Ust six days after the start of the course, including normal oxaliplatin chemotherapy 34th Laboratory data showed on Anemia, thrombocytopenia, and Azot Chemistry. The patient was transferred to our hours Tal for the treatment of acute renal failure At p Chemistry and mild thrombocytopenia Clofarabine Clolar were present one month before admission to the h Capital. At both Chemistry and thrombocytopenia were only VORG Independent chemotherapy proved ineffective, probably due to the observed suppression of the bone marrow. Before entering the h Capital was the renal function in the normal range despite the presence of An Chemistry and mild thrombocytopenia. On admission, the H Hemoglobin and platelet count strongly to 4.6 g / dl and 50 9 103/mm3 or reduced. In addition, increased Hten serum creatinine and blood urea nitrogen to 8.77 and 86 mg / dl. After the last infusion of oxaliplatin, the patient was not aware of a symptom I am not wrong other than back pain, as Makroh Maturie. At the temperature of our h Capital, blood pressure, respiratory rate, were heart rate, and K Body temperature min 130/80 mmHg, 18 breaths /, 82 key GE per minute and 36.0 C, respectively. Laboratory results showed that the level of lactate dehydrogenase, C-reactive Benazepril RAAS inhibitor protein and urine Acid obtained Ht were. Tables 2 and 3 show the detailed results of blood biochemistry and blood gas analysis and urine on admission. Briefly, serum electrolytes all within normal limits, with the exception of sodium and chloride. The blood gas analysis showed no metabolic acidosis. Degree of urine protein was 0.42 g / g creatinine. No microhardness Maturie was present, but the test for H Moglobinurie yielded positive results.
Urine sediment showed granular casts tube with a small number of white S Blutk Rperchen, red blood rperchen, but not proven. Fractional excretion of sodium and fractional excretion of urea nitrogen were used as 7.95 and 53.8%, calculated in accordance with acute Tubul Rer necrosis. The urine volume was 1000 ml / day for 2 weeks after admission. Non-oliguric AKI was diagnosed intrinsic and was before renal ARF based on the conservation of volume of urine high FE Na and FE UN excluded. Serum haptoglobin was below the detection limit. The blood test showed red rperchen Blutk, H reduced Hemoglobin and platelet count, with no evidence of microangiopathic On Chemistry. Peripheral blood smear showed no schistocytes. No evidence of DIC was clear, with a rate of internationalnormalized normal fibrinogen and activated partial thromboplastin time, w While a slight increase in the concentrations of D-dimers in the presence of light-activatable fibrinolysis. The direct Coombs test was positive, and immunoglobulin G with C3b and C3d were detected on the erythrocytes. The indirect Linezolid Coombs test was also positive. Anti-red blood rperchen Antique Body were positive with a positive DAT and IAT, resulting in a diagnosis of acute on Chemistry druginduced autoimmune h haemolytic. However, there were platelet-Antique Body, rheumatoid factor Of, Antique Glomerular body Ren basement membrane, neutrophil cytoplasmic antibody Rpern and other autoimmune Antique rpern At normal levels. Low positive results, however, was not clinically significant for antinukle Re Antique Body and Antique Body-DNA was undetectable observed. Atrophy, hepatomegaly, splenomegaly, and renal failure.