Case series: coronavirus disease 2019 infection as a precipitant of atypical hemolytic uremic syndrome: two case reports

Background Atypical hemolytic uremic syndrome is an exceedingly rare thrombotic microangiopathy caused by accelerated activation of the alternative complement pathway. Case presentation Here, we report two cases of patients presenting with suspected atypical hemolytic uremic syndrome precipitated by coronavirus disease 2019 infection. The first patient, a 25-year-old Hispanic male, had one prior episode of thrombotic microangiopathy presumed to be atypical hemolytic uremic syndrome precipitated by influenza A, and re-presented with thrombocytopenia, microangiopathic hemolytic anemia, nonoliguric renal failure, and normal ADAMTS13 activity, with confirmed coronavirus disease 2019 positivity. The second patient, a 31-year-old Caucasian female, had no personal history of thrombotic microangiopathy, though reported a family history of suspected atypical hemolytic uremic syndrome. She presented with similar laboratory derangements, oliguric renal failure requiring hemodialysis, and confirmed coronavirus disease 2019 positivity. Both patients were treated with eculizumab with complete resolution of their hematologic and renal complications. Conclusion To our knowledge, this represents the largest case series of atypical hemolytic uremic syndrome precipitated by coronavirus disease 2019 in adults.

Furoemside versus mannitol as a renal protection after adult cardiac surgery

Background Occurrence of acute oliguric renal failure in the immediate postoperative period carries important morbidity and mortality after a successful cardiac surgical procedure. Adult cardiac and aortic surgical procedures are especially prone to this complication with the incidence varying between 2% to 15% and the mortality rate as high as 40% to 60%. Aim of the Work to compare between furosemide versus mannitol as a renal protection after adult cardiac surgery. Patients and Methods This prospective comparative trial was conducted at Academy of Cardiothoracic Surgery Ain Shams University on patients undergoing CABG operation consisting of a total of 50 patients with normal renal function, EF of greater than 40%, normal protein and electrolyte levels. Results the study revealed no statistically significant difference between groups according to cystatin-C Conclusion The difference between patients given mannitol and patients given furosemide regarding urinary microalbumin, urinary creatinine and serum cystatin-c was insignificant. Addition of mannitol to the priming solution of the cardiopulmonary bypass acts as a renal protector against AKI postoperative. Finally, giving furosemide infusion to patients undergoing cardiac surgery at the beginning of the CPB improves renal perfusion.

Incidence of Acute Renal Failure in Full Term Neonates with Birth Asphyxia

Introduction: Birth asphyxia is an eventuality having far reaching consequences in the neonatal period. Hypoxia and ischemia can cause damage to almost every tissue and organ in the body and various target organs involved. Renal insult is a recognized complication of birth asphyxia and carries a poor prognosis. Timely detection of renal dysfunction and appropriate management may favorably alter the prognosis in many neonates with birth asphyxia. Objective: The present study was done to find out the incidence of acute renal failure in the full term neonates with birth asphyxia. Methodology: A cross sectional study was conducted at Birat Medical College Teaching Hospital, Morang, Nepal from 1st September 2017 to 28th February 2018. Fifty full term neonates born with Apgar score of <6 at 5 minutes and fulfilling inclusion criteria were enrolled in the study. Asphyxiated neonates having Serum creatinine >1.5gm/dl or urine output<1ml/kg/hr were labeled as cases of Acute Renal Failure. Blood sample for serum creatinine was collected at 24hrs, 48 hrs and 72 hrs of life. Results A total of 50 term asphyxiated neonates were enrolled in the present study. Among them 54% and 46% were males and females respectively with male to female ratio of 1.2:1. In the present study 62% of cases developed acute renal failure in either of the first three days of life with mean urine output 1.02±0.27ml/kg/hr and mean serum creatinine of 1.49±0.32 mg/dL. The incidence of oliguric renal failure was 52% and non oliguric renal failure was 48%.The association between serum creatinine and urine output was statistically significant. Conclusion: In the present study birth asphyxia has been an important cause of neonatal acute renal injury, revealing 31 (62%) cases. Monitoring urine output and serum creatinine has helped in detecting the asphyxiated neonates with acute renal injury in the early stage.

