tetano
Editor, Senior Moderator
J Bras Nefrol. 2013 Sep;35(3):185-190.
Acute kidney injury in patients infected by H1N1: clinical histological correlation in a series of cases.
[Article in English, Portuguese]
Sevignani G, Soares MF, Marques GL, Freitas AK, Gentili A, Chula DC, Nascimento MM.
Abstract
INTRODUCTION:
Influenza A (H1N1) virus was first reported on April 2009 and, since then, several studies have reported the characteristics concerning the clinical presentation and pulmonary involvement. However, accurate information about the acute kidney injury (AKI) and kidney histopathological findings in these patients remain scarce.
OBJECTIVE:
To describe the kidney histopathological findings of 6 patients with H1N1 who developed AKI and underwent kidney biopsy, correlating them with clinical features.
METHODS:
We studied six patients admitted to Hospital de Cl?nicas UFPR with a PCR-confirmed diagnosis of H1N1who developed ARF and underwent kidney biopsy. We reviewed their medical file and the microscopy findings of the biopsy.
RESULTS:
Clinical and/or laboratory evidence of AKI was present in all cases, and only one did not present oliguria. Kidney tissues revealed glomerular lesions in two patients: one patient, with systemic lupus erythematosus, showed changes consistent with lupus nephritis class III A-C according to the ISN/RPS 2003 and focal thrombotic microangiopathy; the other one had intercapillary nodular glomerulosclerosis, but without clinical or laboratory evidence of diabetes. Vacuolar degenerative tubular changes were present in all cases, with focus of oxalosis in two cases. Mild to moderate atherosclerosis was found in two patients.
CONCLUSION:
In this study, varying degrees of vacuolar degenerative tubular changes were present in all patients, but there were no signs of acute tubular necrosis. It seems that in the present study a prerenal cause of acute renal failure was the main involved mechanim to explain the cause of renal failure in these patients.
PMID:
24100737
[PubMed - as supplied by publisher]
Free full text
http://www.ncbi.nlm.nih.gov/pubmed/24100737
Acute kidney injury in patients infected by H1N1: clinical histological correlation in a series of cases.
[Article in English, Portuguese]
Sevignani G, Soares MF, Marques GL, Freitas AK, Gentili A, Chula DC, Nascimento MM.
Abstract
INTRODUCTION:
Influenza A (H1N1) virus was first reported on April 2009 and, since then, several studies have reported the characteristics concerning the clinical presentation and pulmonary involvement. However, accurate information about the acute kidney injury (AKI) and kidney histopathological findings in these patients remain scarce.
OBJECTIVE:
To describe the kidney histopathological findings of 6 patients with H1N1 who developed AKI and underwent kidney biopsy, correlating them with clinical features.
METHODS:
We studied six patients admitted to Hospital de Cl?nicas UFPR with a PCR-confirmed diagnosis of H1N1who developed ARF and underwent kidney biopsy. We reviewed their medical file and the microscopy findings of the biopsy.
RESULTS:
Clinical and/or laboratory evidence of AKI was present in all cases, and only one did not present oliguria. Kidney tissues revealed glomerular lesions in two patients: one patient, with systemic lupus erythematosus, showed changes consistent with lupus nephritis class III A-C according to the ISN/RPS 2003 and focal thrombotic microangiopathy; the other one had intercapillary nodular glomerulosclerosis, but without clinical or laboratory evidence of diabetes. Vacuolar degenerative tubular changes were present in all cases, with focus of oxalosis in two cases. Mild to moderate atherosclerosis was found in two patients.
CONCLUSION:
In this study, varying degrees of vacuolar degenerative tubular changes were present in all patients, but there were no signs of acute tubular necrosis. It seems that in the present study a prerenal cause of acute renal failure was the main involved mechanim to explain the cause of renal failure in these patients.
PMID:
24100737
[PubMed - as supplied by publisher]
Free full text
http://www.ncbi.nlm.nih.gov/pubmed/24100737