PubMed · 31615
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H Schütz. 1978-11-28. [Clinical demonstration (author's transl)].. https://pubmed.ncbi.nlm.nih.gov/31615/
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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.
Dopamine infusion, when commenced 24 h after the insult, was ineffective in modifying the course of uranyl nitrate induced renal failure in rabbits.
In 18 patients with acute renal failure and 11 patients with chronic renal insufficiency serum gastrin levels were estimated before and after a test meal. The results were compared with those obtained in a group of 52 healthy subjects. It was stated that patients with acute as well as chronic renal failure display a "physiological" increase of serum gastrin after stimulation by a test meal. In contrast to healthy subjects the post-test meal gastrin curves in patients with chronic and acute renal insufficiency during the anuric/oliguric phase started from significantly higher fasting values. From the results obtained it seems that diminished renal clearance of gastrin by the insufficient kidneys is only partially responsible for the elevated fasting values found in anuric/oliguric patients with acute renal failure or patients with chronic renal insufficiency.