Match each post-renal transplant clinical scenario and associated biopsy finding with the primary pathophysiologic mechanism responsible for the graft dysfunction.
- A 45-year-old man, 2 months post-renal transplant, presents with a rising creatinine. Biopsy reveals dense interstitial mononuclear cell infiltrates and severe tubulitis.Direct T-lymphocyte mediated cytotoxicity against donor alloantigens
- A 32-year-old man, 1 month post-transplant, presents with acute graft dysfunction. Biopsy reveals peritubular capillaritis, neutrophils in the microcirculation, and diffuse C4d staining.Binding of donor-specific antibodies to graft endothelium with subsequent complement cascade activation
- A 55-year-old man, 4 years post-transplant, has slowly progressive allograft dysfunction and new-onset hypertension. Biopsy demonstrates nodular hyaline deposits in the afferent arterioles and a striped pattern of tubulointerstitial fibrosis.Chronic dose-dependent afferent arteriolar vasoconstriction leading to ischemic fibrotic damage
- A 38-year-old woman, 6 months post-transplant, develops asymptomatic allograft dysfunction. Urinalysis demonstrates enlarged epithelial cells with irregular nuclei. Biopsy shows intranuclear inclusions in tubular epithelial cells.Reactivation of a latent polyomavirus secondary to intense pharmacological immunosuppression
- A 29-year-old woman, 3 weeks post-transplant for end-stage renal disease, develops generalized edema and a urine protein excretion of . Light microscopy of the graft is unremarkable; electron microscopy shows diffuse podocyte effacement.Direct disruption of the glomerular filtration barrier by a circulating systemic permeability factor
Cevap
The correct matches correlate acute cellular rejection with T-cell cytotoxicity, antibody-mediated rejection with complement activation, calcineurin inhibitor toxicity with arteriolar vasoconstriction, BK virus nephropathy with polyomavirus reactivation, and recurrent FSGS with a circulating permeability factor.
Correct matching relies on correlating the post-transplant timeline and specific histopathologic findings with their underlying pathophysiologic mechanisms. T-cell mediated rejection is definitively identified by tubulitis; antibody-mediated rejection by C4d deposition and capillaritis; calcineurin inhibitor toxicity by arteriolar hyalinosis and striped fibrosis; BK virus by intranuclear inclusions; and recurrent FSGS by immediate heavy proteinuria and podocyte effacement in the absence of immune deposits.
Adım Adım Çözüm
Anahtar Kavram
Pathophysiology and histopathologic differentiation of renal allograft dysfunction