OncoNephro Flashcards
2nd most common hematologic malignancy
multiple myeloma
unexplained kidney injury that occurs over less than 6 months with FLC concentration of > 1599 mg/L
cast nephropathy
excess light chains precipitate with tamm horsfall protein in the distal tubule
cast nephropathy
diagnostic for cast nephropathy
serum and urine immunofixation and serum flc analysis
Tx for cast nephropathy
volume resuscitation
proteinuria, renal insufficiency, nodular sclerosing glomerulopathy (mesangial and matrix expansion), crea > 4
light chain deposition disease
more uniform mesangial nodules, irregular thickening and double contours of GBM, linear staining of basement membranes with monotypic light chains
light chain deposition disease
pathogenic light chains unfold and deposit as insoluble fibrils within tissues
Amyloid light chain amyloidosis
AKI more common in allogenic vs autologous
allogenic
AKI typically develops in the first 3 weeks
myeloablative hct
aki distributed over the 1st 3 months
nonmyeloablative hct
pathogenesis of gvhd that lead to ckd
direct Tcell damage via cytokine induced inflammation or through CNI therapy
within first few days of hct, preservation of stem cells causing hemolysis
marrow infusion syndrome, hemoglobinuric AKI
tender hepatomegaly, fluid retention with ascites formation and jaundice; fibrous narrowing of small hepatic venules and sinusoids;
sinusoidal occlusion syndrome
hyperdynamic vital signs, oliguria, hyponatremia and low urinary sodium concentration, minimal proteinuria and muddy brown granular casts, fluid retention resistant to diuretics
sinusoidal occlusion syndrome
commonly associated with pretreatment with cyclophosphamide, busulfan, and/or TBI
sinusoidal occlusion syndrome
Endothelial damage leading to thickened glomerular and arteriolar vessels, the presence of fragmented red blood cells, thrombosis, and endothelial cell swelling
transplant associated thrombotic microangiopathy
(+) schistocytes on peripheral smear, elevated LDH ,doubling of crea, unexplained cns dysfunction, negative coombs, thrombocytopenia, anemia, decreased haptoglobulin
transplant associated thrombotic microangiopathy
Tx options of transplant associated microangiopathy
gvhd prophlaxis, tpe, rituximab, defibrotide
converts uric acid to water solluble allantoin decreasing uric acid levels and urinary acid excretion
rasburicase
gradual onset of nonoliguric AKI, direct tubular toxicity in a low Cl environment
cisplatin nephrotoxicity
decrease in gfr in clisplatin nephrotoxicity occurs when?
3-5 days after the exposure
promotion of better DNA repair and elimination of free radicals that can be used in cisplatin
amifostine
apoptosis of renal proximal tubular cells induced resulting in wasting of K, Mg, Ca and HCO3
cisplatin
alkylating drug that causes renal toxicity either directly or through a metabolite, chloroacetaldehyde, which directly damages tubular epithelial cells
ifosfamide
increased urinary B2 microglobulin
ifosfamide
hemorrhagic cystitis but not tubular injury
cyclophosphamide
increased ADH activity causing hyponatremia
cyclophosphamide
prevention of cyclophosphamide nephrotoxicity
MESNA
synthetic sulfhydryl compound that detoxifies metabolites in the urine preventing hemorrhagic cystitis
MESNA
mechanisms of AKI in methotrexate
intrarenal obstruction, direct tubular toxicity, prerenal azotemia due to efferent arteriolar vasoconstriction
medication that can be given to reduce systemic toxicity associated with MTX and AKI
leucovorin high dose
associated with massive proteinuria
Interferon alfa
systemic capillary leak syndrome
IL2
prevention of IL2 induced AKI medication
low dose dopamine
monoclonal Ab against vegf with assoc hypertension and proteinuria
bevacizumab
monocloal Ab against egfr used in metastatic colon Ca, renal Mg wasting
cetuximab
pathology in CNI causing AKI
direct afferent arteriolar vasoconstriction leading to decrease in the GF pressure and GFR
arteriolar damage, interstitial fibrosis, tubular atrophy and glomerulosclerosis
CNI chronic nephrotoxicity
reason for hyperK in CNI
tubular resistance to aldosterone
Tx for hypercalcemia of malignancy
bisphosphonates
most comon pathologic finding on renal biopsy in bisphosphonate toxicity
acute tubular necrosis
highly protein bound, reducing risk of renal toxicity kind of bisphosphonate
ibandronate
monoclonal antibody antiresorptive not cleared by kidney, preferred; may be used in breast/prostate Ca CKD stage 4
denosumab
mean time to achieve normocalcemia with bisphosphonate
4 days
inhibit osteoclastic bone resorption by decreasing tumor production of locally active cytokine
glucocorticoids
pattern of injury in radiation induced AKI
tubular + glomerular
Tx of radiation induced AKI
RAAS blockade
most common malignancies to metastasize in the kidneys
lymphoma and leukemia
criteria to support diagnosis of metastates to kdiney
renal enlargement without obstruction, absence of other causes of kidney disease, rapid improvement of kidney function and RT and chemotherapy
reactive disorder that results from intense macrophage activation and cytokine release
cytotoxic nephropathy/
hemphagocytic syndrome
Suspected in any patient with malignant lymphoma in whom unexplained multiple-organ dysfunction including AKI develops
cytotoxic nephropathy/
hemphagocytic syndrome
definitive diagnosis fro hemophagocytic syndrome
bone marrow aspiration
Tx for Hemophagocytic syndrome
IVIG, TPE, HCT; dexamehtasone and etoposide
when to do TPE for TMA in patients with cancer?
TMA after bone marrow transplantation.
classic drug that can cause thrombotic microangiopathy
mitomycin C
Nonimmune hemolytic anemia, thrombocytopenia, varying degrees of encephalopathy, and renal failure due to platelet thrombi in the microcirculation of the kidneys
thrombotic microangiopathy
better prognosis
papillary renal cell ca
papillary and clear cell came from
proximal tubule
Chromophone renal cell ca
collecting duct
most common benign tumors
angiomyolipoma
oncocytoma
cut off size T1
4-7
T2
7-10
T3
> 10
when to do active surveillance
2 cm or smaller with high operative risk, monitor q3-6 months
post tx surveillance
bet 3-12 months
yearly up to 3 (partial nephrec) and 5 (ablative therapy)
initial immune therapy
interferon alfa and IL2
targets vegf preventing angiogenesis
bevacizumab
seattle criteria 2 of 3: jaundice, painful hepatomegaky, fluid retention or wt gain within 20’days of hsct
sinusoidal obstruction syndrome
