PubMed · 5763706
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E P Maynard. 1969-02-27. Renal function and cephalothin.. https://pubmed.ncbi.nlm.nih.gov/5763706/
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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.
Cryotherapy is used as a treatment for nonresectable liver tumors and adenocarcinoma of the prostate. Morbidity and mortality following cryotherapy are generally considered to be infrequent, but a syndrome of multiorgan failure, severe coagulopathy, and disseminated intravascular coagulation following hepatic cryotherapy has been described and referred to as the cryoshock phenomenon. In this study we aimed to assess and describe the incidence and clinical features of the cryoshock phenomenon following cryosurgery from the surveyed experience of a large number of clinical centers and to relate the data to the overall mortality and morbidity of this treatment. A questionnaire was sent to all cryotherapy users (n = 299) of whom we were aware. We requested information on the number of patients treated, the occurrence, and the clinical features of cryoshock and mortality and morbidity following cryotherapy of the prostate or liver. Altogether 134 completed questionnaires were returned (44.8%). Seventy-two centers had experience with hepatic cryotherapy and 62 with prostate cryotherapy. Following hepatic cryotherapy, the phenomenon of cryoshock was observed in 21 of 2173 patients (1%) and was responsible for 6 of 33 perioperative deaths (18.2%). Cryoshock was rare following prostate cryotherapy (2 of 5432 patients, 0.04%) and did not contribute to the overall mortality of 0.06%. Hepatic and prostate cryotherapy are safe. Cryoshock is rare after prostate cryotherapy but occurs in 1% of patients following hepatic cryotherapy. Cryoshock is associated with a high risk of death, being responsible for 18.2% of deaths in this survey. Research regarding the mechanism and possible avoidance of cryoshock is required.
Acute interstitial nephritis with severe acute renal failure is reported following tetracycline treatment in a 22-year-old male medical student. Acute renal failure developed within 48 h of a single repeated tetracycline dose and presented 2 days after taking the drug when there was oliguria, nausea, vomiting and bilateral loin pain without rash and fever. The serum creatinine concentration was 8.6 mg/dl and blood urea nitrogen 84 mg/dl. Examination of the urinary sediment revealed 15-20 RBCs per high-power field, and occasional granular and hyaline casts. Percutaneous renal biopsy performed immediately after admission revealed acute interstitial nephritis with immune complexes along the tubular basement membrane and intact glomeruli and was consistent with type 2 interstitial nephritis. Within 4 days of commencement of steroid treatment and hemodialysis, the urine output started to increase with improvement in serum creatinine and BUN levels and after 2 weeks of therapy hemodialysis was discontinued. He remains well 1 year following his illness with complete normalization of his renal function. Although a number of renal side effects of tetracycline antibiotics have been reported, acute interstitial nephritis is rarely caused by tetracycline treatment having been reported just twice following systemic use of minocycline.