key: cord-0026929-6u6hgaim
authors: Chidambaram, Aakash Chandran; Krishnamurthy, Sriram; Deepthi, Bobbity; Karunakar, Pediredla; Maulik, Kaushik; Peela, Sreeram Chandra Murthy; Sistla, Sujatha; Jinkala, Sree Rekha
title: Severe acute kidney injury in a 3-year-old boy with fever and pleural effusion: Questions
date: 2020-05-28
journal: Pediatr Nephrol
DOI: 10.1007/s00467-020-04583-7
sha: 133d6eb27c76254aec7a2cd059ae725cd1a637bf
doc_id: 26929
cord_uid: 6u6hgaim

nan

sign and Brudzinski's sign were negative. There were no focal neurological deficits. The other systemic examinations were unremarkable.

Supplemental oxygen by mask and intravenous (IV) fluids were administered, and he was admitted to the pediatric intensive care unit (PICU). The chest X-ray revealed left-sided pleural effusion (Fig. 1) . He was started on intravenous ceftriaxone and vancomycin, after obtaining necessary blood samples for investigations (Table 1 ). Blood investigations revealed neutrophilic leukocytosis. Serum creatinine was 0.41 mg/dL at this juncture. A diagnostic pleural tap was done after which intercostal drainage tube was inserted (Fig. 1) . The pleural fluid was sent for gram stain, bacterial culture, and molecular diagnostic tests. Nasopharyngeal swabs for influenza A (including H1N1) and influenza B were negative by realtime polymerase chain reaction (RT-PCR). Other investigational workup for pleural effusion, e.g., IgM immunofluorescence for scrub typhus, microscopic agglutination test for leptospirosis, and Widal test (for enteric fever), were negative. Lumbar puncture was done and meningitis was ruled out. Urinalysis did not show any abnormalities. After 24 h of admission, there was worsening respiratory distress with oxygen desaturation and continued absent air entry on the left side. The child required mechanical ventilation. The blood culture and pleural fluid cultures were negative for any organism.

By the 3rd day of admission, the child had a sudden decline in urine output progressing to complete anuria. This was associated with a sudden drop in hemoglobin from 10.1 to 6.5 g/ dL with thrombocytopenia (60,000/μL), without any evidence of ongoing blood loss (Table 1) . Peripheral smear examinations for schistocytes and reticulocyte count were performed. Serum lactate dehydrogenase (LDH) levels were found to be elevated (4049 U/L). Serum complement levels were normal [C3-94 mg/dL (reference range 80-140 mg/dL); C4-24 mg/ dL (reference range 12-42 mg/dL)] and direct Coombs test (DCT) was positive. The serum aspartate transaminase (AST) and alanine transaminase (ALT) were high (545 U/L and 166 U/L, respectively). The d-dimer and fibrin degradation products (FDP) were negative, and the prothrombin time (PT) and activated partial thromboplastin time (aPTT) were normal. Repeat urinalysis could not be performed, as the child was completely anuric.

Peritoneal dialysis was initiated in view of anuria and washed packed red blood cells were transfused. Despite the ongoing renal replacement therapy (which was transited to sustained low efficiency dialysis (SLED) due to the development of shock), continued mechanical ventilation, and intravenous antibiotics, the child showed no improvement in the ventilator settings and progressed to acute respiratory distress syndrome (ARDS). He subsequently developed catecholamine refractory septic shock, altered sensorium, and remained completely anuric throughout the further course of illness. He died on day 10 of hospital stay. Postmortem biopsy of the kidney was performed (Fig. 2) . 1 a Chest X-ray revealed left-sided pleural effusion. b Diagnostic pleural tap after which intercostal drainage tube was inserted Fig. 2 a, b Postmortem biopsy of the kidney

What are the differential diagnoses of AKI in this case? 2. What are the strategies for the management of AKI in this case? What is the role of performing complement studies and treating with plasma exchanges in this patient?

What could be the reason for complete anuria in this child? What are the histopathological findings in Fig. 2?

Authors' contributors Aakash Chandran Chidambaram, Sriram Krishnamurthy, Bobbity Deepthi, Pediredla Karunakar, and Kaushik Maulik managed the patient, reviewed the literature, and drafted the manuscript. Sriram Krishnamurthy critically revised the manuscript. Sreeram Chandra Murthy Peela and Sujatha Sistla interpreted the microbiological reports. Sree Rekha Jinkala interpreted the histopathological findings. All authors contributed to reviewing of literature and drafting of the manuscript and approved the final version of the manuscript. Sriram Krishnamurthy shall act as the guarantor of the paper.

Conflict of interest The authors declare that they have no conflicts of interest.Publisher's note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.