, and
neurologic disorders, meds that cloud the
sensorium, osmotic diuretics, tube feedings with
high protein and glucose, bowel cathartics
• Neurologic sequelae can include obtundation,
stupor, coma, and death
• Correct free water deficits over 72 hours by
encouraging oral fluid intake, or administering IV
or enteral free water
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HYPO/HYPERVOLEMIA
• Hypovolemia
 Sodium and water deficit
 Older adults at increased risk due to decreased RAAS
activity and increased atrial natriuretic hormone
 May be due to medications such as diuretics, or conditions
such as diarrhea or vomiting
 Treatment: replace both salt and water
• Hypervolemia
– May be due to underlying conditions or medications
– Treatment: treat underlying conditions, discontinue
offending medications, judicious use of diuretics
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HYPOKALEMIA
• Causes in older adults:
• Volume depletion leading to stimulation of the RAAS
• GI losses from vomiting, diarrhea, fistula drainage
• Medications (loop and thiazide diuretics, cathartics)
• Inadequate intake of potassium
• Treatment: correct volume depletion,
discontinue offending medications, increase
potassium intake
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HYPERKALEMIA
• Increased risk in older adults due to age-related decline in
aldosterone levels
• May be spurious due to hemolysis, should repeat
• Treatment of severe hyperkalemia:
• Hospital admission
• IV calcium to stabilize the myocardium
• IV insulin and glucose, sodium bicarbonate, nebulized albuterol
to shift potassium into cells
• Meds that remove potassium including diuretics, sodium
polystyrene (Kayexalate), and patiromer (Veltessa)
• Dialysis may be necessary in severe cases
DISORDERS OF ACID-BASE BALANCE
• Metabolic acidosis
 When severe may lead to shortness of breath as the
respiratory system attempts to blow off CO2
 Chronic acidosis contributes to bone loss and progression
of CKD
 Treatment: administration of exogenous base (sodium
bicarbonate tablets or powder, or citrate salts)
• Metabolic alkalosis
 When severe may decrease respiratory drive
 Treatment: cessation of diuretics and administration of
saline to volume-depleted patients, acetazolamide to
volume-overloaded patients
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SECONDARY HYPERTENSION
• Suspect secondary cause in patients with
new onset, very severe, or accelerated
hypertension
• Most hypertension is idiopathic but secondary
causes include renal arterial disease,
mineralocorticoid HTN, hypercortisolism,
pheochromocytoma, CKD
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RENAL ARTERY DISEASE
• Risk factors: smoking, HTN, hyperlipidemia,
diabetes mellitus, dissecting aortic aneurysms
• Suspect in patients with other vascular disease,
new-onset HTN, acceleration of previously
controlled HTN, resistant HTN, progressive
azotemia after starting ACE inhibitor or ARB
• Management:
– Medical: BP control with ACE inhibitor or ARB
– Renal angiography and stenting is not indicated except in
extreme cases of uncontrollable HTN or progressive
kidney failure from severe stenosis
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HEMATURIA AND NEPHROLITHIASIS
• Hematuria may be due to glomerular disease,
infection, stones, AV malformations, neoplasms
• Evaluation:
Urine culture
Microscopic evaluation of the urine
Imaging depends on setting, may include plain
abdominal radiograph, CT scan with/without
contrast, ultrasound
Urology consultation and cystoscopy often
recommended
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ACUTE KIDNEY INJURY (AKI)
• Acute increase in creatinine, and oliguria (<5
mL/kg/hr urine output over at least 6h)
• Even minor increases in creatinine have been
associated with increased risk of prolonged
hospitalization and death
• Differential diagnosis of AKI
 Prerenal
 Intrinsic renal
 Postrenal
• Most common cause of AKI in older adults is acute
tubular necrosis, followed by prerenal azotemia
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PRERENAL AZOTEMIA
• Diagnosis is suggested by BUN:creatinine ratio >20,
fractional excretion of sodium (FENa)<1%
• Risks: physiologic changes with aging, acute illness
leading to poor oral intake, GI fluid loss,
comorbidities such as CHF and renal artery disease,
meds such as diuretics, ACE inhibitors, ARBs,
NSAIDs, reduced access to fluids
• Treatment:
 Volume resuscitation
 Discontinue or reduce offending meds
 Consider colloid infusion in hypoalbuminemic states
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CARDIORENAL SYNDROME
• Acute and chronic kidney injury that occurs in
systolic or diastolic heart failure due to a
