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Acute Care I - Spring 2017 > Module 10: Renal Dysfunction > Flashcards

Module 10: Renal Dysfunction Flashcards

1
Q

what are the main functions of the kidney

A
  1. Regulatory function: water and electrolyte (Na, K, Ca, glucose) homeostasis; maintenance of acid/base balance
  2. excretion of metabolic waste through urine
  3. hormone secretion: erythropoietin (red blood cell production); activation vitamin D (bone health); renin production (BP regulation)
  4. metabolic function: metabolism of drugs and endogenous substances
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2
Q

how is kidney function measured

A
  1. creatinine is freely filtered across the glomerulus and is neither reabsorned nor metabolized by the kidney. ~10-40% of urinary creatinine is derived from tubular secretion
  2. creatinine clearance, tends to exceed the true glomerular filtration rate by ~10-20%.
    3.
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3
Q

what is GFR

A

GFR is equal to the sum of the filtration rates in all of the functioning nephrons

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4
Q

how much does the glomeruli filter / day?

A

180 L /day

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5
Q

what does GFR depend upon?

A

age, sex, body size. 130 in men, 120 in women

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6
Q

what does serum Cr measure

A

kidney function. not a marker of kidney injury (there are some, but mostly for research purposes)

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7
Q

how do you estimate ckd stage?

A
  • not used w/ AKI
  • cause use Cockroft-Gault equation (but not used that much)
  • can used modification of diet in renal disease study group (MDRD) formula. more accurate than creatinine clearnce measured from 24 hour urine collections or estimated by cockcroft-gault formula.
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8
Q

when is MDRD formula not accurate?

A

if GFR > 60 ml/min, or at extreme weights/age.

-not validated if age > 70

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9
Q

CKD-EPI creatinine equation, why deveolped?

A

in an effort to create a formula more accurate than MDRD formula, especially when actual GFR>60

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10
Q

what does cystatin C equation do?

A

takes out muscle mass form the equation

  • it’s an endogenous compound that has been evaluated to measure GFR b/c of the imperfections of using serum creatinine
  • it is a protein that is produced by all nucleated cells that is freely filtered by the glomerulus
  • not secreted or absorbed as an intact molecule
  • reported to be generated at a relatively constant rate, independent of age, sex, muscle mass
  • not yet routinely used clinically
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11
Q

what is good about CKD-EPI creatinine cystatin equation

A
  • may be more accurate than Cr in some populations
  • may provide more accurate estimates in patients w/ extremes of muscle mass, or those outside the boundaries of where the MDRD equation has been validated
  • may be useful in estimating GFR change over time in people with changing muslce mass or diet
  • may help identify CKD patients who have highest risk for complications
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12
Q

what is CKD

A

-presence of kidney damage:

urinary albumin excretion > 30 mg/day

OR

decreased kidney function - GFR <60

for > 3 months regardless of cause

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13
Q

what distinguishes CKD from AKI

A

persistence of damage or decreased function for > 3 months

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14
Q

is it normal to have normal creatinine and protein in the urine?

A

no - should refer to nephrologist.

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15
Q

what is stage 1 of CKD

A

gfr: 90+
description: normal kidney function but urine findings or structural abnormalities or genetic trait point to kidney disease
treatment: observation, control BP

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16
Q

what is stage 2 ckd

A

gfr: 60-89
description: mildly reduced kidney function, other findings that point to kidney disease
treatment: observation, control BP & other risk factors

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17
Q

what is stage 3A ckd

A

gfr: 45-59
description: moderately reduced kidney function
treatment: observation, control BP & risk factors

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18
Q

what is stage 3b ckd

A

gfr: 30-44
description: moderately reduced kidney function
treatment: observation, control BP & risk factors

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19
Q

what is stage 4 ckd

A

gfr: 15-29
description: severely reduced kidney function
treatment: planning for esrd

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20
Q

what is stge 5 ckd

A

gfr: < 15; or on dialysis
description: very severe; or end stage kidney failure/established renal failure
treatment: dialysis

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21
Q

what is definition of chronic kidney disease

A

2 samples at least 90 days apart.

