PubMed · 9277987
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M Hata. 1997. [Nephropathy associated with solid tumor].. https://pubmed.ncbi.nlm.nih.gov/9277987/
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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.
In two patients, a woman aged 34 and a man aged 38, toxic shock-like syndrome was diagnosed. This is a serious and potentially lethal disease characterized by multiorgan failure, fever, skin lesions and shock and caused by the exotoxin of Streptococcus pyogenes. Both patients had an invasive Lancefield group A beta haemolytic streptococcal infection. The first patient presented with a skin wound at the right knee and later developed shock and thrombosis, in the second a flu-like disease was complicated by respiratory insufficiency, rhabdomyolysis and acute renal insufficiency. Timely recognition of this infection may reduce the risk of complications such as adult respiratory distress syndrome, disseminated intravasal coagulation and necrotizing fasciitis. Both patients eventually recovered after antibiotic and intensive supporting therapy. This infection can be life-threatening and the fatality rate is 15-35% even if patients received appropriate antimicrobial therapy, supportive care, and, where necessary, surgical debridement.
HISTORY AND CLINICAL FINDINGS: A 20 year old, previously healthy woman presented with a four week history of progressive oedema of the legs and the eyelids and a weight gain of 10 kg. INVESTIGATIONS: Biochemical tests revealed a nephrotic syndrome with a protein-loss in urine of 13.6 g/24 hours and a serum-albumin of 1.2 g/dl. Serological tests showed positive response for antinuclear antibodies, anti-double-stranded-DNA antibodies and cardiolipin antibodies. Renal histology revealed a lupus-associated diffuse membranous nephropathy (WHO-type Vd). DIAGNOSIS, TREATMENT AND COURSE: We first started a treatment regimen with oral steroids and intravenous loop-diuretics without improvement of the nephrotic syndrome. Two weeks after initial presentation the patient developed dialysis-dependent, acute renal failure. Having excluded a renal vein-thrombosis and the transition to diffuse proliferative form of the glomerulonephritis we suggested a nephrotic etiology of the acute renal failure. We initiated cyclophosphamide pulse-therapy which led to dramatic improvement of the nephrotic syndrome after the first cycle with reduction of protein-loss to 6 g/24 hours. Concurrently renal function recovered and treatment with hemodialysis could be stopped after 3 weeks. CONCLUSION: Acute renal failure in nephrotic syndrome has also to be considered in an acute form of a membranous lupus nephritis. Renal recovery is much better when acute renal failure is caused by nephrotic syndrome.