Vol 10, Issue 11, 2017 Online - 2455-3891 Print - 0974-2441 DIABETIC NEPHROPATHY AN OBVIOUS COMPLICATION IN LONG TERM TYPE 1 DIABETES MELLITUS: A CASE STUDY JAHIDUL ISLAM MOHAMMAD 1 *, SRIDEVI CHIGURUPATI 2 *, AZLI SHAHRIL OTHMAN 1 , MUHAMMAD ZAHID IQBAL 3 1 Department of Pharmacology, Faculty of Medicine, Cyberjaya University College of Medical Sciences, CUCMS, Cyberjaya, Malaysia. 2 Department of Pharmaceutical Chemistry, Faculty of Pharmacy, AIMST University, Semeling, Bedong, Kedah, Malaysia. 3 Department of Clinical Pharmacy, Faculty of Pharmacy, AIMST University, Semeling, Bedong, Kedah, Malaysia. Email: dr.jahid1980@gmail.com Received: 14 June 2017, Revised and Accepted: 07 August 2017 ABSTRACT Most overwhelming complications of Type 1 diabetes mellitus patients are responsible for complications related to the microvascular system most likely with kidney. In the kidney, hyperglycemia induced microangiopathy resulting not only thickening of the glomerular capillary basement membrane but also to the proliferation of the mesangial matrix and solidifying of the tubular basement membrane. Several biochemical and pathological, factors are concerned for the development of diabetic renal microangiopathy. These include the glomerular hyperperfusion and hyperfiltration, transformed morphology of podocytes accompanies these basement membrane modifications, Type IV collagen augmented synthesis following the hyperglycemia, and increased expression of tissue matrix metalloproteinase. The aim of this case review is to highlight the recent advances in understanding the pathogenesis, diagnosis, the overview and the potential renoprotective therapeutic agents that would prevent the development or the progression of diabetic nephropathy. Keywords: Type 1 diabetesmellitus, Albuminuria, Diabetic nephropathy. INTRODUCTION Diabetic nephropathy (DN) signifies one of the utmost common microvascular problems of Type 1 diabetes mellitus (T1DM) with an increasing frequency worldwide [1]. Which is well-defined as the presence of trace albuminuria followed by a diminished glomerular filtration rate (GFR) [2]. This signifies the inability of kidneys to prevent urinary protein leakage characterizes a significant primary sign of renal impairment in patients with T1DM [3]. One-third of T1DM patient’s progress to DN, on the other hand, this incidence is much lower with T1DM [4]. The most common complications of diabetes include macrovascular and microvascular events likewise-retinopathy induced blindness, heart attack, kidney failure, stroke, and leg amputation [5]. At present antidiabetic drugs are effective but implies very cost burden to the family. Moreover, a lot of cofactors such as patient devotion, education interrelated to diabetes, lifestyle modification, and associated comorbid diseases has an association with glycemic control [6]. The hall mark characteristics of DN is accompanied by numerous histological and functional anomalies, which includes loss of podocyte, thickening of glomerular basement membrane mesangial growth due to increased density of mesangial matrix and hypertrophy of mesangial cells (MCs) and hemodynamic changes in the initiation and progression of diabetic glomerulosclerosis, which resulting interruption and crumbling of the normal glomerular architecture which resulting microaneurysm formation [7]. American Diabetes Association characterized DN based on the extent of albuminuria and GFR. Renal hyperfunction and hypertrophy are categorized by the earliest stage (Stage 1) of DN. In the course of time and with the coexistence of risk factor such as uncontrolled hypertension, and persistent increase in urine albumin excretion (UAE) develops. This stage is called incipient nephropathy (Stage 3) characterized by GFR 30-59 ml/min/1.73 m 2 , UAE>30 mg/day, >20 µg/min, or urine albumin to creatinine ratio (ACR) > 33 mg/g of creatinine. Stage 4 or overt nephropathy (renal failure) characterized as GFR shows a consistent decline (15-29 ml/min/1.73 m 2 ) that becomes distinct with the continuous increase of UAE above 300 mg/day, 200 µg/min, or when urine ACR exceeds 300 mg/g. Stage 5 renal failure or end-stage renal disease signify constant increase of UAE above 300 mg/day and GFR below 15 ml/min/1.73 m 2 [8-10]. CASE REPORT A 37-year-old woman is brought to the emergency department of a hospital with the complaints of unintentional weight loss, confused mental status, and dyspnea since last night. According to the patient, she is a known case of T1DM since her age is 8. It was treated with insulin lispro since diagnosis. Her family transfers to a new place and started an irregular follow-up in the diabetic outpatient care unit. The patient noticed that recently she has lost 5 kg body weight without dieting and has been complaining of fatigue for 2 or 3 weeks. She appeared confused, forgetfulness, carelessness in dress and daily hygiene for the last 3 days. She also observed that her daughter is dyspneic during walking around the house, washing, dressing, and even during eating since last night. 6 months before the admission, the patient also noticed swelling of the face and legs which are associated with scanty micturition during daytime and frequently at night, which disturbs her sleep. For the last 1 month, she noticed gradual swelling of whole body and puffiness of the face, which is more marked after getting up from sleep in the morning. She is hypertensive for past 5 years but no history of allergy or bronchial asthma. She is under medication with insulin lispro and tablet losartan. Her parents are suffering from hypertension with dyslipidemia. However, they denied about diabetes or bronchial asthma. She was experiencing severe emotional trauma because of sudden loss of her 5 years old younger brother. There is no history of fever, abdominal pain, loin pain, itching, joint pain, skin rash, or hematuria. On general examination, the patient is ill looking and pale, with puffy face and baggy eyelids, moderately anemic, pitting edema-present, she appears dehydrated with a dry tongue, loss of skin turgor, no clubbing, jaundice, cyanosis or koilonychia, no lymphadenopathy or thyromegaly, © 2017 The Authors. Published by Innovare Academic Sciences Pvt Ltd. This is an open access article under the CC BY license (http://creativecommons. org/licenses/by/4. 0/) DOI: http://dx.doi.org/10.22159/ajpcr.2017.v10i11.20699 Case Report