combination of diminished forward flow and
increased central venous pressure
• Poor prognosis
• Treatment:
 Optimize cardiac function, typically with diuretics and
afterload-reducing agents
 Occasionally inotropic support
 Discontinue or reduce meds that impair renal
autoregulation
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OBSTRUCTIVE UROPATHY
• Common and often reversible cause of AKI
• Bladder outlet obstruction
 BPH most common cause in men
 Functional bladder outlet obstruction can occur in both
genders, caused by anticholinergic medications
 Other causes include bladder carcinoma and urethral
stricture
• Ureteral obstruction
 Often caused by stones, strictures, retroperitoneal
malignancies
 Additional imaging and urology consultation is usually
warranted
INTRINSIC RENAL DISEASE:
ACUTE TUBULAR NECROSIS
• Ischemia is the most common cause in older adults
• Evolution of prerenal azotemia to frank ATN is more
common in older patients with AKI (23%) than in
younger ones (15%)
• Diagnosis of ATN:
 Urine sediment includes renal tubular epithelial cells and
granular “muddy brown” casts
 In oliguria, FENa >2% (in setting of diuretic use, fractional
excretion of urea >35%)
• Treatment of ATN is generally supportive; often
reversible over days to weeks
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INTRINSIC RENAL DISEASE:
ACUTE INTERSTITIAL NEPHRITIS
• Most commonly an allergic response to medication,
though can also be caused by viral infections
• Any med can cause it, but antibiotics are most commonly
implicated, particularly β-lactams and fluoroquinolones
• Diagnostic clues: sterile pyuria, with WBC casts and/or
eosinophils on UA, CBC with diff with eosinophilia
• Therapy: Discontinue the offending agent
 Recent retrospective data suggest that a course of
corticosteroids may speed recovery
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INTRINSIC RENAL DISEASE: MULTIPLE
MYELOMA
• Malignant plasma cells generate monoclonal
proteins that form casts and obstruct renal tubules =
“myeloma kidney”
• Abnormal proteins can deposit in renal parenchyma
(“light-chain” or “heavy-chain deposition disease”) or
form fibrils that deposit as amyloid
• Associated with heavy proteinuria, severe
hypercalcemia, low anion gap, increased protein
gap, anemia, bone pain
• Treatment: chemotherapy such as melphalan and
prednisone, may result in improvement of the
associated kidney problems
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INTRINSIC RENAL DISEASE: VASCULAR
DISEASE
• Atheroembolic disease: cholesterol microemboli lodge in
small vessels of kidneys, risks include angiography and
use of warfarin
• Thrombotic microangiopathy: platelet microthrombi
occlude small renal arterioles, such as in
thrombocytopenic purpura (TTP) and hemolytic uremic
syndrome (HUS), or malignant HTN, catastrophic
antiphospholipid antibody syndrome, and scleroderma
renal crisis
• Acute renal artery occlusion: can occur in renal artery
stenosis or as result of embolism from afib or
paradoxical venous thromboembolism
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INTRINSIC RENAL DISEASE:
GLOMERULAR DISEASE (1 of 3)
• Rapidly progressive glomerulonephritis (RPGN):
– most common form of acute glomerulonephritis in older
adults
– Many causes, including ANCA-associated vasculitis,
Goodpasture’s disease, lupus nephritis, IgA nephropathy,
infection-associated glomerulonephritis
– Therapy: IV followed by oral steroids and additional
immunosuppression, plasmapheresis in severe acute
cases; once remission achieved, maintenance with
azathioprine or mycophenolate
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INTRINSIC RENAL DISEASE:
GLOMERULAR DISEASE (2 of 3)
• Acute nephritic syndrome:
 Decreasing kidney function, hematuria with dysmorphic
red cells and red cell casts, variable proteinuria, HTN, and
fluid retention
 Diagnosis may be delayed in older adults due to
incorrectly attributing symptoms to common conditions like
UTI, heart failure, or venous stasis disease
• Postinfectious glomerulonephritis:
 Occurs in the setting of infections such as streptococcal
infection of throat and skin, or staphylococcal infections
 Treatment: supportive. Postinfectious glomerulonephritis is
generally self limited with favorable prognosis
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INTRINSIC RENAL DISEASE:
GLOMERULAR DISEASE (3 of 3)
• IgA nephropathy (Berger disease):
 Presents as acute or chronic nephritis syndrome with
variable proteinuria
 May be primary or secondary to cirrhosis, celiac disease,
or infection with HIV, CMV, Haemophilus parainfluenzae,
Staphylococcus aureus, disseminated tuberculosis, and
toxoplasmosis
 Treatment: control underlying condition, BP control with
