RESUMEN
BACKGROUND: Granulomatous interstitial nephritis in sarcoidosis (sGIN) is generally clinically silent, but in <1% causes acute kidney injury (AKI). METHODS: This Italian multicentric retrospective study included 39 sarcoidosis-patients with renal involvement at renal biopsy: 31 sGIN-AKI, 5 with other patterns (No-sGIN-AKI), 3 with nephrotic proteinuria. We investigate the predictive value of clinical features, laboratory, radiological parameters and histological patterns regarding steroid response. Primary endpoint: incident chronic kidney disease (CKD) beyond the 1°follow-up (FU) year; secondary endpoint: response at 1°line steroid therapy; combined endpoint: the association of initial steroid response and outcome at the end of FU. RESULTS: Complete recovery in all 5 No-sGIN-AKI-patients, only in 45% (13/29) sGIN-AKI-patients (p=0.046) (one lost in follow-up, for another not available renal function after steroids). Nobody had not response. Primary endpoint of 22 sGIN-AKI subjects: 65% (13/20) starting with normal renal function developed CKD (2/22 had basal CKD; median FU 77 months, 15-300). Combined endpoint: 29% (6/21) had complete recovery and final normal renal function (one with renal relapse), 48% (10/21) had partial recovery and final CKD (3 with renal relapse, of whom one with basal CKD) (p=0.024). Acute onset and hypercalcaemia were associated to milder AKI and better recovery than subacute onset and patients without hypercalcaemia, women had better endpoints than men. Giant cells, severe interstitial infiltrate and interstitial fibrosis seemed negative predictors in terms of endpoints. CONCLUSIONS: sGIN-AKI-patients with no complete recovery at 1°line steroid should be treated with other immunosuppressive to avoid CKD, in particular if males with subacute onset and III stage-not hypercalcaemic AKI.
RESUMEN
A case of transcutaneous diethylene glycol poisoning with severe acute kidney injury, but a positive outcome, is described. A man without significant medical history was admitted to our hospital due to anuria, gastrointestinal symptoms, and hypertension. Ultrasonography excluded vascular damage and postrenal obstruction. Laboratory tests showed acute kidney injury and metabolic acidosis with increased anion gap; hemodialysis therapy was started. The brother of the patient reported that the patient had been smearing his skin with brake fluid containing diethylene glycol to treat a "dermatitis." Only supportive therapy was given due to the lack of a specific antidote. Continuous venovenous hemofiltration was performed. The kidney biopsy showed acute toxic proximal tubulonecrosis, without deposition of oxalate crystals. His neurologic condition worsened dramatically; supportive care was continued. Over time, acute kidney injury and neurologic damage gradually improved; 33 days after admission, he went to a rehabilitation unit for 5 months, with complete clinical recovery. Historically, diethylene glycol has been the cause of large-scale poisonings from ingestion of contaminated drugs. The clinical evolution is unpredictable. Treatment is not well defined; early hemodialysis treatment reduces levels of toxic metabolites, and fomepizole could be useful in cases with an early diagnosis. A comparison of the characteristics of diethylene glycol versus ethylene glycol poisoning is given.