Chronic Kidney Disease Part 2 Flashcards
one or both: abnormalities of ca, phos, PTH, vitamin D metabolism; abnormalities in bone turnover, mineralization, volume, linear growth or strength, vascular or other soft tissue calcification
CKD-MBD
alteration of bone morphology in patients with CKD, one measure of skeletal component
renal osteodystrophy
most important regulator of intestinal absorption of Phos
high dietary Phos
major site of intestinal calcium absorption
duodenum
vitamin D independent nonsaturable pathway
paracellular pahtway
vitamin D dependent, saturable pathway
transcellular pathway
inactivation of CaSR: Calcium and PTH
decrease in Calcium, increase PTH secretion
most important determinant of minute to minute secretion of PTH From stored secretory granules
extracellular concentration of ionized calcium
major source of the circulating levels of calcitriol
kidney
circulating factors that regulate phos excretion
phosphatonins - FGF23 and MEPE
surrogate of bone turnover in patients with CKD
PTH
bone turnover, microarchitecture, microfractures and mineralization
bone quality
alignment of strands of collagen has an irregular woven pattern
osteitis fibrosa cystica
histologically by absence of cellular activity, osteoid formation and endosteal fibrosis
low turnover (adynamic bone disease)
excess of unmineralized osteoid, wide osteoid seams, decreased mineralization rates
osteomalacia
bone biopsies with secondary hyperparathyroidism with mineralization defect: extensive osteoclastic and osteoblastic activity and increased endosteal peritrabecular fibrosis
mixed uremic osteodystrophy
assess the presence or absence of vascular calcification
plain radiographs
Vit D deficiency
less than 10 ng/mL
vit D insufficiency
10-30 ng/mL
decreased stratum corneum hydration and abnormal eccrine gland function
xerosis
mainstay of treatment of xerosis
hydration of skin
skin develops patterned scale with hyperkeratosis and occasionally epidermal hypogranulosis
acquired ichthyosis
most common alteration in pigment of hd patients
yellowish tint
cause of hyperpigmentation
increased melanin production, inc B melanocyte stimulating hormone
perforating folliculitis, Kyrle’s disease, reactive perforating collagenosis
acquired perforating dermatosis
crateriform, umbilicated or centrally hyperkeratotic papules and nodules resolve with scarring after 6-8 weeks
acquired perforating dermatosis
mainstay of treatment of calciphylaxis
supportive and preventive measures
calcium deposits in the tissue
metastatic calcification
trauma may result to
dystrophic calcification
deficiency of uroporphyringogen decarboxylase
porphria cutanea tarda
noninflamed blisters, erosions and crusts in dorsal of hands and forearms, blisters may heal with scarring
porphyria cutanea tarda
subepidermal cleft with minimal inflammation; festooning of the papillary dermis at the base of the celft; thickened vessel walls
porphyria cutanea tarda
IF findings in porphyria cutanea tarda
granular to linear staining of immunoglobulin G and C3 at the dermoepidermal junction
noninflamed blisters on the extremities: hands and forearms and other sun exposed areas
pseudophrphyria
drugs associated with pseudoporphyria
tetracycline, furosemide, naproxen, amoidarone and nalidixic acid
yellowish orange smooth papules and plaques that rapidly appear on buttocks and proximal extremities
eruptive xanthomas
histopathologic findings in eruptive xanthomas
extracellular lipid and foamy macrophages
vascular proliferation near or over an AV shunt
pseudo-kaposi’s sarcoma
ESRD patients who receive intravenous contrast with translucent papulonodular or vegetative lesions
iododerma
marked epidermal hyperplasia with intraepidermal pustules of neutrophils and eosinophils
iododerma
bound down indurated skin, cobblestone apperance, edema and erythema early on; exposure to gadolinium
nephrogenic systemic fibrosis
Histopath: increased dermal and/or subcutaneous fibroblast-like cells
cells stain with procollagen I and CD34
nephrogenic systemic fibrosis
rare complication of fistula construction leading to decreased distal perfusion involving brachial area
dialysis associated steal syndrome
pallor or a reticulated pink to blue discoloration of the skin with necrosis, ulceration or gangrene
dialysis associated steal syndrome
effective treatment of dialysis associated steal syndrome
fistula ligation and/or binding
B2 microglobulin deposition, carpal tunnel syndrome and destructive arthropathy
dialysis related amyloidosis
melanin deposition in the nail bed and plate, proximal white to normal half and a red brown distal half
lindsay’s half and half nail
leukocytoclasia, fibrin thrombi, nonblanching papules and plaques in lower extremities
leukocytoclastic vasculitis
numerous flesh-colored to slightly tan, smooth papules on the face that histopathologically are fibrofolliculomas or trichodiscomas
