case_images: PMC8387732_01
case_images: Carbon dioxide angiography performed at 4.5 months post-transplant demonstrates two transplant renal arteries (R1 and R2) which were 4 mm apart on the donor aortic patch. The caudal renal artery (R2) was divided into two branches. A: A high-grade stenosis or kink at the level just distal to the anastomosis of the cephalad renal artery (R1) and wide patent of the caudal renal artery (R2). B: A marked improvement and more brisk flow through to cephalad renal artery (R1) into the kidney allograft after a 2.5 mm x 2 cm Ultraverse balloon angioplasty at the level of the stenosis.
case_images: CNCS-9-093-01.jpg
case_images: PMC8387732_01_CNCS-9-093-01.jpg
case_images: Figure1
case_images: Only cephalad renal artery with high-grade stenosis at the level just distal to the anastomosis was successfully intervened by CO2 balloon angioplasty and the caudal renal artery was wide patent (Figure 1).
case_images: Abdomen and pelvis CT scan with contrast on hospital day 9 revealed abnormal, heterogeneous parenchymal enhancement of the transplant kidney allograft with multifocal, peripherally located areas of nonenhancement with an appearance suggestive of multiple renal infarcts (blue arrows). No hydronephrosis (1A: cross-sectional view, 1B: coronal view, and 1C: sagittal view).
case_images: CNCS-9-093-02.jpg
case_images: PMC8387732_01_CNCS-9-093-02.jpg
case_images: Figure2
case_images: Transplant kidney ultrasound with color Doppler duplex on hospital day 13 revealed no flow detected in the upper and mid poles of transplant kidney allograft. Lower pole parenchyma demonstrates low resistive waveform, which may be related to ischemia (2A: upper pole, 2B: mid pole, and 2C: lower pole).
case_images: CNCS-9-093-03.jpg
case_images: PMC8387732_01_CNCS-9-093-03.jpg
case_images: Figure3
case_images: U/S showed no flow in the mid and upper pole of allograft and low resistive waveform in the lower pole parenchyma (Figure 3).
case_images: Figure 4. Explanted allograft kidney demonstrated diffuse thrombotic microangiopathy (TMA) with extensive cortical infarction. (A) Extensive glomerular, arteriolar, and interlobular artery thrombosis (B) Extensive cortical necrosis (C) Interlobar artery thrombosis (H & E stained sections). (D) Fibrinogen staining of arterial thrombosis. (E, F) Electron micrographs of glomerular capillary loops involved by thrombosis. Dysmorphic red blood cells and fibrin tactoids distend capillary loops. Endothelial cells are denuded from basement membranes. Podocyte foot processes are detached. Light microscopy and immunofluorescence microscopy images are x 400.
case_images: CNCS-9-093-04.jpg
case_images: PMC8387732_01_CNCS-9-093-04.jpg
case_images: Figure4
case_images: No viral particles were present in any compartment (Figure 4).
case_images: Clinical course during hospitalization relating to different biomarkers. AF = atrial fibrillation; Cr = serum creatinine; CVVHDF = continuous venovenous hemodiafiltration; hsCRP = high-sensitive c-reactive protein; hsTrop-I = high-sensitive Troponin I; LDH = lactate dehydrogenase; VF = ventricular fibrillation.
case_images: CNCS-9-093-05.jpg
case_images: PMC8387732_01_CNCS-9-093-05.jpg
case_images: Figure5
case_images: Clinical course and biomarkers indicating thrombotic risk and inflammation related to COVID-19 are shown in Figure 5.