Module 10: Renal Dysfunction Flashcards
what are the main functions of the kidney
- Regulatory function: water and electrolyte (Na, K, Ca, glucose) homeostasis; maintenance of acid/base balance
- excretion of metabolic waste through urine
- hormone secretion: erythropoietin (red blood cell production); activation vitamin D (bone health); renin production (BP regulation)
- metabolic function: metabolism of drugs and endogenous substances
how is kidney function measured
- 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
- creatinine clearance, tends to exceed the true glomerular filtration rate by ~10-20%.
3.
what is GFR
GFR is equal to the sum of the filtration rates in all of the functioning nephrons
how much does the glomeruli filter / day?
180 L /day
what does GFR depend upon?
age, sex, body size. 130 in men, 120 in women
what does serum Cr measure
kidney function. not a marker of kidney injury (there are some, but mostly for research purposes)
how do you estimate ckd stage?
- 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.
when is MDRD formula not accurate?
if GFR > 60 ml/min, or at extreme weights/age.
-not validated if age > 70
CKD-EPI creatinine equation, why deveolped?
in an effort to create a formula more accurate than MDRD formula, especially when actual GFR>60
what does cystatin C equation do?
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
what is good about CKD-EPI creatinine cystatin equation
- 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
what is CKD
-presence of kidney damage:
urinary albumin excretion > 30 mg/day
OR
decreased kidney function - GFR <60
for > 3 months regardless of cause
what distinguishes CKD from AKI
persistence of damage or decreased function for > 3 months
is it normal to have normal creatinine and protein in the urine?
no - should refer to nephrologist.
what is stage 1 of CKD
gfr: 90+
description: normal kidney function but urine findings or structural abnormalities or genetic trait point to kidney disease
treatment: observation, control BP
what is stage 2 ckd
gfr: 60-89
description: mildly reduced kidney function, other findings that point to kidney disease
treatment: observation, control BP & other risk factors
what is stage 3A ckd
gfr: 45-59
description: moderately reduced kidney function
treatment: observation, control BP & risk factors
what is stage 3b ckd
gfr: 30-44
description: moderately reduced kidney function
treatment: observation, control BP & risk factors
what is stage 4 ckd
gfr: 15-29
description: severely reduced kidney function
treatment: planning for esrd
what is stge 5 ckd
gfr: < 15; or on dialysis
description: very severe; or end stage kidney failure/established renal failure
treatment: dialysis
what is definition of chronic kidney disease
2 samples at least 90 days apart.
what was acute kidney injury formerly called?
acute renal failure
what is aki?
rise in serum creatinine or decline in urine output that has developed within hours to days
criteria for aki?
- 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.
should you assume that admission Cr is the baseline
no, may have an AKI on admission
epidemiology of aki
- incidence varies
- more common in hospitalized elders
- very common in icu patients
- associated w/ high mortality
- may have progressive kidney dysfunction after severe aki.
risk factors for aki
- 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
aki prevention/consideration
- 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.
3 causes of aki
pre-renal
intra renal
post renal
pre renal aki
sudden and severe drop in BP (shock) or interruption of blood flow to the kidneys from severe injury or illness
intra renal aki?
direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply
post renal aki?
sudden obstruction of urine flow d/t enlarged prostate, kidney stones, bladder tumor, injury
important clues for aki
- age
- race
- family history
- occupation
- allergies
- medications
signs / symptoms of aki
-dry mouth, thirst, lightheadedness, rash, pericardial rub, asterixis
admitting dx & pmx
- 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)
how do you search for causes of renal issues?
-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
hematuria with dysmorphic red blood cells, red blood cell casts, varying degrees of albuminuria goes with what kidney disease
proliferative glumerulonephritis (IgA nephropathy, ANCA-assocaited vasculitis, lupus nephritis)
heavy albuminuria with with minimal or absent hematuria goes with what kidney disease
acute tubular necrosis in a patient with underlying acute kidney injury
isolated pyuria goes with what kidney disease
infection (bacterial, mycobacterial or tubulointerstitial disease)
normal urinalysis with few cells, no casts and no or minimal proteinuria goes with with kidney disease
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
how do you make an aki diagnosis?
