PubMed · 9277745
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I Ishikawa. 1997. [Patchy renal vasoconstriction].. https://pubmed.ncbi.nlm.nih.gov/9277745/
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Early transplant dysfunction and failure because of immunological and nonimmunological factors still presents a significant clinical problem for transplant recipients. A critical unmet need is the noninvasive detection and prediction of immune injury such that acute injury can be reversed by proactive immunosuppression titration. In this study, we used iTRAQ -based proteomic discovery and targeted ELISA validation to discover and validate candidate urine protein biomarkers from 262 renal allograft recipients with biopsy-confirmed allograft injury. Urine samples were randomly split into a training set of 108 patients and an independent validation set of 154 patients, which comprised the clinical biopsy-confirmed phenotypes of acute rejection (AR) (n = 74), stable graft (STA) (n = 74), chronic allograft injury (CAI) (n = 58), BK virus nephritis (BKVN) (n = 38), nephrotic syndrome (NS) (n = 8), and healthy, normal control (HC) (n = 10). A total of 389 proteins were measured that displayed differential abundances across urine specimens of the injury types (p < 0.05) with a significant finding that SUMO2 (small ubiquitin-related modifier 2) was identified as a "hub" protein for graft injury irrespective of causation. Sixty-nine urine proteins had differences in abundance (p < 0.01) in AR compared with stable graft, of which 12 proteins were up-regulated in AR with a mean fold increase of 2.8. Nine urine proteins were highly specific for AR because of their significant differences (p < 0.01; fold increase >1.5) from all other transplant categories (HLA class II protein HLA-DRB1, KRT14, HIST1H4B, FGG, ACTB, FGB, FGA, KRT7, DPP4). Increased levels of three of these proteins, fibrinogen beta (FGB; p = 0.04), fibrinogen gamma (FGG; p = 0.03), and HLA DRB1 (p = 0.003) were validated by ELISA in AR using an independent sample set. The fibrinogen proteins further segregated AR from BK virus nephritis (FGB p = 0.03, FGG p = 0.02), a finding that supports the utility of monitoring these urinary proteins for the specific and sensitive noninvasive diagnosis of acute renal allograft rejection.
BACKGROUND: Three people with clinical manifestations of acute renal failure with neurological involvement of unknown cause were admitted to a hospital in Mumbai, India. We describe clinical presentations and investigations of the cause. METHODS: We analysed case reports and laboratory findings for the patients (age 37-43 years, two men, one woman) that were provided by the clinicians in charge. Serum and cerebrospinal fluid were tested for viral cause by IgM ELISA to Japanese encephalitis, West Nile fever, dengue, and measles. Samples were inoculated in vero-cell culture for virus isolation. The virus isolates were confirmed with indirect immunofluoresence with antimeasles immune sera and mouse monoclonal antibodies to measles HA and F proteins and with neutralisation tests using antimeasles immune sera. FINDINGS: Clinical features were fever, vomiting, oliguria or anuria, bilateral facial weakness, impaired hearing, blindness, proximal and distal areflexic limb paralysis, and respiratory paralysis. No patient had a macropapular rash. Blood urea nitrogen (4.64-27.8 mmol/L) and creatinine (601.1-1105.0 micromol/L) were high, and cerebrospinal fluid contained high concentrations of proteins and pleocytosis. Kidney biopsy samples in two patients showed severe interstitial nephritis. IgM antibodies to measles were found in blood and cerebrospinal fluid. Vero-cell cultures from serum and cerebrospinal fluid of one patient and cerebrospinal fluid of two patients, showed cytopathic effects characteristic of measles. INTERPRETATION: Unusual manifestations of acute renal failure with neurological involvement associated with measles virus in adults presenting without rash was confirmed. Our findings may affect the development of measles-elimination programmes.
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