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22
Q

what was acute kidney injury formerly called?

A

acute renal failure

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23
Q

what is aki?

A

rise in serum creatinine or decline in urine output that has developed within hours to days

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24
Q

criteria for aki?

A
  • increase in serum creatinine by > 0.3 within 48 hours
  • increase to > 1.5 presumed baseline S Cr that is known or presumed to have occurred w/in the prior week
  • decrease in urine volume to < 3 mL / kg over 6 hours.
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25
Q

should you assume that admission Cr is the baseline

A

no, may have an AKI on admission

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26
Q

epidemiology of aki

A
  • incidence varies
  • more common in hospitalized elders
  • very common in icu patients
  • associated w/ high mortality
  • may have progressive kidney dysfunction after severe aki.
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27
Q

risk factors for aki

A
  • pre-existing ckd or previous aki
  • older age
  • comorbid conditions: dm, htn, cvd, surgery, infections, CHF, shock,
  • potentially nephrotoxic medications
  • exposure to iodinated iv contrast
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28
Q

aki prevention/consideration

A
  • anticipate risks
  • maintain adequate perfusion
  • attention to medications
  • be aware and avoid nephrotoxic drugs (NSAID, iodinated iv/ia contrast, aminoglycosides)
  • med dose adjustment
  • med dosing may change if kidney function is changing.
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29
Q

3 causes of aki

A

pre-renal
intra renal
post renal

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30
Q

pre renal aki

A

sudden and severe drop in BP (shock) or interruption of blood flow to the kidneys from severe injury or illness

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31
Q

intra renal aki?

A

direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply

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32
Q

post renal aki?

A

sudden obstruction of urine flow d/t enlarged prostate, kidney stones, bladder tumor, injury

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33
Q

important clues for aki

A
  • age
  • race
  • family history
  • occupation
  • allergies
  • medications
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34
Q

signs / symptoms of aki

A

-dry mouth, thirst, lightheadedness, rash, pericardial rub, asterixis

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35
Q

admitting dx & pmx

A
  • pre-existing ckd
  • dm, htn, smoking
  • cvd, ca, trauma
  • pvd, renal artery stenosis, anemia
  • bph, nephrolithiasis
  • infections
  • recent surgery/npo/fluid restriction
  • therapies/tests (cardiac catheterization)
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36
Q

how do you search for causes of renal issues?

A

-strict i&o
-urine output: oliguria < 500 mL/day or <0.3 mL/kg body weight
anuria < 50-100 mL/day
-send UA with micro, urine protein/cr ration (may be affected in AKI) CBC, chem panel
-may need kidney biopsy

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37
Q

hematuria with dysmorphic red blood cells, red blood cell casts, varying degrees of albuminuria goes with what kidney disease

A

proliferative glumerulonephritis (IgA nephropathy, ANCA-assocaited vasculitis, lupus nephritis)

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38
Q

heavy albuminuria with with minimal or absent hematuria goes with what kidney disease

A

acute tubular necrosis in a patient with underlying acute kidney injury

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39
Q

isolated pyuria goes with what kidney disease

A

infection (bacterial, mycobacterial or tubulointerstitial disease)

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40
Q

normal urinalysis with few cells, no casts and no or minimal proteinuria goes with with kidney disease

A

in presence of aki: pre-renal disease, urinary tract obstruction, hypercalcemia, acute phosphate neuropathy, myeloma cast nephropathy

in presence of ckd: ischemic nephropathy, hypertensive nephrosclerosis, urinary tract obstruction, hepato renal disease, cardiorenal disease

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41
Q

how do you make an aki diagnosis?

