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Immunologically mediated drug-induced acute renal failure.

D Kleinknecht·A Kanfer·L Morel-Maroger·J P Méry
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Abstract

(1) AIN is the most frequent pattern of drug-induced immunologically mediated renal injury. A number of drugs may be responsible for AIN, namely methicillin and other penicillin derivatives, rifampicin, phenindione and sulfonamides. Particular clinical and pathological features often suggest an immune pathogenetic mechanism. IgG anti-TBM and IgE antibodies have been found in only a few cases and it is likely that antibody-mediated and cell-mediated injury may operate in the same patient. (2) Only few examples of drug-induced vasculitis and glomerulonephritis are known, and the pathophysiology of this kind of renal damage is poorly understood.

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Acute Kidney InjuryAntigensBasement MembraneDrug HypersensitivityGlafenineGlomerulonephritisHumansKidneyKidney GlomerulusKidney TubulesMethicillinNephritis, InterstitialPenicillin GPenicillinsPhenindioneRifampinSulfonamidesVasculitisJournal ArticleReview

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D Kleinknecht, A Kanfer, L Morel-Maroger, J P Méry. 1978. Immunologically mediated drug-induced acute renal failure.. https://doi.org/10.1159/000401522

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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.

Acute Kidney Injury↗
PubMed1979

[Serum gastrin in patients with acute kidney failure].

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.

Acute Kidney Injury↗