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