A
  • pay attention to the timing of potential culprits
  • ensure that patients are not taking their own home meds during the hospital stay (NSAIDs, bactrim)
  • check for previous aki
  • ask if all urine is being measured
  • foley catheter/imaging if concerned for urinary retention
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42
Q

what to do for aki intervention

A
  • early recognition
  • restore adequate fluid balance (maximize cardiac output and renal blood flow)
  • search for causes
  • there is no evidence for lasix use or renal-dose dopamine for renal ‘protection’
  • get a renal consult
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43
Q

intervention for post renal issues

A

renal ultrasound, post void residual, may need foley catheter placement

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44
Q

intervention for pre renal issues

A

fluids/re-establish renal perfusion

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45
Q

intervention for intra-renal issues

A

remove causative agent if possible and prevent further administration

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46
Q

what does fractional excretion of Na+ tell us?

A

<1% is pre renal, interstitial, vasculitis or obstruction

<1% w/o decrease in volume = cirrhosis, severe CHF, contrast nephropathy, acute glomerulonephritis, rhabdo

1-2% mixed and non diagnostic

> 2% acute tubular nephritis
2% w pre renal state: diuretics, severe CRF

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47
Q

pre renal aki?

A
  • look at i/o, history (nausea, diarrhea, poor intake, lightheadedness, dark urine),
  • exam: poor skin turgid, dry mucous membranes, check orthostatic VS
  • can give NS fluid challenge if uncertain, but monitor urine output/fluid status closely
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48
Q

what can cause afferent vasoconstriction?

A
  • nsaid/cox-2 inhibitors
  • contrast
  • amphoterecin B
  • cyclosporine/tacrolimus
  • hypercalcemia
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49
Q

what causes efferent vasoconstriction

A

ace inhibitors/arbs

50
Q

what is the time frame for contrast induced nephropathy

A
  • s cr > 25% or 0.5 w/in 48-72 hours of contrast administration in absence of another alternative etiology
  • usually not oliguric & generally reversible
  • occurs w/in minutes after contrast administration
  • decline that starts within 3-7 days
51
Q

what causes contrast induced nephropathy

A

exact pathogenesis unknown. likely ATN via renal vasoconstriction, direct tubular injury

52
Q

what’s the risk for patients for contrast induced nephropathy

A

very low in patients without risk factors,

-associated w/ long term adverse events for unclear reasons

53
Q

risk factors for contrast induced nephropathy

A

-ckd, diabetic nephropathy, volume depletion, multiple myeloma, CHF, high dose contrast, IA>IV

54
Q

how to prevent contrast induced nephropathy

A
  • identify patients at risk
  • avoid IV/IA contrast
  • avoid nephrotoxins
  • limit contrast dose & exposures
  • patient consent
  • NS 1 ml/kg/hr x 6-12 hours before & after contrast
  • possible statin benefit
55
Q

causes of post renal obstruction

A
  • bilateral obstruction or unilateral if solitary kidney
  • prostate, tumor, clots, stones, medications
  • u/o variable
56
Q

how to diagnose post renal obstruction?

A

ultrasound & post void residuals

57
Q

Rx for post renal obstruction?

A

potentially foley, stent, nephrostomy (depending on findings)

58
Q

infrarenal etiologies

A
  • acute tubular necrosis
  • rhabdomyolysis
  • nephrotoxins
  • infections
  • immunologic
59
Q

what is acute tubular necrosis

A

-ischemic: look for hypotension including intra-operatively

-nephrotoxic:
1. ahminoglycosides (aki during 5-10 days of exposure is usually non-oliguric)
2. amphotericin, foscarnet, cifofovir, pentamidine
-tenofovir, ritonovir, rifampin, cisplatin & other chemo
rhabdomyolysis caused by cocaine, statins, trauma, heavy exercise

60
Q

what will acute tubular necrosis casts look like

A

muddy brown granular casts

61
Q

what is treatment for acute tubular necrosis

A

supportive (avoid hyper K+ & fluid overload)

avoid further injury

62
Q

is vancomycin nephrotoxic?

A

yes.

  • increased nephrotoxicity associated w/ concurrent use of vancomycin & zosyn.
  • monitor throughs & small changes in S Cr.
63
Q

what does medication-induced acute interstitial nephritis look like?