ACE inhibitor if possible, management of CKD, steroids or
other immunosuppressants are sometimes used for severe
exacerbations
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INTRODUCTION TO
NEPHROTIC SYNDROME
• Defined as urinary excretion >3.5 g of protein per day, with
associated hypoalbuminemia, hyperlipidemia, and edema
• Hypertension and renal failure are seen in about 1/3 of cases
in older adults
• Can result from primary glomerular disease or from infection,
malignancy, exposure to allergens or medications, diabetes, or
HTN
• Renal biopsy is essential for early diagnosis and appropriate
therapy
• Therapy: BP control, use of RAAS blockers, sodium restriction,
statins for hyperlipidemia, anticoagulation when plasma
albumin <2.8 g/dL
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MEMBRANOUS NEPHROPATHY
• Most common histopathology in the geriatric population
• Most patients have idiopathic disease; NSAID use and
malignancy are the 2 most common causes of
secondary membranous nephropathy
 Up to 20% of patients have solid organ tumors
• The prognosis for older adults is quite variable and
correlates somewhat to the severity of the syndrome
• Therapy includes calcineurin inhibitors, with or without
low-dose steroids, or cyclic corticosteroids and
cytotoxic agents
FOCAL SEGMENTAL
GLOMERULOSCLEROSIS (FSGS)
• Primary FSGS is idiopathic, secondary causes include
infections such as hepatitis B, parvovirus, or HIV;
malignancies including lymphoma; medications including
pamidronate; morbid obesity; many forms of advanced
CKD
• Basic treatment principles: correct reversible causes,
control blood pressure, use ACE inhibitors or ARBs to
minimize proteinuria, moderately restrict dietary protein,
and in primary disease, a prolonged course of steroid
therapy or calcineurin inhibitor therapy
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MINIMAL CHANGE DISEASE
• Can be idiopathic or associated with hypersensitivity
reactions, hematologic malignancies, or drugs,
particularly NSAIDs
• In older adults, presents with abrupt onset of fullblown nephrotic syndrome and normal BP; risk of
AKI is increased
• Treatment: prolonged course of high-dose steroids;
other agents such as calcineurin inhibitors or
cyclophosphamide may be tried when steroids are
not tolerated
• Up to 80% of older patients respond to initial therapy
with steroids, but with relapse rates up to 33%
AMYLOIDOSIS AND OTHER PROTEIN
DEPOSITION DISEASES
• For evaluation, use renal biopsy or abdominal fat pad
biopsy stained with Congo red or thioflavine T
• Renal tissue should be examined by electron
microscopy for myeloid fibrils
• Paraproteinemia can be found in up to 68% of patients
with primary amyloidosis
 Order both serum and urine immunoelectrophoresis for all
older adults with nephrotic syndrome; if findings are abnormal,
order bone marrow biopsy to exclude multiple myeloma
• Treatment with appropriate chemotherapy regimen can
delay progression to ESRD
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CHRONIC KIDNEY DISEASE
• Kidney function as measured by GFR declines
on average 8mL/min per decade after age 40
• Renal glomerular and tubulointerstitial fibrosis
increases with age, leading to CKD
• Frequently manifests with a decompensation of
preexisting medical illness such as heart failure,
diabetes mellitus, HTN, or dementia
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STAGES OF CKD
GFR
(mL/min/1.73 m2)
Stage
Description
1
Kidney damage with normal or
↑ GFR
2
Kidney damage with mildly ↓
GFR
60–89
3A
Mildly to moderately ↓ GFR
45–59
3B
Moderately to severely ↓ GFR
30–44
4
Severely ↓ GFR
15–29
5
Kidney failure (end-stage renal
disease)
>90
<15
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PRINCIPLES OF MANAGING CKD
• Emphasize preservation of residual renal
function and limiting complications
• Correct reversible causes
• Control blood pressure
• Use RAAS blockers to decrease proteinuria
• Control diabetes
• Moderately restrict dietary protein
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RISK OF CARDIOVASCULAR EVENTS
• Patients with CKD of all stages are at increased risk
of cardiovascular events
• Far more likely to die of cardiovascular disease than
to require dialysis
• Aggressively manage CV risk factors
 BP control
 Lipid-lowering therapy
 Smoking cessation
 Attention to diet and exercise
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MEDICATION USE IN CKD
• Complicated by diminished renal clearance
• Compounded by age-associated changes in
pharmacokinetics and pharmacodynamics
• Many medications or their metabolites are renally
excreted
• Verify renal dosing of any new medication being
prescribed
• Avoid or use extreme care prescribing nephrotoxic
