PubMed · 14176460
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A M PARFITT. 1964-07-25. HYPERCALCAEMIC NEPHROPATHY.. https://doi.org/10.5694/j.1326-5377.1964.tb115035.x
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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.
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UNLABELLED: Non-steroidal anti-inflammatory drugs (NSAIDs) are known to have adverse effects on kidney function. Situations with a stimulated renin-angiotensin system such as volume depletion or pre-existing chronic renal failure predispose to acute renal failure (ARF) via inhibition of prostaglandin synthesis by NSAIDs. To date, NSAIDs are frequently used as antipyretic drugs even in situations predisposing to ARF. Within 20 months, seven children presenting with diarrhoea and/or vomiting and fever were treated with therapeutic doses (11.5-32 mg/kg per day) of ibuprofen for 1 to 3 days before developing ARF. Maximum plasma creatinine levels were 180-650 micromol/l. One patient required emergency dialysis for hyperkalaemia, uraemia, and hyperphosphataemia. After cessation of NSAID treatment and rehydration, all patients recovered completely with a normalised creatinine level after 3 to 9 days. Once the acute phase is controlled, long-term outcome is excellent. Interstitial nephritis, another possible adverse effect of NSAIDs, might require steroid treatment and is the major differential diagnosis. Only histological examination can confirm the exact pathomechanism of ARF after NSAID exposure. If immunological events are responsible for the ARF, the recovery period is usually longer. CONCLUSION: non-steroidal anti-inflammatory drugs are potentially dangerous in situations with even moderate volume depletion.