A

fever/rash/eosinophilia not specific/sensitive

may have pyuria (eosnophiluria) wbc casts, peripheral eosinophilia

64
Q

what drugs cause medication-induced acute interstitial nephritis

A 
PCN
cephalosporins
nsaid
cox 2 inhibitors
rifampin
bactrim
diuretics
quinolone
cimetidine
allopurinol
ppo
indinavir
mesalamine
65
Q

treatment for medication-induced acute interstitial nephritis

A

discontinue medication, consider steroid if aki does not resole

66
Q

obstruction & aki in oncology patients

A

retroperitoneal adenopathy, pelvic neoplasms, tumor lysis syndrome, more likely w/ higher tumor burden

67
Q

obstruction & aki in bone marrow transplant patient

A

-sepsis & nephrotoxic antibodies
cyclosporine/tacrolimus->check trough levels
thrombotic microangiopathy 4-12 months after BMT

68
Q

what is tumor lysis syndrome

A

tumor load/chemotherapy causes massive release of intracellular contents

69
Q

risks for tumor lysis syndrome

A

dehydration, ckd

70
Q

treatment for tumor lysis syndrome

A

ivf, alkalinize urine, allopurinol/rasburicase (to treat high uric acid), phosphate bind, HD

71
Q

when should dialysis be started

A

volume overload, uremia, hyperkalemia, extreme acidemia

72
Q

what can cause a high BUN

A

steroid administration, GI bleed, high protein diet,

73
Q

CKD causes

A
  • pre renal (CHF, cirrhosis - from persistently decreased renal perfusion)
  • intrinsic renal vascular disease (nephrosclerosis from HTN, renal artery stenosis)
  • intrinsic tubular & interstitial disease (polycystic kidney disease, nephrocalcinosis)
  • obstruction (prostate disease, metastatic CA)
74
Q

what’s the workout for CKD

A
  • doesn’t have to take place in hospital
  • CMP, CBC, UA, urine protein/creatinine ratio, CK
  • renal US
  • possible serologies: SPEP/UPEP, HIV, HCV, HBV, C3/C4, ANA, ANCA, anti-GBM, ASO
75
Q

considerations for hematuria?

A

foley catheter, trauma, uti, glomerular bleeding, stones, malignancy

76
Q

how is glomerular bleeding suggested?

A

presence of proteinuria, active urine sediment +/- elevated serum cr

77
Q

when should you request cystoscopy

A

if other causes of hematuria have been elxcluded

78
Q

what tests should you think about for hematuria?

A

urine cytology, imaging of kidney & collecting system, may need kidney biopsy

79
Q

who should have a renal biopsy

A
  • evaluate risk/benefit ratio
  • unclear etiology of aki/ckd (including substantial proteinuria even with normal serum cr) or of hematuria in setting of proteinuria/elevated SCr
  • not if kidneys are small/scarred - likely too late to change management
80
Q

medication considerations pre kidney biopsy

A

hold asa, fish oil, nsaid, plavix x 1 week before. hold heparin a few hours before. timing of restarting should be discussed w/ nephrologist.

81
Q

what are risk factors for ESRD

A
  • heritable: race, renal disease
  • DM, htn, aging > 60 yo, autoimmune diseases
  • ca, chf, systemic infection
  • nephrolithiasis, uti
  • previous aki
  • genetics (PKD, alports)
  • med-induced
82
Q

what are causes of nephrotic syndrome?

A
  • DM, SLE, cancer (membranous nephropathy) amyloidosis
  • infection (strep, mono, hepatitis)
  • exposure to allergens or medications
  • genetic or multisystem
83
Q

what is definition of nephrotic syndrome?

