CKD pt 1 Flashcards
(115 cards)
1
Q
official definition of CKD
A
- presence of markers of kidney damage for 3+ months
- Structural or functional abnormalities of the kidney (+/- a current decrease in GFR) that can ultimately lead to decreased GFR
- Manifested by either pathological abnormalities or other markers of kidney damage, including abnormalities in the composition of blood or urine, or abnormalities in imaging tests.
OR - The presence of GFR <60 mL/min/1.73 m2 for 3+ months with or without other signs of kidney damage
2
Q
what is CKD (short definition)
A
Spectrum of disorders associated with abnormal kidney function and/or progressive decline in GFR
3
Q
Decline in function usually _____ even if cause is removed
CKD is due to _____
A
persists
nephron overwork injury
4
Q
pathophys of CKD
A
Kidneys respond to a reduction in the number of functional nephrons by signaling changes that lead to:
1. hyperfiltration
2. hypertrophy
3. RAAS plays a role in these changes
5
Q
how does hypertrophy change glomerular architecture? result?
A
Glomerular architecture becomes distorted with hypertrophy, hindering filtering abilities
Inflammation and fibrosis ensue
6
Q
what is “the renal rebound”
A
- may see an improvement in markers like BUN, Creatinine, and GFR in some circumstances!
- Recovery from AKI-on-CKD
- Removal of toxic substances
- Diet changes
- Improved hydration
- Control of other disease states
does NOT reflect the restoration of renal tissue, but rather the removal of disease burden on still-functioning nephrons.
7
Q
Over 70% of cases of late-stage CKD (Stage 5 or ESRD) are due to ?
A
DM
HTN/vascular disease
Other cases - glomerulonephritis, polycystic kidney disease,
chronic tubulointerstitial disease, etc.
8
Q
CKD is an independent risk factor for ?
A
CVD
9
Q
what type of CKD can ↑ risk of CV mortality
A
proteinuric CKD
10
Q
risk factors for CKD
A
- Patient Demographics
- Older age
- sub-Sarahan African ancestry - Historical Factors
- Previous episode of AKI
- FHx of renal disease
- Smoking
- Lead exposure - GU Conditions
- Structural urinary tract abnormalities
- Proteinuria
- Abnormal urinary sediment - Metabolic Conditions
- DM
- Low HDL
- Obesity
- MetS - Other Conditions
- HTN
- Autoimmune disease
- Cardiorenal Syndrome
11
Q
Deterioration of one organ results in deterioration of the other
A
Cardiorenal Syndrome (Renocardiac Syndrome)
12
Q
types of Cardiorenal Syndrome (Renocardiac Syndrome)
A
Type 1 (Acute CRS) - AKI caused by acute cardiac disease
Type 2 (Chronic CRS) - CKD caused by chronic cardiac disease
Type 3 (Acute RCS) - Acute cardiac disease caused by AKI
Type 4 (Chronic RCS) - Chronic cardiac decompensation caused by CKD
Type 5 (Secondary CRS) - Simultaneous heart and kidney dysfunction
caused by another acute or chronic systemic disorder
13
Q
Newer recommendation of staging CKD
A
GFR and albuminuria
14
Q
Higher levels of albuminuria =____ mortality risk, ____ CKD progression, _____ risk of ESRD - regardless of GFR
A
higher
15
Q
Early CKD
Kidney damage with normal GFR
GFR >90
what staging?
A
1
16
Q
Kidney damage with mildly decreased GFR
GFR 60-89
what staging?
A
2
17
Q
Mildly to moderately decreased GFR
GFR 45-59
what staging?
A
3a
18
Q
Moderately to severely decreased GFR
GFR 30-44
what staging
A
3b
19
Q
Severely decreased GFR
GFR 15-29
what staging
A
4
20
Q
Kidney failure / ESRD
May add D if treated with dialysis
GFR <15
what staging
A
5
21
Q
albumin Normal to mildly increased
AER < 30
what is the staging?
A
A1
22
Q
Moderately increased (microalbuminuria)
AER 30-300
what staging?
A
A2
23
Q
Severely increased (macroalbuminuria)
May be subdivided into nephrotic and non-nephrotic
AER >300
what staging?
A
A3
24
Q
s/s of early-mid CKD
A
asx
25
eventual s/s of early-mid CKD
slow onset of nonspecific s/s
26
MC PE finding of CKD overall
HTN
Present in early CKD, and worsens as CKD progresses
Later stages - volume overload
27
Late CKD s/s
waste build up - GFR ~10 mL/min/1.73 m2
Leads to S/S of uremia
S/S of uremia warrants admission and dialysis consult
Dialysis normally improves uremic syndrome
28
what specific sign can be seen in uncontrolled prolonged CKD?