- 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
what to do for aki intervention
- 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
intervention for post renal issues
renal ultrasound, post void residual, may need foley catheter placement
intervention for pre renal issues
fluids/re-establish renal perfusion
intervention for intra-renal issues
remove causative agent if possible and prevent further administration
what does fractional excretion of Na+ tell us?
<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
pre renal aki?
- 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
what can cause afferent vasoconstriction?
- nsaid/cox-2 inhibitors
- contrast
- amphoterecin B
- cyclosporine/tacrolimus
- hypercalcemia
what causes efferent vasoconstriction
ace inhibitors/arbs
what is the time frame for contrast induced nephropathy
- 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
what causes contrast induced nephropathy
exact pathogenesis unknown. likely ATN via renal vasoconstriction, direct tubular injury
what’s the risk for patients for contrast induced nephropathy
very low in patients without risk factors,
-associated w/ long term adverse events for unclear reasons
risk factors for contrast induced nephropathy
-ckd, diabetic nephropathy, volume depletion, multiple myeloma, CHF, high dose contrast, IA>IV
how to prevent contrast induced nephropathy
- 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
causes of post renal obstruction
- bilateral obstruction or unilateral if solitary kidney
- prostate, tumor, clots, stones, medications
- u/o variable
how to diagnose post renal obstruction?
ultrasound & post void residuals
Rx for post renal obstruction?
potentially foley, stent, nephrostomy (depending on findings)
infrarenal etiologies
- acute tubular necrosis
- rhabdomyolysis
- nephrotoxins
- infections
- immunologic
what is acute tubular necrosis
-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
what will acute tubular necrosis casts look like
muddy brown granular casts
what is treatment for acute tubular necrosis
supportive (avoid hyper K+ & fluid overload)
avoid further injury
is vancomycin nephrotoxic?
yes.
- increased nephrotoxicity associated w/ concurrent use of vancomycin & zosyn.
- monitor throughs & small changes in S Cr.
what does medication-induced acute interstitial nephritis look like?
fever/rash/eosinophilia not specific/sensitive
may have pyuria (eosnophiluria) wbc casts, peripheral eosinophilia
what drugs cause medication-induced acute interstitial nephritis
PCN cephalosporins nsaid cox 2 inhibitors rifampin bactrim diuretics quinolone cimetidine allopurinol ppo indinavir mesalamine
treatment for medication-induced acute interstitial nephritis
discontinue medication, consider steroid if aki does not resole
obstruction & aki in oncology patients
retroperitoneal adenopathy, pelvic neoplasms, tumor lysis syndrome, more likely w/ higher tumor burden
obstruction & aki in bone marrow transplant patient
-sepsis & nephrotoxic antibodies
cyclosporine/tacrolimus->check trough levels
thrombotic microangiopathy 4-12 months after BMT
what is tumor lysis syndrome
tumor load/chemotherapy causes massive release of intracellular contents
risks for tumor lysis syndrome
dehydration, ckd
treatment for tumor lysis syndrome
ivf, alkalinize urine, allopurinol/rasburicase (to treat high uric acid), phosphate bind, HD
when should dialysis be started
volume overload, uremia, hyperkalemia, extreme acidemia
what can cause a high BUN
steroid administration, GI bleed, high protein diet,
CKD causes
- 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)
what’s the workout for CKD
- 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
considerations for hematuria?
foley catheter, trauma, uti, glomerular bleeding, stones, malignancy
how is glomerular bleeding suggested?
presence of proteinuria, active urine sediment +/- elevated serum cr
when should you request cystoscopy
if other causes of hematuria have been elxcluded
what tests should you think about for hematuria?
urine cytology, imaging of kidney & collecting system, may need kidney biopsy
who should have a renal biopsy
- 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
medication considerations pre kidney biopsy
hold asa, fish oil, nsaid, plavix x 1 week before. hold heparin a few hours before. timing of restarting should be discussed w/ nephrologist.
what are risk factors for ESRD
- heritable: race, renal disease
- DM, htn, aging > 60 yo, autoimmune diseases
- ca, chf, systemic infection
- nephrolithiasis, uti
- previous aki
- genetics (PKD, alports)
- med-induced
what are causes of nephrotic syndrome?
