Vakrani Girish P, Nambakam Tanuja
Department of Nephrology, Vydehi Institute of Medical Sciences and Research Centre, #82, EPIP Area, Whitefield, Bengaluru 560066, Karnataka, India.
Department of General Medicine, Vydehi Institute of Medical Sciences and Research Centre, #82, EPIP Area, Whitefield, Bengaluru 560066, Karnataka, India.
Int J Nephrol. 2021 Jun 4;2021:6682838. doi: 10.1155/2021/6682838. eCollection 2021.
Cholera is gastroenteritis caused by . It presents with vomiting, severe secretory diarrhoea, and dehydration. It can cause severe complications with severe electrolyte imbalances and oligoanuric acute kidney injury due to acute tubular necrosis secondary to dehydration or infection itself. However, cholera presenting with significant proteinuria and acute kidney injury has not been reported. Hence, this study was conducted. This aim of this study was to assess clinical features, treatment, and prognosis of AKI in cholera patients; to correlate proteinuria with AKI in cholera patients; and to compare cholera patients with normal kidney function and those with AKI. . It was a retrospective observational study involving patients with cholera. Information regarding cholera patients with acute kidney injury, proteinuria, and prognosis were collected.
Most of the patients had significant vomiting, moderate-to-severe diarrhoea, dehydration, and hypovolaemic shock. Cholera caused severe complications such as severe electrolyte imbalances including hyponatraemia and hypokalaemia, acute kidney injury, and proteinuria secondary to dehydration or infection. A surprising finding noted was the lack of significant association between the onset of acute kidney injury and usual risk factors such as hypovolaemic shock and dehydration. It was found that proteinuria had influenced the onset of acute kidney injury, but it did not influence recovery. As there was complete recovery in kidney function, none of the cases required kidney biopsy. There was no mortality noted.
This study points towards the rare occurrence of proteinuria and acute kidney injury in infection with spontaneous remission of kidney disease with appropriate therapy.
霍乱是由[病原体未提及]引起的肠胃炎。其症状表现为呕吐、严重的分泌性腹泻和脱水。它可导致严重并发症,出现严重的电解质失衡以及因脱水或感染本身继发急性肾小管坏死而引起的少尿性急性肾损伤。然而,霍乱伴有大量蛋白尿和急性肾损伤的情况尚未见报道。因此,开展了本研究。本研究的目的是评估霍乱患者急性肾损伤的临床特征、治疗及预后;探讨霍乱患者蛋白尿与急性肾损伤的相关性;比较肾功能正常的霍乱患者与急性肾损伤患者。这是一项涉及霍乱患者的回顾性观察研究。收集了有关急性肾损伤、蛋白尿及预后的霍乱患者的信息。
大多数患者有严重呕吐、中重度腹泻、脱水和低血容量性休克。霍乱引发了严重并发症,如包括低钠血症和低钾血症在内的严重电解质失衡、急性肾损伤以及脱水或感染继发的蛋白尿。一个令人惊讶的发现是,急性肾损伤的发生与诸如低血容量性休克和脱水等常见危险因素之间缺乏显著关联。研究发现蛋白尿影响了急性肾损伤的发生,但不影响恢复。由于肾功能完全恢复,无一例需要进行肾活检。未观察到死亡病例。
本研究表明,在[病原体未提及]感染中,蛋白尿和急性肾损伤罕见发生,经适当治疗后肾病可自发缓解。