Uremic Frost: crystallized urea excreted in sweat
29
low serums seen in CKD
Heme - RBC, H&H (normocytic, normochromic anemia)
Lytes/Acid-Base - Ca, Na, pH (Met. acidosis)
Renal - GFR
Others - vitamin D, HDL
30
high serums seen in CKD
Lytes/Acid-Base - K
Renal - BUN, sCr
Others - phosphate, PTH, triglycerides, uric acid
31
Broad, waxy casts in UA is seen in what condition?
CKD
32
what is often present in CKD UA?
proteinuria
glucosuria may be present
33
stage 1 and 2 CKD s/s
Usually no symptoms from decreased GFR
May see s/s from underlying disease
Edema, HTN
34
Anemia, fatigue, anorexia
Abnormal calcium, phosphorus, vitamin D, PTH
Abnormal Na, K, water, and acid-base balance
what stage of CKD could they be in?
stage 3 and 4
More likely to have S/S, abnormal labs
All organ systems usually affected by this point
35
marked disturbance in ADL, well being, nutrition, water and electrolyte homeostasis
uremic syndrome
what stage of CKD
stage 5/ESRD
36
does an abnormal renal imaging indicate CKD?
Yes!
Abnormal renal imaging can
indicate CKD even if there is
normal Cr/GFR
- Polycystic kidneys
- Small kidneys ( < 9-10 cm )
- Asymmetric kidneys (vascular disease)
37
main tx goal of CKD
slow progression
1. Control underlying process
2. Reduce intraglomerular HTN - ACE/ARB
3. Reduce proteinuria - ACE/ARB, dietary protein restriction
4. Avoid further injury - Obstruction, nephrotoxins, flare of underlying disease
5. If DM - control glucose (HbA1c <7%) - SGLT-2 inhibitors
6. Adjust medication doses as needed
38
80% of CKD pts die before needing dialysis, primarily due to ?
CV disease
_MC complication of CKD_
39
CV complications of CKD include:
Hypertension (HTN)
Coronary Artery Disease (CAD) / Hyperlipidemia
Heart Failure (HF)
Atrial Fibrillation
Pericarditis
40
HTN can be Exacerbated by ___ and ____ for CKD
hyperreninemia, exogenous EPO
41
goal bp for HTN complication of CKD
< 130/80 (or 140/90) mmHg
42
nonpharm tx for HTN - CKD
diet, exercise, wt loss
Treatment of OSA (if present)
Low sodium diet - 2300 mg/day
43
pharm tx for HTN - CKD
1. ACE inhibitors or ARBs
- _Check sCr and K+ in 7-14 d_ - starting or ￪ dose
- Hyperkalemia or >30% Cr increase - reduce or stop
2. Diuretics _nearly always needed_
- _Thiazides_ - early CKD
- _Loop_ - more effective in later CKD (GFR < 30)
- Overdiuresis or low vascular volume → AKI
3. Other anti-HTN rx - CCBs, BBs
44
primary finding + other labs of hyperlipidemia - CKD
**Hypertriglyceridemia**
Total cholesterol concentration - usually normal
Lower HDL and increased lipoprotein (a) also common
45
what CAD/hyperlipidemia condition is accelerated especially in ESRD?
atherosclerosis
46
tx for CAD / Hyperlipidemia - CKD
1. Lifestyle changes
2. Statins - recommended for most patients with CKD due to CV risk
3. PSK9 inhibitors and ezetimibe - may be used as adjunct to statin therapy
4. Fibrates - increased rhabdomyolysis risk when paired with statins in CKD pts
- Not shown to reduce risk of mortality
47
Increased cardiac workload in CKD can lead to what CV complication?
HF
48
HF from CKD is due to ?
HTN, volume overload, anemia, atherosclerosis
49
HF - CKD can lead to what dysfunction
LVH and diastolic dysfunction
Systolic dysfunction may also develop
50
what HF medication is higher risk for toxicity than non-CKD pts
digoxin
Due to electrolyte disturbances common in CKD
51
tx for HF - CKD
_Diuretics, ACE/ARB, fluid and salt restriction_
- Thiazides - early CKD
- Loop - later CKD (GFR <30)
- ACE/ARB - can help with progression of HF
Monitor closely for hyperkalemia
52
Disproportionately high rates of what irregular heart rhythm in late-stage and end-stage CKD? tx?