A

urinary excretion > 3-3.5 g of protein / day

  • hypoalbuminemia, hyperlipidemia, hypercoagulable
  • edema, weight gain, fatigue, anorexia, foamy urine
84
Q

therapy for nephrotic syndrome

A

control bp, lipids, steroid, low Na diet, avoid high protein intake

85
Q

what is membranous nephropathy

A

inflammation & thickening of structures, protein loss

  • edema, weight gain, faigute, anorexia, foamy UA
  • prognosis correlates w/ severity
86
Q

causes of membranous nephropathy

A

1 is idiopathic

  • toxins (gold, mercury)
  • infections (hep b, syphilis, malaria)
  • medications (nsaids, penicillamine, trimethadione)
  • cancer, sle, ra, graves
87
Q

therapy for membranous nephropathy

A

bp & lipid control, steroids, cytotoxic agents, low Na diet

88
Q

what causes minimal change disease

A
  • idiopathic

- possible hypersensitivy reaction (drug/vaccine), viral illness, tumors

89
Q

minimal change disease characterized by

A

normal histopathology,

edema, weight gain, anorexia, foamy UA

90
Q

older adults & minimal change disease?

A

more aki
severe proteinuria
lower albumin

91
Q

therapy for minimal change disease

A

steroids

cytotoxic agents if needed

92
Q

causes of glomerulonephritis

A

infection (strep throat, endocardtitis, abscess,)

autoimmune (sle, ra, IgA nephropathy)

93
Q

definition of glomerulonephritis

A

rapid onsite & progression, inflammation of renal capillaries & glomerulus

94
Q

characteristic of glomerulonephritis

A

hematuria (rusty), proteinuria, htn, cough, sob, fever, ill feeling, arthralgias

95
Q

therapy for glomerulonephritis

A
  • nephrology consult
  • bp control, steroids/other immunosuppression
  • plasmapheresis
  • low Na diet
96
Q

when should you suspect renal artery stenosis

A

new onset HTN
uncontrolled HTN despite maximal doses of 3 anti-htn agents

abruptly worsening of previously stable htn

aki induced by acei or arb

htn in vasculopaths

asymmetrical kidneys on imagining

97
Q

what are diagnostic options for renal artery stenosis

A

renal artery duplex, ultrasonography, cta (ct angiography), mra (magnetic resonance angiography)

98
Q

therapy for renal artery stenosis

A
  • aggressive control of risk factors
  • angiotensin blockade for renovascular htn
  • lipid & dm control
  • renal artery angioplasty +/- stenting
99
Q

signs/symptoms of ckd

A
  • fatigue/ha/somnolence
  • anorexia, nausea, vomiting
  • pruritis
  • chest pain, sob
  • decreased urination
  • extremities numbness, restless leg, cramping
  • increase bp, arrhythmia
  • sallow pale complexion, bruising, uremic frost
  • jvd
  • pericardial rub
  • crackles on lung exam
  • edema
  • asterixis, myoclonus, change in MS
100
Q

lab abnormalities of ckd

A

-hyperkalemia
-hyperphosphatemia
-hypocalcemia
-metabolic acidosis
hyperuricemia
-elevated pth
-anemia

101
Q

hyperkalemia ecg changes?

A 
peaked t waves
prolonged PR
diminished P waves
widened QRS
prolonged QT
sine wave pattern
102
Q

hyperkalemia reminders

A
  • low K diet
  • remind staff not to give orange juice if the patient is hypoglycemic
  • limit intake of ensure, use nepro instead
103
Q

treatment of hyperkalemia

A
  • calcium glucoante
  • albuterol neb
  • insulin
  • bicarbonate
  • kayexalate
104
Q

things to remember about CKD

A
  • avoidance of potential nephrotoxins
  • avoid sucralfate long term (risk of aluminum toxicity)
  • medication dosing adjustments
  • avoidance of gadolimium, esp if gfr <30, r/f nephrogenic systemic fibrosis
  • hyperphosphatemia is more common once gfr < 45
  • PTH may become elevated even with a mild gfr redution
  • sometimes ckd duration is unknown, so clues may include symptoms, degree of anemia, hyperparathyroidism
105
Q

nutrition related consequences of ckd?

