Journal of Clinical and Diagnostic Research, 2022 Mar, Vol-16(3): OD01-OD03 1 1 DOI: 10.7860/JCDR/2022/52470.16079 Case Report Internal Medicine Section Immune Complex-Mediated Crescentic Glomerulonephritis CASE REPORT A 33-year-old male with no known co-morbidities presented with chief complaint of fever since one week. Patient was apparently well one week prior to admission and later developed generalised fatigue followed by fever. Fever was insidious in onset, intermittent, low grade with evening rise of temperature and relieved with medication. Two days prior to admission, the fever was continuous, high grade, and was associated with chills and rigors. No history of night sweats, rash, sore throat, or weight loss. He had a history of high coloured urine, burning micturition, decreased urine output and decreased frequency for a week. There was no history of abdominal pain or flank pain. However, he reported a history of facial puffiness, swelling of hands and feet for two days prior to admission. He had history of five episodes of loose stools one day prior to admission. Loose stools were watery in consistency, non blood tinged and non foul smelling. Patient also had one episode of vomiting on the day of admission. Vomitus contained food particles, it was non bilious and non blood tinged. On presentation, patient was conscious and oriented. All vitals like temperature (97°F), pulse rate (87/min), Blood Pressure (140/80 mmHg), Saturation of Peripheral Oxygen (SpO2) (98%) on room air and respiratory rate (18/minute) were within normal limits. General examination revealed facial puffiness with mild swelling of hands and feet. Swelling of the feet was confined to the medial malleolus, pitting in nature. Systemic examination was normal. Routine investigations on the day of admission revealed elevated total counts (14,000 cells/mm 3 ) with normal haemoglobin and platelet count. Renal parameters were deranged {Urea: 46 mg/dL (Normal range: 15-45 mg/dL), Creatinine: 2.40 mg/dL (Normal range: 0.5-1.1 mg/dL)} and hypoalbuminemia (Albumin: 3 g/dL) was present. The urine routine showed albuminuria, 12-15 pus cells, 18-20 Red Blood Cells (RBCs) and granular casts. There was elevated urine protein creatinine ratio of 8.1 (Normal range: 0.1) and elevated 24 hour urinary protein excretion of 4.9 grams in 24 hours. Erythrocyte Sedimentation Rate (ESR) was elevated (90 mm/hour) and C-Reactive Protein (CRP) was negative. Fever profile for dengue, scrub, malaria and typhoid were negative. Lipid profile revealed hypertriglyceridemia (248 mg/dL). Human Immunodeficiency Virus (HIV), Hepatitis B Virus (HBV) and HCV markers were negative. Ultrasonography of abdomen and pelvis showed normal sized kidneys and corticomedullary differentiation was maintained. On admission, patient was provisionally diagnosed with probable infective diarrhoea and AKI. During the hospital stay, since day 2 of admission, the patient had persistent high blood pressure recordings (BP>170/100 mmHg) which were managed with calcium channel blockers (Oral nifedipine 20 mg 8 th hourly). Due to elevated total counts and possible infective aetiology, patient was empirically treated with antibiotics and supportive medication such as intravenous fluids (0.9% normal saline). Due to a history of fever and high coloured urine, statically elevated renal parameters and high blood pressure recordings in the hospital, our differential diagnosis included Acute Glomerulonephritis (AGN). Nephrology opinion was sought and they have advised for renal biopsy. On day 4 of admission, BP continued to be elevated. Repeat renal parameters did not show any improvement (urea: 34 mg/dL and creatinine: 2.58 mg/dL). Total counts were on an improving trend. Blood and urine cultures were sterile. Renal biopsy was performed in strong suspicion of AGN. After the procedure, patient was monitored for hematoma and bleeding manifestations. On day 6 of admission, renal biopsy findings were as follows: Immunofluorescence revealed granular positivity on the capillary loops and focally on the mesangium with C3 (+3) and IgG (+1) positive. No light chain restriction was seen. IgM, IgA and C1q were negative [Table/Fig-1,2]. Light microscopy with Haematoxylin and Eosin stain, special stains like Periodic Acid-Schiff (PAS), Jones methenamine silver and Masson trichrome were done on the renal cortical tissue. Endocapillary hyper cellularity was noted in all glomeruli. Cellular crescents were identified in five out of seven glomeruli. RBC casts were seen in many of the tubules with tubular epithelial cell injury and focal inflammatory infiltrate in the interstitium [Table/Fig-3]. DHRUVI REDDY 1 , SIVA RANGANTHAN GREEN 2 , R HEMACHANDAR 3 Keywords: Acute nephritis, C3 glomerulopathy, Chronic kidney disease, Immunoglobulin, Infection-related ABSTRACT Immune complex-mediated Glomerulonephritis (GN) comprises a group of disorders including Immunoglobulin A (IgA) nephropathy, IgA vasculitis, lupus nephritis, infection-related GN {poststreptococcal, Hepatitis C Virus (HCV)}, and fibrillary GN with polyclonal Ig deposits. Infection-Related Glomerulonephritis (IRGN) is an immune complex-mediated injury which is triggered by an infection other than renal causes. With new evolving histopathological variants such as C3 Glomerulonephritis (C3GN), it can be challenging to consultants in both diagnostic and management aspects in differentiating it from IRGN. It is seen to occur alongside infection in adults with a greater risk of disease progression to End-Stage Renal Disease (ESRD). Here, the authors report a case of 33- year-old male who presented with gastrointestinal and urinary symptoms. Patient was initially diagnosed as infective diarrhea with Acute Kidney Injury (AKI), and on further evaluation, renal biopsy was suggestive of immune-complex mediated crescentic GN. Patient was treated with steroids and there was an improving trend of renal function and positive outcome after treatment, with an overall good prognosis. Aetiology of this immune-complex mediated crescentic GN is however unclear due to similarities between Postinfectious Glomerulonephritis (PIGN) and C3 glomerulopathy pathologically.