atrial fibrillation
Stage 1-4 CKD patients - treated similarly to general population
Stage 5/ESRD patients - higher bleeding risk with anticoag
53
Rare CV complication, but may develop in uremic patients
Always an indication for hospitalization and initiation of hemodialysis
Pericarditis
54
CKD is experiencing retrosternal chest pain, friction rub
what could they be experincing?
pericarditis
Uremic pericardial effusion - pulsus paradoxus, enlarged cardiac silhouette, low voltage QRS
Cardiac tamponade may develop
55
uremic pericardial effusions are generally ____, therefore you must avoid these medications
hemorrhagic
anticoags
56
MC mineral metabolism complication patterns
Abnormal calcium, phosphorus, PTH, active vitamin D
1. Hyperphosphatemia
- Decreased excretion by kidney
2. Hypovitaminosis D
- Decreased production by kidney
3. Hypocalcemia
- Phosphorus complexes with Ca
--- soft tissue deposits
- ￬ gut Ca absorption due to ￬ vitamin D
4. Secondary hyperparathyroidism
- Due to ￪ phosphate, ￬ calcium
57
mineral metabolism complicatoin commonly leads to what? how to diagnose it?
Renal Osteodystrophy
bone bx
58
which renal osteodystrophy is Due to hyperparathyroidism → osteoclast stimulation
High rates of bone turnover
Bone pain, proximal muscle weakness
Osteitis fibrosa cystica
59
types of renal osteodystrophy
1. **Osteitis fibrosa cystica MC**
2. Adynamic bone disease
3. Osteomalacia
_All_ increase the risk of fracture
60
which renal osteodystrophy is d/t - low bone turnover
Suppression of PTH or low endogenous PTH
adynamic bone disease
61
which renal osteodystrophy is d/t lack of bone mineralization. what were the MC causes in the past and now?
Osteomalacia
In the past → aluminum toxicity
Currently → due to hypovitaminosis D, bisphosphonates
62
first step tx for mineral metabolism
control hyperphosphatemia (≥ 4.5 mg/dL or ≥ 5.5 mg/dL in ESRD)
1. Initially - dietary phosphorus restriction
- Meats (especially processed), Colas, Baked, goods/mixes, Fast food, Frozen premade foods
2. Later - Oral phosphorus binders
- Calcium carbonate or calcium acetate
--- Block absorption of phosphorus in GI tract; dosed TID w/ meals
- _Non-calcium-based - first-line therapy_ - **Sevelamer** or **Lanthanum**
- Aluminum hydroxide - highly effective, but limited d/t SE
- Iron-based agents - ferric citrate, sucroferric oxyhydroxide - Limited evidence
63
which oral phosphorus binder may cause increased vascular calcification, hypercalcemia?
Calcium carbonate or calcium acetate
64
which oral phosphorous binder is Safe to combine either with a calcium-based phosphate binder
non-calcium-based - **Sevelamer** or **Lanthanum**
65
what are the potential SE of aluminum hydroxide as a oral phosphorus binder?
Osteomalacia, neurologic complications
May use if severe hyperphosphatemia (>7 mg/dL) or short periods (< 3 weeks)
66
overall tx plan for mineral metabolism
1. control hyperphosphatemia
2. manage PTH
67
After phosphorus levels are controlled, what is the next step of tx for mineral metabolism complication? how?
manage PTH:
1. **Vitamin D3 (calcitriol)**
* 0.25 or 0.5 mcg orally daily or every other day
* For secondary hyperparathyroidism in stage 3-5 CKD
* Measure and normalize vitamin D before using to tx elevated PTH
* Will increase serum Ca and phosphorus - Routine labs to monitor required
2. **Cinacalcet (Sensipar)** 30-90 mg orally once daily
* Targets calcium-sensing receptors of parathyroid gland
* Good option if ￪ phosphorus or Ca prohibit use of calcitriol
* May cause hypocalcemia
68
Goal PTH levels in late CKD are ? why?
higher - To avoid adynamic bone disease
69
anemia primarly due to ?
| Hematologic Complications - CKD
**decreased erythropoietin**
Often becomes significant during stage 3 CKD
70
Prior to tx with erythropoiesis-stimulating agents for anemia (CKD), what must we do beforehand?
must rule out other anemia causes
71
many CKD pts have what type of anemia? why?