- DM, SLE, cancer (membranous nephropathy) amyloidosis
- infection (strep, mono, hepatitis)
- exposure to allergens or medications
- genetic or multisystem
what is definition of nephrotic syndrome?
urinary excretion > 3-3.5 g of protein / day
- hypoalbuminemia, hyperlipidemia, hypercoagulable
- edema, weight gain, fatigue, anorexia, foamy urine
therapy for nephrotic syndrome
control bp, lipids, steroid, low Na diet, avoid high protein intake
what is membranous nephropathy
inflammation & thickening of structures, protein loss
- edema, weight gain, faigute, anorexia, foamy UA
- prognosis correlates w/ severity
causes of membranous nephropathy
1 is idiopathic
- toxins (gold, mercury)
- infections (hep b, syphilis, malaria)
- medications (nsaids, penicillamine, trimethadione)
- cancer, sle, ra, graves
therapy for membranous nephropathy
bp & lipid control, steroids, cytotoxic agents, low Na diet
what causes minimal change disease
- idiopathic
- possible hypersensitivy reaction (drug/vaccine), viral illness, tumors
minimal change disease characterized by
normal histopathology,
edema, weight gain, anorexia, foamy UA
older adults & minimal change disease?
more aki
severe proteinuria
lower albumin
therapy for minimal change disease
steroids
cytotoxic agents if needed
causes of glomerulonephritis
infection (strep throat, endocardtitis, abscess,)
autoimmune (sle, ra, IgA nephropathy)
definition of glomerulonephritis
rapid onsite & progression, inflammation of renal capillaries & glomerulus
characteristic of glomerulonephritis
hematuria (rusty), proteinuria, htn, cough, sob, fever, ill feeling, arthralgias
therapy for glomerulonephritis
- nephrology consult
- bp control, steroids/other immunosuppression
- plasmapheresis
- low Na diet
when should you suspect renal artery stenosis
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
what are diagnostic options for renal artery stenosis
renal artery duplex, ultrasonography, cta (ct angiography), mra (magnetic resonance angiography)
therapy for renal artery stenosis
- aggressive control of risk factors
- angiotensin blockade for renovascular htn
- lipid & dm control
- renal artery angioplasty +/- stenting
signs/symptoms of ckd
- 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
lab abnormalities of ckd
-hyperkalemia
-hyperphosphatemia
-hypocalcemia
-metabolic acidosis
hyperuricemia
-elevated pth
-anemia
hyperkalemia ecg changes?
peaked t waves prolonged PR diminished P waves widened QRS prolonged QT sine wave pattern
hyperkalemia reminders
- low K diet
- remind staff not to give orange juice if the patient is hypoglycemic
- limit intake of ensure, use nepro instead
treatment of hyperkalemia
- calcium glucoante
- albuterol neb
- insulin
- bicarbonate
- kayexalate
things to remember about CKD
- 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
nutrition related consequences of ckd?
- 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
goals of nutritional management for ckd
- prevent ckd
- slow down the rate of ckd progression (diet/lifestyle changes may be of benefit)
- optimizing nutritional status, including preventing protein-energy malnutrition
protein energy malnutrition
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
what to think about with dialysis patients
- 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)
anemia in esrd
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)
renal osteodystrophy
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
HTN in ESRD
- 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
potential complications of kidney disease
- cardiovascular disease
- pulmonary edema
- high output CHF
- pneumothorax after catheter placement
- pericarditis
- arrhythmias
- malnutrition
- infections
- avoid PICC in dialysis patients
CVD in CKD
- primary cause of death in CKD patients is CVD
- there is controversy re: statin using in dialysis patients
- troponin levels may be chronically elevated
malnutrition & CKD
- 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
AKI causes in elderly?
- 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)
aging & the kidney
- 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
impact of aging on renal concentrating capacity
decrease in tubular water transport in response to arginine vasopressin release leading to decrease response to hyperosmolar and volume deprived conditions
impact of aging on renal diluting capacity
unclear
may be due to decrease in GFR leading to decrease response to hyperosmolar and volume overloaded conditions
impact of aging on acid and ammonium excretion
decrease in GFR and renal mass leads to increased susceptibility to metabolic acidosis
impact of aging on GFR
numerous
increased susceptibility to acute and chronic kidney disease
impact of aging on sodium conservation
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.
impact of aging on sodium excretion
decrease in GFR and response to atrial natriuretic peptide leading to percentage of nocturnal sodium load excretion contributing to nocturia, and susceptibility to hypernatremia