medications in patients with CKD
 NSAIDs, radiocontrast agents, gadolinium, aminoglycosides,
amphotericin B
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MANAGING ANEMIA IN CKD
• Screen for anemia starting at stage 3B CKD
• Exclude other causes of anemia before treating
• Erythropoiesis-stimulating agents (ESAs) are
often used to prevent the need for blood
transfusions
• Iron should be replaced prior to starting ESA
• Goal ferritin >100 ng/mL and transferrin saturation
>20%
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CALCIUM, PHOSPHORUS,
AND BONE DISEASE IN CKD (1 of 2)
• Screening for calcium, phosphorus, and PTH
abnormalities should begin in Stage 3 CKD
• Maintain phosphorus concentrations between 2.7
and 4.6 mg/dL in patients with stage 3 or 4 CKD
 Start dietary phosphorus restriction if PTH is
increased, even if serum phosphorus is normal
 Use phosphorus binders when PTH starts to
increase
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CALCIUM, PHOSPHORUS,
AND BONE DISEASE IN CKD (2 of 2)
• Markedly increased PTH is associated with high
bone turnover disease, which increases fracture risk
 Can be suppressed with active vitamin D metabolites, but
must monitor calcium levels
• Bisphosphonates are the recommended treatment
of choice for osteoporosis in the early stages of
CKD
 Efficacious in the transplant population
 Contraindicated in adynamic bone disease
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MANAGING DEPRESSION IN CKD
• Screening for depression is warranted for all patients
with CKD
 Diagnosis can be difficult; vegetative symptoms can be
similar to those of uremia or insufficient dialysis
 Functional and cognitive decline are common presenting
symptoms of depression in older adults with CKD
 Most depression screening instruments have been
validated in the kidney failure population
• Very low doses of SSRIs are safe, but avoid the longacting medications
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NUTRITION AND CKD
• Dietary requirements for patients with CKD
are complex
 Intake of protein, phosphorus, and potassium
all need to be controlled while maintaining
adequate energy intake
• Once a patient reaches stage 4 CKD, an
experienced renal dietician should be
involved in the patient’s nutritional
management
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END-STAGE RENAL DISEASE (ESRD)
• More than 38% of patients with ESRD are ≥65
• Although incidence rates in older adults have
plateaued in recent years, the number of affected
individuals continues to increase as the
population ages
• There has been a trend to offer dialysis to older
and sicker patients
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RENAL REPLACEMENT THERAPY
• Patients with Stage 4 CKD should be referred to a
nephrologist to discuss preparations for ESRD
• Dialysis is initiated when clear indications arise,
usually with an eGFR <10 mL/min
• Decision to pursue dialysis is highly individualized
and should always include a cogent discussion
regarding goals of care and potential benefits and
harms
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LIFE EXPECTANCY WITH DIALYSIS AND
KIDNEY TRANSPLANTATION
Remaining life expectancy, yr
Age, yr
General
Population
Dialysis
Population
Transplant
Population
40–44
30.1–40.8
6.7–9.2
30.1–40.8
50–54
22.5–31.5
5.1–6.9
22.5–31.5
60–64
16.0–22.8
3.7–5.1
16.0–22.8
70–74
10.8–15.2
2.7–3.5
10.8–15.2
80–84
6.9–8.8
2.0–2.4
6.9–8.8
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KIDNEY TRANSPLANTATION
• As in younger patients, mortality rates in older patients
with kidney transplants are considerably less than in
those maintained on dialysis
• Older kidney recipients demonstrate lower acute
rejection rates, lower incidence of chronic rejection, and
higher risk of infection and sepsis than younger
recipients
• Suitable older patients and their families should explore
the option of transplantation before the need for renal
replacement therapy arises
NONAGGRESSIVE RENAL CARE
AND HOSPICE
• Patients with advanced CKD who opt for
nonaggressive renal care have several options for
symptomatic treatment




Diuretics for fluid overload and hyperkalemia
Low-protein diet to limit production of uremic toxins
Iron and erythropoietin to limit symptomatic anemia
Stop unnecessary meds like statins and some BP meds
• Once a chronic dialysis patient stops dialysis, death
usually occurs within 7-14 days
• Failure to thrive is the driving reason to stop dialysis
in almost half of cases
• Less than half use hospice
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CHOOSING WISELY®
• Do not use antimicrobials to treat bacteriuria in older
adults unless specific urinary tract symptoms are
present.
