Non steroidal anti- inflammatory drugs (NSAIDs) are one of the most commonly used Over the Counter (OTC) drugs. NSAIDs exert their anti- inflammatory effect via Cyclooxygenase (COX) inhibition. Their common adverse effects include gastrointestinal ulcers, cardiac toxicity, bleeding diathesis, allergic reactions and renal complications, with acute kidney injury [2, 3] being the most common form of NSAIDs – induced renal injury. NSAIDs can reduce renal blood flow, cause tubular obstruction through crystal deposition, and induce direct cytotoxicity and cell- mediated immune injury mechanisms leading to the occurrence of AKI [4]. Other manifestations include hypertension, oedema, hyponatremia, hyperkalemia, nephritic syndrome, papillary necrosis and interstitial nephritis. The major signs and symptoms of AKI include swelling on legs, ankles, and around the eyes, fatigue or tiredness, decreased urine output, confusion, lower abdominal pain. These incidences of AKI are mainly determined as per the stage which it was belonged to. Mostly AKI has 3 stages [5] (Table 1). Etiological factors contributing to AKI differs and which includes infections, cardio renal syndrome, drug use, obstructive condition of the urinary tract, dehydration, etc (Figure 1). In this article we report a known case of CLD who developed AKI (Grade III) by taking NSAIDs. Thereby rapidly withdraw the suspected drug which causes the reaction.

Table 1: Staging of Acute Kidney Injury according to current kidney Disease Improving Global Outcomes definition.

CASE REPORT:

A 53-year-old female patient came to the Gastroenterology department for her routine review. On evaluation, serum Creatinine shows acute elevation (4.7mg/dL). She had a past medical history of Chronic Liver Disease (CLD) for 8 months and Hypothyroidism for the past 2 years. And was on medical treatment with TAB. URSODEOXYCHOLIC ACID 300mg, PROTEIN SUPPLEMENTS 30gm, and DIETARY SUPPLEMENTS 500+400mg, HEME IRON POLYPEPTIDES 12mg, TAB. THYROXINE 100mcg. She was admitted to the hospital with the chief complaints of abdominal pain and pedal oedema 8 months back. And show alterations in renal function and thought to be as Hepato Renal Syndrome (HRS). On taking her family and social history, came to know about the intake of ACECLOFENAC and PARACETAMOL tablet for toothache. Thus concluded this case as NSAID induced AKI. She was admitted 12 days in the hospital.  Admission examination showed: Blood pressure of 120/80mmHg, heart rate of 72beats/min, no abnormalities in the auscultation of the lungs, Oxygen saturation at rate of 97 %, no murmur in the heart, pallor positive, no abdominal tenderness. The patient was anaemic. ESR, SGOT, SGPT, ALP, Urinary epithelial cells and pus cells were found to be elevated than normal limits. Albumin level monitored on LFT was below the limit. It is declined to 2.8 mg/dL. Urea (58 mg/dL) and serum Creatinine (4.7mg/dL) on the day of admission was declined. Due to the elevation of urinary pus cells and epithelial cells, urine culture is done and it is sterile. USG of abdomen and pelvis was taken, and it shows mildly coarsened hepatic echo texture with Splenomegaly and bilateral Grade I parenchyma echoes. Serum urea, Creatinine and levels were monitored for 11 days for her hospital stay (Table 2). PTINR was monitored for 4 days (Table 3).

(Table 3): Determination of PTINR value on Day 2, Day 6, Day 7, and Day 8

She was treated with vasopressin agonist (INJ. TERLIPRESSIN 1mg), Proton pump inhibitor (TAB. PANTOPRAZOLE 40mg), Hepatoprotective agent (TAB. UDILIV 300mg), and Rifamycin antibiotic (TAB. RIFAXIMIN 550mg). During nephrologist’s consultation, it was advised to give ALBUMIN – TERLIPRESSIN infusion. So INJ TERLIPRESSIN changed from 1mg Q6H to BD. Also added TAB. SODIUM BICARBONATE 500mg, TAB. FOLIC ACID 5mg, and Inj. ACETYL CYSTEINE 1.2gm, and Inj. HUMAN ALBUMIN was given on daily basis. Potassium and sodium level declination found on the eight day and was corrected with Ivf. NORMAL SALINE 500ml with Inj POTASSIUM CHLORIDE 40mEq. Creatinine levels gradually declined. She was clinically stable and discharged after 12 days of hospital stay.

DISCUSSION:

The aetiology of AKI is conceptually classified into three general categories: Pre-renal, Intra-renal and Post-renal (Table 4) [6]. This patient was admitted with elevated serum Creatinine (4.7mg/dL). The points in favour NSAID induced AKI was reduced urine output, history of taking NSAIDs, declined serum Creatinine. ALBUMIN infusion was given to correct hypoalbuminemia. Patient was admitted for 12 days in the hospital and was clinically better. On twelfth day, her serum Urea and Creatinine were 40 and 2.3 respectively.  Discontinuation of the drug is important in case of drug induced diseases. Cirrhotic patients are more prone to develop drug induced AKI than normal individuals. Here the drug was stopped due to renal impairment. NSAIDs have an inhibitory effect on both COX – 1 and COX – 2, that is enzymes that inhibit Prostaglandin (PG) synthesis. Both forms of this isoenzyme are found in the kidney [7]. Blocking one or both of these enzymes can defect different kidney functions [8,9,10]. COX – 2 derived PGs have profound effects on renal homeostasis, suggesting that selective COX – 2 inhibitors such as CELECOXIB may have the same potential for renal adverse effects as traditional non- selective NSAIDs, especially in clinical situations associated with a renal impairment such as sodium depletion, hypovolemia, cirrhosis, heart failure, Nephrotic syndrome, and CKD.