Supplementary Material
Evaluation of kidney functions of the study cohort: All patients were assessed for the presence and development of AKI (AKI) at baseline and during hospitalization. AKI at admission was defined as based on admission serum creatinine≥1.5 mg/dl in the absence of chronic kidney disease [7]. In-hospital kidney injury was defined using the AKIN criteria [7]. Serum creatinine was monitored until death, recovery or a maximum of 14 days. Following discharge, all patients were followed-up after one week and subsequently at 1 month and 3 months. AKI was classified as functional and structural [1]. Functional AKI was further categorized as pre-renal volume responsive or pre-renal volume non-responsive or hepatorenal syndrome (HRS). Pre-renal volume responsive AKI was considered in the presence of recent history of diuretics, gastrointestinal bleed, diarrhea, vomiting or large volume paracentesis, bacterial infections with an initial response (assessed at 2 days) to fluid resuscitation, blood transfusion, withdrawal of diuretics, antibiotics and volume expansion with albumin in the absence of other known causes of AKI. HRS was defined as volume non-responsive AKI after institution of all the above measures [6] which included patients with and without associated bacterial infections. Structural AKI was defined as kidney damage secondary to nephrotoxicity or ATN in the presence of shock (hypovolemic or septic), history of nephrotoxic medications with the presence of granular casts and high urine spot sodium (>40 meq) or microhematuria with 50 RBCs/HPFor proteinuria >500 mg/day and/or urine osmolality under 350 mOsm/kg. -Progression of AKI was defined as progression to higher AKIN stage or requirement of RRT [7,8,]. Peak AKIN stage was defined as the highest AKIN stage reached during the hospital. Resolution of AKI was defined as decrease of serum creatinine to baseline value or less than 1.5mg/dl [7]. MOF was defined as simultaneous presence of two or more organ failures. Patients were managed according to the standard of care [1]
Patients with volume non-responsive AKI were treated with intravenous terlipressin which was administered at a dose of 2mg continuous infusion with dose stepped up to a max of 12 mg/day based on response. Treatment with terlipressin was continued in responders i.e. patients who had AKI resolution (as described) or a maximum of 14 days. Terlipressin non-response was defined as AKI progression, requirement of RRT or discontinuation due to side-effects. Terlipressin was discontinued in case of severe adverse effects and patients were switched to alternative therapy with noradrenaline. Noradrenaline was the first drug of choice in patients with contraindications to terlipressin. Renal replacement therapy was used for patients with severe volume overload, metabolic acidosis, or hyperkalemia unresponsive to standard medical therapy as described.
Urine Microscopy: Fresh urine samples were obtained from the patients and were examined within 1 h. 10ml of urine was centrifuged at 1,500 rpm for 5 min in a standard centrifuge. Samples were examined at low power (×10) and then at high power (×40) on the bright-field microscope. The supernatant was fully decanted; and a small amount of urine which remained with the residue at the bottom of the centrifuge tube was mixed back into solution by gently agitating the tube. A single drop of this was pipetted onto a slide and covered with a cover slip. Polarization microscopy was used for the identification of crystals and casts. Urinary sediment was analyzed for the presence and number of red and white blood cells, renal tubular epithelial cells, granular casts, and hyaline casts which were semi-quantified. Urine sediments were verified by two physicians [9].