Improving acute peritoneal dialysis outcome with use of soft peritoneal dialysis catheter (Cook Mac-Loc Multipurpose Drainage catheter®) among infants < 1500 g in a low resource setting.

BACKGROUND: Despite its utility, uncertainty exists on the feasibility of acute peritoneal dialysis (PD) and optimal PD catheter type for very low birth weight (VLBW < 1500 g) and extremely low birth weight (ELBW < 1000 g) infants. We hereby report our experience of acute PD among these high-risk infants and compare the outcome between stylet-based rigid catheter (SRC) and Cook Mac-Loc Multipurpose Drainage catheters® (CMMDC). METHODS: Case notes of infants < 1500 g undergoing PD between 2012 and 2021 in a network of five participating neonatal units supported by a tertiary paediatric nephrology centre in Kolkata, India, were retrospectively reviewed. PD was conducted either with SRC or after 2018 with CMMDC. Outcome parameters included complications, survival during PD, and survival to discharge. RESULTS: 24 infants (VLBW: n = 13 and ELBW: n = 11) underwent PD at median age 4.5 days (IQR 3-6) with either CMMDC (n = 14) or SRC (n = 10). Significant improvement in biochemical parameters and fluid removal was seen in both ELBW and VLBW infants. CMMDC was associated with significantly fewer PD-related complications 7/14 (50%) vs. 9/10 (90%) (p = 0.04) and higher survival during PD 13/14 (93%) vs. 5/10 (50%) (p = 0.02), without significant difference in survival to hospital discharge 8/14 (57%) vs. 3/10 (30%) (p = 0.25). CMMDC also enabled longer duration of PD, higher ultrafiltration, and better control of acidosis. Consumable cost was higher for CMMDC (USD$60) than SRC (USD$14). CONCLUSIONS: In a low resource setting, CMMDC had lower PD complications and superior short-term survival among ELBW/VLBW infants. A higher resolution version of the Graphical abstract is available as Supplementary information.

Snake bite associated with acute kidney injury.

Acute kidney injury (AKI) is a well-known life-threatening systemic effect of snake envenomation which commonly happens secondary to snake bites from families of Viperidae and Elapidae. Enzymatic toxins in snake venom result in injuries to all kidney cell types including glomerular, tubulo-interstitial and kidney vasculature. Pathogenesis of kidney injury due to snake envenomation includes ischaemia secondary to decreased kidney blood flow caused by systemic bleeding and vascular leakage, proteolytic degradation of the glomerular basement membrane by snake venom metalloproteinases (SVMPs), deposition of microthrombi in the kidney microvasculature (thrombotic microangiopathy), direct cytotoxic action of venom, systemic myotoxicity (rhabdomyolysis) and accumulation of large amounts of myoglobin in kidney tubules. Clinical features of AKI include fatigue, loss of appetite, headache, nausea, vomiting, oliguria and anuria. Monitoring of blood pressure, fluid balance, serum creatinine, blood urea nitrogen and serum electrolytes is useful in managing AKI induced by snake envenomation. Early initiation of anti-snake venom and early diagnosis of AKI are always desirable. Biomarkers which will help in early prediction of AKI are being explored, and current studies suggest that urinary clusterin, urinary neutrophil gelatinase-associated lipocalin, and serum cystatin C may play an important clinical role in the future. Apart from fluid and electrolyte management, kidney support including early and prompt initiation of kidney replacement therapy when indicated forms the bedrock in managing snake bite-associated AKI. Long-term follow-up is important because of chances of progression towards CKD.

Experience with Cidofovir as an adjunctive therapy in a patient of adenovirus-induced macrophage activation syndrome in systemic arthritis.

A 5-year-old female child, with known systemic juvenile idiopathic arthritis diagnosed at 18 months of age (on low dose Prednisolone + Methotrexate + Leflunomide + Tocilizumab), presented with fever for 1 day, vomiting, drowsiness followed by seizures. On admission to PICU, she was drowsy, tachycardic, tachypneic, with rashes, and hepatosplenomegaly. Lab findings showed thrombocytopenia, leucopenia, low ESR, normal CRP, elevated liver enzymes, high ferritin, LDH, and triglycerides suggestive of macrophage activation syndrome (MAS). Chest X-ray showed left basal pneumonia and DNA PCR of throat swab revealed adenovirus. She was diagnosed as adenovirus-triggered MAS and was initiated on pulse methylprednisolone (6 mg/kg). Because of suboptimal response after 2 doses, manifested by increasing drowsiness, further fall in platelets and rising ferritin, methylprednisolone dosage was increased to 30 mg/kg/day with the addition of oral cyclosporine (4 mg/kg/day). In view of worsening of the chest X-ray and increasing oxygen requirement, Cidofovir infusion (1 mg/kg thrice weekly) was also started simultaneously considering increased activity of the adenoviral infection concurrent to immunosuppression. Within 48 h, the child showed signs of recovery with improved consciousness, lower oxygen requirements, and improving lab parameters. She was discharged after 3 weeks of IV Cidofovir, on oral prednisolone and cyclosporine. To the best of our knowledge, this is the first reported use of Cidofovir in adenovirus-induced MAS.