A
  • decreased excretion of nutrients and waste –> electrolyte imbalances (sodium retention - edema, HTN); potassium retention (arrhythmias), metabolic acidosis
  • abnormal metabolism of Ca/PO4 –> bone disease
  • poor appetitie/malnutrition/weight loss
  • anemia (impaired erythropoiesis/low iron stores)
  • cardiovascular disease and mortality
106
Q

goals of nutritional management for ckd

A
  • prevent ckd
  • slow down the rate of ckd progression (diet/lifestyle changes may be of benefit)
  • optimizing nutritional status, including preventing protein-energy malnutrition
107
Q

protein energy malnutrition

A

caused by

  • inadequate food intake (anorexia, nausea, altered taste, concurrent illness, depression, bland diets, excessive restrictions, limited access)
  • catabolic response and chronic inflammation caused by illnesses
  • removal of nutrients by dialysis
  • strong associated w/ morbidity & mortality in CKD
108
Q

what to think about with dialysis patients

A
  • are they truely ESRD?
  • ensure RNs are documenting i/o & weight
  • avoid gadolinum (r/f NSF)
  • caution with nephrotoxins if residual renal function
  • med dosing (Cipro, gabapentin, vanco)
  • no dietary protein restrictions (hd takes off amino acids so don’t want to limit proteins)
109
Q

anemia in esrd

A

chronic anemia

  • typically receive erythropoiesis-stimulating agent
  • oral iron not effective in esrd, typically receive iv iron
  • avoid iv iron in setting of infetion
  • renal vitamins (folate and replace water-soluble vitamins removed from dialysis)
110
Q

renal osteodystrophy

A

vitamin d deficiency & inadequate conversion of vitamin d to active form

  • secondary hyperparathyroidism
  • hyperphosphatemia (associated with negative outcomes) PO4 binders - given w/ meals & dietary PO4 restriction (limit dark sodas, hot dogs
111
Q

HTN in ESRD

A
  • ideal BP is not known, BP may improve w/ volume removal
  • consider holding at least some anti-HTN meds pre-HD if BP tends to drop which limits volume removal
  • Na intake < 2 g / day
  • many anti-HTN meds are removed w/ HD
112
Q

potential complications of kidney disease

A
  • cardiovascular disease
  • pulmonary edema
  • high output CHF
  • pneumothorax after catheter placement
  • pericarditis
  • arrhythmias
  • malnutrition
  • infections
  • avoid PICC in dialysis patients
113
Q

CVD in CKD

A
  • primary cause of death in CKD patients is CVD
  • there is controversy re: statin using in dialysis patients
  • troponin levels may be chronically elevated
114
Q

malnutrition & CKD

A
  • commonly occurs b/c of anorexia, limited food choices, depression, decreased access to optimal foods
  • associated w/ increased inflammation, poor overall outcomes
  • dietitian consult could be helpful
115
Q

AKI causes in elderly?

A
  • sepsis: may be an inflammatory event
  • polypharmacy & drug toxicity: age related changes in renal function & pharmacokinetics increase the risk for toxicities
  • contrast induced nephropathy: risk increases w/ age (& with comorbidities that increase w/ age)
116
Q

aging & the kidney

A
  • the rate of GFR decline w/ age varies widely
  • elderly patients may have decreased thirst response
  • decreased muscle mass may mean a normal creatinine could be abnormal kidney function
117
Q

impact of aging on renal concentrating capacity

A

decrease in tubular water transport in response to arginine vasopressin release leading to decrease response to hyperosmolar and volume deprived conditions

118
Q

impact of aging on renal diluting capacity

A

unclear

may be due to decrease in GFR leading to decrease response to hyperosmolar and volume overloaded conditions

119
Q

impact of aging on acid and ammonium excretion

A

decrease in GFR and renal mass leads to increased susceptibility to metabolic acidosis

120
Q

impact of aging on GFR

A

numerous

increased susceptibility to acute and chronic kidney disease

121
Q

impact of aging on sodium conservation

A

decrease distal tubular Na reabsorption, renin levels & activity & aldosterone levels leading to increased susceptibility to hyponatremia from salt loss caused by excessive diaphoresis, GI losses, etc.

122
Q

impact of aging on sodium excretion

A

decrease in GFR and response to atrial natriuretic peptide leading to percentage of nocturnal sodium load excretion contributing to nocturia, and susceptibility to hypernatremia

Acute Care I - Spring 2017 (10 decks)

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