P. falciparum Malaria induced Renal impairment

Introduction: The involvement of the kidney in falciparum malaria has been known for decades. In 1944, Spitz observed acute renal failure due to falciparum infection in soldiers during World War II. This observation was later supported by other workers who detected oliguria developing in patients with black water fever. The initial clinical pattern is that of reversible renal dysfunction or pre-renal azotemia, which rapidly progresses to acute tubular necrosis if treatment is not started early. Patients with malaria induced renal failure are hypercatabolic with blood urea and serum creatinine levels rising rapidly.Oliguric as well non-oliguric renal failure are observed and duration of oliguric renal failure ranges from a few days to several weeks depending on the severity of renal dysfunction. Acute renal failure in falciparum malaria is usually associated either with acute intravascular haemolysis or heavy parasitemia. Acute renal failure in falciparum malaria is also observed in patients with severe intravascular haemolysis resulting in haemoglobinuria. It may be induced by malarial fever or by anti-malarial drugs in a patient with or without G6-PD deficiency. Materials and Methods: This is a hospital based cross sectional study carried out in a total of 50 cases of acute renal failure who were selected from diagnosed patients of P. falciparum malaria. Cases were confirmed either by P. falciparum antigen test and/or peripheral blood smear test(both thick and thin smear).Malarial ARF (MARF) is diagnosed when serum creatinine level > 3 mg/dl, and/or urine output < 400 ml/24hrs despite adequate rehydration. Result: Out of 174 cases of falciparum malaria 50 patients (28.7%) had acute renal failure in falciparum malaria. 36 (72%) cases were males and 14 (28%) were females, indicating a much higher incidence in males. Approximately 78% of the cases in the present study were below the age of 40 years. The youngest was 15 years old and the oldest was 61 years old (Mean age – 32 ± 11.6 years). All were febrile (100%) and a majority had oliguria or anuria (72%); jaundice was detected in 30 (60%) patients on presentation. Hepatomegaly & Splenomegaly were found in 76% & 66% of the cases respectively. Out of the total 50 cases of malaria induced ARF, 14 cases (28%) had pre-renal ARF while in the majority, 72% the clinical course was that of ATN. The pathogenesis of ATN in the 36 cases was found to be heavy parasitaemia in 40% of the cases, IV hemolysis with haemoglobinuria in 3 (6%) of cases; and cholestatic jaundice in 26% of falciparum patients. Examination of the urinary sediments revealed that albumin was present in urine in 40 cases (80%). Majority of the patients had significant rise in blood urea level with a mean value of 177 mg. S. creatinine levels ranged between 3.2 - 13.6 mg with a mean value of 7.83 mg. The mean creatinine clearance rate was 11.71 ml/min. The overall mortality rate was 26%. Conclusion: AKI is common in Falciparum malaria. The pathogenesis of AKI is largely unknown but may be related to the erythrocyte sequestration and agglutination within the renal microcirculation interfering with flow and metabolism. Clinically and pathologically, this syndrome manifests as Pre-renal azotemia and acute tubular necrosis. Acute renal failure may occur simultaneously with other vital-organ dysfunction (in which case the mortality risk is high) or may progress as other disease manifestations resolve. Early dialysis or hemofiltration considerably enhances the likelihood of a patient’s survival, particularly in acute hypercatabolic renal failure. Severity of oliguria and presence of one or more associated complications like pulmonary oedema, acidosis, and altered sensorium have considerable influence on the outcome of the patients.

PROLONGED PYREXIA WITH ACUTE RENAL INSULT - UNRAVELING THE PUZZLE AND SOLVING THE ENIGMA

A middle aged man with prolonged pyrexia was referred to us with a diagnosis of FUO (Fever of unknown origin). He was evaluated by various investigations and a diagnosis of Tuberculosis was established. On anti tubercular treatment (ATT) he developed complication of acute renal injury –non oliguric renal failure, from which he recovered fully after the puzzle was successfully solved & managed accordingly. Even though he was proved to have rifampicin induced acute intersticial nephritis(AIN) by biopsy , he had varied & unconventional presentation like without oliguria, without peripheral blood eosinophilia, and more so particularly on the maiden administration of rifampicin. Thus our case highlights the importance of quickly establishing the cause for FUO, and also need for greater vigilance on part of physicians to solve unconventional presentations of complications arising out of treatment.