Author: Cha, Ran-hui; Yang, Seung Hee; Moon, Kyung Chul; Joh, Joon-Sung; Lee, Ji Yeon; Shin, Hyoung-Shik; Kim, Dong Ki; Kim, Yon Su
Title: A Case Report of a Middle East Respiratory Syndrome Survivor with Kidney Biopsy Results Document date: 2016_3_10
ID: rkwz1pwh_24
Snippet: There are several reports about the AKI in H1N1 infected patients. And pathophysiologic mechanism of AKI in H1N1 infected patients are multifactorial including hyperperfusion, re- The kidney tissue samples were co-stained for MERS-CoV (human IgG; green) and dipeptidyl peptidase 4 (DPP 4; red). DPP 4 was primarily stained in proximal tubules (aquaporin-1; violet). The first and second rows indicate the reaction using patient serum 9 weeks after sy.....
Document: There are several reports about the AKI in H1N1 infected patients. And pathophysiologic mechanism of AKI in H1N1 infected patients are multifactorial including hyperperfusion, re- The kidney tissue samples were co-stained for MERS-CoV (human IgG; green) and dipeptidyl peptidase 4 (DPP 4; red). DPP 4 was primarily stained in proximal tubules (aquaporin-1; violet). The first and second rows indicate the reaction using patient serum 9 weeks after symptom onset and the serum from a convalescent plasma donor. The third row is the negative control. nal vasoconstriction, rhabdomyolysis in the setting of severe inflammatory response syndrome. In addition, a report showed viral particles in the glomerulus macrophage cytoplasm and it might be an evidence of circulating virus (17, 18) . The kidney injury in this case may be related to antibiotics, such as colistimethate and tigecycline as high doses of the latter were used to treat MDR AB and MRSA. Acute tubulointerstitial nephritis supports this rationale. However, the interpretation of these results was limited by autolysis of the tissues, and direct renal involvement by MERS-CoV could not be ruled out. In addition, we suggest that the renal pathological changes associated with MERS-CoV may be caused indirectly by a systemic toxic reaction resulting from respiratory failure or a harmful immune response and cytokine reaction induced by viral infection, as well as directly by the cytopathic effect mediated by virus replication. SARS-CoV patients developed AKI at a median duration of 20 days from the onset of infection, which was compatible with the late viremic or the hyperimmune response phase of the infection (19) . The polymerase chain reaction of coronavirus fragments was detected in urine between the second and third weeks of viral infection (14) . One report showed that the MERS-CoV polymerase chain reaction was positive after 3 weeks in the blood (4). 26.7% of the patients in our MERS-CoV cohort (8 patients in a total of 30 patients) showed AKI, and the median time of AKI occurrence was 16 days from the onset of symptoms. The mean urinary PCR was highest approximately 4 weeks after the symptom onset (20) . In this case, urinary protein excretion started to increase in 2 weeks after the onset of symptoms and steadily increased till 5 weeks. And the highest SCr was observed at 5 weeks after symptom onset. The elapsed time from symptom onset to the evidence of kidney injury is compatible with previous reports. We performed urinary MERS-CoV polymerase chain reaction and kidney biopsy too late (6 and 8 weeks after the onset of symptoms) than previous reports because of the general condition of the patient and the fear of in-hospital virus transmission. Direct involvement of the kidneys by MERS-CoV still could not be ruled out.
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