• Avoid NSAIDs in individuals with hypertension or heart
failure or chronic kidney disease of all causes, including
diabetes mellitus.
• Do not initiate erythropoiesis-stimulating agents to
patients with chronic kidney disease with Hb ≥10 g/dL
without signs or symptoms.
• Do not perform routine cancer screening for dialysis
patients with limited life expectancies without signs or
symptoms.
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SUMMARY (1 of 2)
• As people age, their kidneys become less able to
maintain homeostasis in response to physiologic
stress.
• Serum creatinine is a poor marker of kidney function.
Kidney function is best approximated by the estimated
glomerular filtration rate (eGFR).
• Causes of acute kidney injury are divided into prerenal
azotemia, urinary tract obstruction, and intrinsic kidney
disease, which may be glomerular, tubulointerstitial, or
vascular in origin.
58
SUMMARY (2 of 2)
• Chronic kidney disease (CKD) is a disease of the older
population and is classified into stages based on GFR.
Preventing progression of CKD is important at any
age.
• Referral to a nephrologist is recommended when
eGFR decreases to <30 mL/min (Stage 4 CKD) for
help in management of CKD-related complications and
discussions regarding dialysis and transplantation
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CASE 1 (1 of 4)
• A 73-year-old man is brought to the emergency
department because of chest pain.
 EKG is consistent with myocardial ischemia.
• History: diabetes mellitus, gout, hypertension,
hyperlipidemia, chronic kidney disease (serum
creatinine 2.8 mg/dL)
60
CASE 1 (2 of 4)
• Hospital course
 Before cardiac catheterization, fluids administered
intravenously to reduce contrast-associated renal injury.
 During procedure, 120 mL of noniodinated, low-osmolarity
contrast is administered.
 Transient hypotension develops.
 Over the next few days, severe hypertension and GI bleeding
develop, and toes on his right foot turn purple.
 Serum creatinine level increases to 6.5 mg/dL, necessitating
hemodialysis.
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CASE 1 (3 of 4)
Which one of the following most likely caused his
renal failure?
A. Cholesterol embolization to the small arteries
and arterioles in the kidney
B. Heart failure with prerenal azotemia
C. Ischemic acute tubular necrosis caused by
hypotension during catheterization
D. Radiocontrast-induced nephrotoxicity
62
CASE 1 (4 of 4)
Which one of the following most likely caused his
renal failure?
A. Cholesterol embolization to the small arteries
and arterioles in the kidney
B. Heart failure with prerenal azotemia
C. Ischemic acute tubular necrosis caused by
hypotension during catheterization
D. Radiocontrast-induced nephrotoxicity
63
CASE 2 (1 of 4)
• A 67-year-old man is admitted to the hospital because
he has an abscess in his right arm.
 Cultures are positive for Staphylococcus aureus.
 He improves after treatment with nafcillin and is discharged
home on a 6-week course of dicloxacillin.
 The next day, a fever develops and he returns to the hospital.
• Examination
 Temperature 38.6°C (101.5°F), blood pressure 118/68 mmHg,
pulse 78 bpm
 Lung, heart, and abdominal findings are unremarkable.
 No rashes
 No lower-extremity edema
64
CASE 2 (2 of 4)
• Laboratory findings
 Serum creatinine 3.2 mg/dL (up from 1.1 mg/dL 1 week ago)
 Urinalysis
 pH 6.5, specific gravity 1.020, +1 blood, trace protein
 Leukocyte esterase and nitrite are negative
 Microscopically, there are sheets of white cells and 1–5 red
cells/hpf that are homogeneous
65
CASE 2 (3 of 4)
Which one of the following is the most likely
cause of his acute kidney injury?
A. Acute tubular necrosis
B. Urinary tract infection
C. Acute interstitial nephritis
D. Postinfectious glomerulonephritis
E. Immunoglobulin A nephropathy
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CASE 2 (4 of 4)
Which one of the following is the most likely
cause of his acute kidney injury?
A. Acute tubular necrosis
B. Urinary tract infection
C. Acute interstitial nephritis
D. Postinfectious glomerulonephritis
E. Immunoglobulin A nephropathy
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GRS9 Slides Editor:
Tia Kostas, MD
GRS9 Chapter Authors:
Joshua I. Bernstein, MD
Josette A. Rivera, MD
GRS9 Question Writers:
Emaad Abdel-Rahman, MD, PhD, FASN
Managing Editor:
Andrea N. Sherman, MS
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American Geriatrics Society