Birt Hogg Dube syndrome
Birt Hogg Dubb syndrome is associated with what renal findings
renal cell carcinoma
adenoma sebaceum associated with angiomyolipoma
tuberous sclerosis
port wine stain, cysts, clear cell renal cell Ca
VHL syndrome
sebaceous neoplasia, genitourinary carcinoma
muir-torre syndrome
diagnosis of DKD
urine ACR 30 mg/g or higher, eGFR < 60 ml/min
most important risk factor in DM
duration
screening of DKD in type 2 DM is recommended at
time of diagnosis
screening of DKD in type 1 DM is recommended after
5 years of type 1 DM
important predictor of progression of advanced kidney disease, clinical hallmark of diabetes
hyperglycemia
abnormalities in heart rate and vascular dynamics: resting tachycardia and orthostatic hypotension
cardiac autonomic neuropathy
best currently available risk marker for DKD
albuminuria
hallmark of DKD
accumulation of extracellular matrix
early finding in DKD
tubular basement/GB membrane thickening
first lesion detected by light microscopy
mesangial expansion
first lesion identified by electron microscopy
GBM thickening
prominent round expansion of hypocellular mesangial matrix with palisading mesangial cells in the periphery of the nodule surrounded by glomerular capillaries
nodular glomerulosclerosis, kimmelstiel wilson nodules
where can nodular glomerulosclerosis be seen
DKD, light chain deposition disease, immune complex processes, idiopathic nodular glomerulosclerosis
fraying of the mesangial matrix, precursor of nodular lesions
mesangiolysis
subendothelial accumulations of hyaline in the glomerular capillary
fibrin caps
accumulation of hyaline under the parietal epithelial cell lining of Bowman’s capsule
capsular drops
Kidney biopsy in DM patients
sudden onset proteinuria, onset of proteinuria less than 5 years from type 1 DM, proteinuria in absence of retinopathy, AKI, active urinary sediment, hematuria
Class 3 DKD Glomerular lesions
nodular lesions (KWL_ at least one
RAAS blocker of choice: Type 1 DM, Htn, Albuminuria
ACEi
Type 2 DM. htn, microalb RAAS blocker
ARB
Overt DKD
ARB
target Hba1c for prevention of DKD
7%
treatment goal of dyslipidemia
LDL < 70-100
protein intake for DKD
0.8 g/kg/day
DM patients on dialysis with spontaneous resolultion of hyperglycemia with Hba1c less than 6%
Burnt-out DM
screening for anemia should begin at CKD stage
stage 3
EPO is produced in what cells within renal cortex
peritubular interstitial cells, fibroblasts
low hepcidin
iron mobilization
high hepcidin
iron overload
gold standard to monitor patients with iron overload disorders
liver magnetic resonance imaging
decrease ferritin
vitamin C deficiency, hypothyroidism
threshold tsat value below which iron therapy is indicated
20%
dual markers of iron status as well as of nutritional and protein balance
transferrin and TIBC
most sensitive indicator of functional iron deficiency
Retic Hegmoglobin content
reversal agent for LMW and UFH
protamine sulfate
thrombocytopenia 5-10 days after the start of heparin therapy, persistence of any acute thrombotic event, normal platelet count before heparin, trhombocytopenia with no other causes; resolution after heparin cesation; HIT antibody seroconversion
heparin induced thrombocytopenia
first 2 days after exposire to heparin and platelet count normalizes with continued heparin therapy
Type 1 HIT
immune mediated disorder that typically occurs 4-10 days after exposure to heparin and has life and limb threatening thrombotic complications
Type 2 HIT
acute confusional state characterized by recent onset of fluctuating awareness, disorganized thinking, impairment of memory and attention
delirium disorders
syndrome of delirium seen in inadequately treated ESKD - lethargy, confusion and seizures or coma
uremic encephalopathy
headache, visual disturbance, nausea, agitation,
dialysis dysequlibrium
syndrome of progressive dementia related to aluminum intoxication
dialysis dementia
management of chronic cognitive impairment mild to moderate dementia
cholinesterase inhibitors
treatment of moderate to severe Alzheimer’s dementia
Memantine
distal symmetric, mixed sensorimotor polyneuropathy, symmetric muscle weakness, areflexia and loss of vibratory sense
uremic polyneuropathy
compression or ischemia of the ulnar or median nerves and often dialysis related, amyloidosis or AVF
mononeuropathy
repetitive cessation of respiration during sleep
sleep apnea
apnea associated with continued respiratory effort
obstructive
apnea associated with absence of respiratory effort
central
treatment of sleep apnea
CPAP
urge to move the legs associated with feelings of discomfort or paresthesias
restless leg syndrome
first line therapy for more severe symptoms
levodopa
second line for restless leg syndrome
gabapentin
sudden and repetitive movements of the lower extremities during sleep
periodic limb movements of sleep