**iron deficiency**
**Hepcidin** - blocks GI iron absorption and mobilization
of iron from body stores - **Elevated** in CKD patients
72
what is necessary before erythropoiesis - stimulating rx
what ranges make someone iron deficient?
| anemia - CKD
Adequate iron stores
Goal of higher iron stores in CKD patients
Ferritin < 100-200 ng/mL OR iron saturation < 20% = iron deficiency
73
iron deficiency tx for anemia complication from CKD
1. Oral therapy preferred for pre-ESRD CKD
* Ferrous sulfate, ferrous gluconate, or ferrous fumarate
* **Auryxia (ferric citrate)** - FDA-approved
2. If oral iron isn’t tolerated OR has poor response → parenteral iron
3. Do not give iron supplementation if ferritin
>500-800 ng/mL - Even if iron saturation <20%
74
Erythropoietin Tx for anemia complication from CKD
Goal Hb of 10-11 g/dL
* Higher Hb goal → increased risk of CV events
* Hb should rise at most 1 g/dL every 3-4 weeks
* Likely no benefit to starting tx if Hb > 9 g/dL
1. **epoetin** - given 1-2x/week
2. **darbepoetin** - given every 2-4 weeks
* Both may be given IV (hemodialysis) or SC
* **SC dosing - 30% more effective**
75
potention Se of erythropoietin tx for anemia complication
| CKD
HTN
76
what Coagulopathy is mainly d/t platelet dysfunction?
How would they present?
| CKD
Hypocoagulability
Prolonged bleeding time, petechiae, purpura
77
management for coagulopathy
1. Tx only indicated if symptomatic
* Raising Hb to 9-10 g/dL can reduce risk
* **Desmopressin** 25 mcg IV every 8-12 hrs x 2 doses
--- Short-lived; mainly used in preparation for surgery
* **Dialysis** - improves bleeding time
* Other Tx - conjugated estrogens, cryoprecipitate - rarely used
78
If severe proteinuria you may see what coagulopathy complication?
| CKD
**hyper**coagulability
79
what complication Usually manifests in stages 4-5
Can occur earlier in high potassium diet, DM pts, hemolysis, rhabdomyolysis, medications
| CKD
Hyperkalemia
80
what medicatoins can lead CKD ito hyperkalemia?
1. Decrease K+ secretion - triamterene, spironolactone, NSAIDs, ACE, ARB
2. Block K+ uptake by cells - BBs
81
tx for chronic hyperkalemia
1. Dietary K+ restriction
2. Reduce or stop medications that affect K+ metabolism
3. Loop diuretics (if not volume-depleted)
82
Loss of ability to excrete acid in the urine would lead to what acid-base complication?
| CKD
metabolic acidosis
83
Loss of ability to excrete acid in the urine is primarily due to what?
1. **loss of renal mass**
2. Distal tubules may be unable to help excrete
3. May lead to chronic metabolic acidosis
84
metabolic acidosis can contribute to what other CKD complication?
**renal osteodystrophy**
Calcium pulled from bones to help buffer acidosis
85
tx for metabolic acidosis
| CKD
Maintain serum bicarbonate at > 21 mEq/L
**Oral sodium bicarbonate** - given BID
86
this CKD complicatoin is Due to aggregation of uremic toxins
Uremic Encephalopathy
87
s/s of Uremic Encephalopathy
Early - difficulty concentrating
Later - lethargy, confusion, seizure, coma
Exam - altered mental status, asterixis, weakness
88
tx for uremic encephalopathy
Dialysis
89
Distal, symmetrical, mixed peripheral neuropathy
what is this CKD complication
Uremic Neuropathy
Indication to start dialysis
Can occur in some pts already on dialysis
90
s/s of Uremic Neuropathy
Sensory precedes motor
1. Initial - loss of position and vibration sense in toes, decreased DTRs
2. Sensory - paresthesias, burning, pain, RLS
3. Motor - may lead to muscle atrophy, myoclonus, eventual paralysis
91
diagnostic test for uremic neuropathy?
electrophysiologic studies
92
tx for uremic neurpathy
1. **dialysis** - Less improvement if sx present for a long time prior to dialysis
2. Symptomatic tx for neuropathic pain - **TCAs, anticonvulsants**
3. RLS - may improve with tx of anemia, iron deficiency
93
how does CKD affect renal clearance of insulin?
