Acute Renal Failure after Abdominal Trauma: Renal Artery Spasm Hypothesis in Ischemic Infarction in a 12-Year-Old Girl

Posttraumatic renal failure is often due to postischemic renal infarction, caused by identified vascular lesions. In our patient, a 12-year-old girl with acute anuric renal failure requiring hemodialysis after severe abdominal trauma, no vascular lesion or thrombosis was identified. Nevertheless, CT-scan and renal biopsy showed typical lesions of diffuse bilateral renal ischemic necrosis. The main hypothesis is a severe bilateral arterial vasospasm after a blunt abdominal trauma. The patient recovered only partially with persisting chronic renal failure.

P0315SUCCESFUL TREATMENT OF A STRETOCOCCUS-PNEUMONIAE-ASSOCIATED HAEMOLYTIC URAEMIC SYNDROME BY A SHORT COURSE OF ECULZIMAB

Background and Aims Hemolytic uraemic syndrome (HUS) is a known rare complication of Streptococcus pneumonia infections (SP-HUS) and is characterized by microangiopathic hemolytic anemia, thrombocytopenia and renal failure. In adults it is associated with a higher mortality than HUS due to other etiologies. Method Case Report Results A 33-years old female patient with a history of alcohol abuse was referred to hospital with hypotension and symptoms of infection, including high fever and diarrhea, which had occurred since three days. On admission the patient presented with septic shock and was transferred to the intensive care unit. There she showed signs of hemolytic uraemic syndrome, including severe thrombocytopenia (11 Gpt/l), schistocytosis, elevated lactate-dehydrogenase (LDH; max. 2300 U/l), low haptoglobine (<0,3g/l) and acute anuric renal failure with need of continuous renal replacement therapy. Severe confusion and necrotic lesions of the extremities completed the clinical picture. Plasma exchange (PE) was initiated under suspected thrombocytopenic thrombotic purpura (TTP). Under PE the clinical situation did not ameliorate and signs of severe HUS persisted. A total of four PE were realized, TTP was excluded by Factor VIII-ADAMTS13-activity above the diagnostic limit. In the peripheral blood cultures Streptococcus pneumonia was detected, and antimicrobial was deescalated from piperacillin/tazobactam to penicillin G. Under the clinical picture of a persistent severe pneumococcal associated HUS, without clinical benefit of PE, we decided to start therapy with eculizumab, a monoclonal anti-C5-antibody, approved for the therapy of aHUS and with anecdotical evidence of efficacy in SP-HUS. We started with 1200 mg of ECZ, followed by doses of 900 mg weekly with a total of four doses. Under therapy thrombocyte count normalized, renal function ameliorated and dialysis could be discontinued, the levels of haptoglobin and LDH normalized. The patient could be referred to a rehabilitation clinic, where renal function normalized and no further signs of hemolysis were seen three months after discontinuation of therapy under monitoring. The forefoot remained necrotic with need of surgery in future, the ischemic lesions of the hands completely disappeared. Conclusion Eculizumab could provide a therapeutic option of pneumococcal associated HUS. Therapy could be safely discontinued after 1 month under strict monitoring of signs of HUS. Further studies are required to document the benefit of complement blockade therapy in severe forms of SP-HUS.

Profound Hypokalaemia Resulting in Maternal Cardiac Arrest: A Catastrophic Complication of Hyperemesis Gravidarum?

We present a case of a 39-year-old G8P6 Pacific Islander woman who at 15+5 weeks’ gestation had an out-of-hospital cardiac arrest secondary to profound hypokalaemia which was associated with severe hyperemesis gravidarum (HG). Her clinical course after arrest was complicated by a second 5-minute cardiac arrest in the Intensive Care Unit (ICU) (pre-arrest potassium 1.8), anuric renal failure requiring dialysis, ischaemic hepatitis, and encephalopathy and unfortunately fetal demise and a spontaneous miscarriage on day 2 of admission. Despite these complications, she was discharged home 4 weeks later with a full recovery. Following a plethora of inpatient and outpatient investigations, the cause of her cardiac arrest was determined to be profound hypokalaemia. The hypokalaemia was presumed second to a perfect storm of HG with subsequent nutritional deficiencies causing electrolyte wasting, extracellular fluid (ECF) volume reduction, and activation of the renin-angiotensin-aldosterone axis (RAAS). This combined with the physiological changes that promote potassium wasting in pregnancy including volume expansion, increased renal blood flow, increased glomerular filtration rate, and increase in cortisol contributed to the patient having a profoundly low total body potassium level. This diagnosis is further strengthened by the fact that her pre- and post-pregnancy potassium levels were within normal limits in the absence of supplementary potassium. This case highlights the potentially life-threatening electrolyte imbalances that can occur with HG and the importance of recognising the disease, comprehensive electrolyte monitoring, and aggressive management in pregnancy.

Féloldali vese gyűjtőcsatornás daganatának eredményes palliatív kemoterápiás kezelése anuria mellett

The case of a 54-year-old woman is presented. She underwent right sided unilateral nephrectomy for metastatic bilateral renal tumour of the Bellini collecting ducts. Progression of the contralateral tumour resulted in acute complete anuric renal failure. Haemodialysis was started along with palliative gemcitabine (1000 mg/m2)–cisplatine (70 mg/m2) chemotherapy. In parallel, renal function was improving and dialysis could be stopped at the end of the chemotherapy line comprising 6 cycles. Half a year later the patient was lost of uncontrolled local and pulmonary progression. The potentially nephrotoxic cisplatine chemotherapy associated to complex supportive treatment improved the renal function by controlling diffusely infiltrative tumour growth and allowed a survival benefit over one year with active household keeping capacity. Orv. Hetil., 2016, 157(11), 436–439.

What's new in the diagnosis and pathophysiology of thrombotic thrombocytopenic purpura

Severe ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) deficiency causes thrombotic thrombocytopenic purpura (TTP), which is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and the absence of oliguric or anuric renal failure. However, some patients with this constellation of findings do not have ADAMTS13 deficiency, and some patients with ADAMTS13 deficiency have renal failure or relatively normal blood counts. Consequently, many investigators and clinicians have incorporated severe ADAMTS13 deficiency into the case definition of TTP. This change has facilitated the timely initiation of treatment for patients with atypical clinical features who otherwise would not be recognized as having TTP. Conversely, excluding severe ADAMTS13 deficiency focuses attention on the diagnosis and treatment of other causes of thrombotic microangiopathy that require different treatment. The rapid return of ADAMTS13 data is important to make the best use of this information.