CKD → **decreased** renal clearance of insulin
Increased risk of **hypoglycemia**
May need _dose adjustment_ of oral medication, exogenous insulin
94
management for hypoglycemia complication from CKD
**Metformin** - discontinue after serum Cr > 1.4-1.5 or GFR < 30
Increased risk of lactic acidosis
95
reproductive changes in CKD complication
1. Decreased libido and ED are common
* Men - decreased testosterone
* Women - often anovulatory
2. Pregnancy - if serum Cr >1.4, CKD may progress faster
* Fetal mortality almost 50% in female ESRD pts
* Surviving infants are often premature
96
Best odds for healthy pregnancy for CKD pts
**transplant**
97
dietary changes in CKD
1. Protein restriction - Avoid if cachectic, low albumin
2. Sodium restriction - 2 g/d
* > 3-4 g/d → HTN, volume overload
* < 1 g/d → hypotension, volume depletion
3. Water restriction - 2 L/d (if volume overload)
4. Potassium restriction - *If GFR < 10-20 mL/min OR hyperkalemia*
5. Phosphorus restriction
If GFR < 20-30 mL/min - phosphate binders
98
medication changes in CKD
1. Renally excreted drugs - insulin, BBs, abx, etc.
- Adjust dose based on pt’s GFR and clinical presentation
2. AVOID
* Magnesium-containing drugs - laxatives, antacids, etc.
* Phosphorus-containing drugs - e.g., cathartic laxatives
* Nephrotoxic drugs - NSAIDs, IV contrast, etc.
* Morphine - metabolites can accumulate in late CKD - Not seen with other opioids
99
indications for dialysis in CKD
1. GFR <10
2. Uremic symptoms
3. metabolic disturbances
4. Fluid overload unresponsive to diuretics
100
Ideal method of renal replacement therapy
**Renal Transplantation**
No standardized criteria for recipients; 2-6 yr wait for transplant
101
most renal transplants are ?
deceased
2/3 transplants
102
which type of renal transplant has a better survival rate
living donors
103
factors determining renal transplant match
* ABO blood groups and major histocompatibility
* Age and race of recipient, age of donor
* Comorbidities (hyperlipidemia, HTN, CMV)
* Length of time spent on dialysis
104
what is the management for renal transplants afterward?
**immunosuppressive regimens**
* Must balance between avoiding rejection of graft and risk of side effects
* Cancer, infection, new-onset DM
* Transplant nephrologist usually also will follow the patient to manage medical regimen
105
which dialysis Requires a constant flow of blood along one side of a semipermeable membrane
hemodialysis
Diffusion and convection → removal of unwanted substances in blood and replacement of needed substances
MC modality for ESRD
106
types of hemodialysis
1. **Arteriovenous fistula (preferred)**
* Lasts longest
* Requires 6-8 wks for maturation after
* surgical construction
2. Prosthetic graft
* Shorter duration, but only needs 2 wks to mature
* Higher risk of infection, thrombosis, aneurysm than fistulas
3. Indwelling vascular catheter
* Very high risk of infection
* Temporary only
107
where can hemodialysis be done?
1. hemodialysis center
* 3x/wk for 3-5 hrs at a time
2. home with assistance
* 3-6x/wk for shorter sessions
108
how does the peritoneal dialysis work?
Peritoneal membrane acts as “dialyzer”
* Dialysate put in peritoneal cavity via indwelling catheter
* Water and solutes move across capillary bed in peritoneum between blood and dialysate
* Dialysate is periodically drained and new dialysate instilled
109
what are the types of peritoneal dialysis
* Continuous Ambulatory Peritoneal Dialysis (CAPD) - patient manually exchanges dialysate 4-6x/day
* Continuous Cyclic Peritoneal Dialysis (CCPD) - cycler machine automatically exchanges dialysate at night
110
pros vs cons of peritoneal dialysis
**Benefits**:
* Increased patient autonomy
* Continuous - less symptomatic volume and electrolyte shifts
* Poorly dialyzable compounds are better cleared → less diet restrictions
* May be better for pts with limited transport
* Allows pt to stay in their home
**Risks**:
* Removes large amounts of albumin
* Requires mental/physical ability to understand and complete exchanges
* Access may not be possible in patients with significant intra-abdominal adhesions or scarring
* Risk of peritonitis
111
MC complication of peritoneal dialysis
Peritonitis
112
pt on peritoneal dialysis is now experincing N/V/D/C, abd pain, fever, cloudy dialysate
their Peritoneal fluid >100 WBC/mcL, 51% PMNs
what are they experiencing?
peritonitis
112
MC pathogen to cause peritonitis
**staphylococcus aureus**
Gram negative rods, strep also common
May do culture for organism
Tx - abx for appropriate organism
112
prognosis for ESRD and dialysis
Higher mortality > renal transplant pts
* Little difference in survival for PD vs. HD
* Overall 5-year survival - 39%
* Estimated life expectancy - 3-5 years
113
MCC death of ESRD
cardiac disease (>50%)
Poor prognostic indicators - DM, advanced age, hypoalbuminemia, low socioeconomic status, inadequate dialysis, high fibroblast growth factor
