HbA1c in Diagnosis of Diabetes Mellitus without Ketonuria in Young AdultK Nazimuddin et alhigh risk individuals.HbA1c measurement improvesthe sensitivity of screening in high-risk individuals 6.All these studies support our findings of sensitivityHbA1c as initial test for detection of diabetesmellitus. In this study HbA 1c was shown to have 85%sensitivity (table-4).HbA1c in the diagnosis of diabetes of young caseswithout spontaneous ketonuria showed positivecorrelation with blood glucose and a cut off at 6.5%was 85% sensitive to diagnose diabetes. So HbA1ccan be used as a diagnostic tool with fairly goodsensitivity in our young population.References:1. Allen DW, Schoroeder WA,Balog J.Observations on thechromatographic heterogeneity of normal adult and foetalhuman hemoglobin. Jam Chem Soc 1959;80:1628-34.2. Pickup JC. Diabetic control and it's measurements. In :PickupJC,Williums G,eds.Text book of diabetes.3rd edn.Oxford.Blackwell, 2003. p34.3-34.53.3. Ito C, Maeda R , S,Sasaki H,Harada H . Correlation amongfasting glucose, two hours plasma glucose level in OGTT andHbA1C. Diabetes Res Clin Pract 2000;50:225-30.4. Takahshi Y, Noda M, Tsugane S, Kuzuya T, Ito C,kadowakiT.Prevalence of diabetes estimated by plasma glucose criteriacombined with standered measurement of HbA1c amonghealth check-up participants on Miyako island. Diabetes Care2000; 23: 1092-6.5. Rohlfing CL, Little RR, Wiedmeyer HM, England JD, MadsenR, Harris MI et al. Use of GHb(HbA1C) in screening forundiagnosed diabetes in US population. Diabetes Care2000;23:187-91.6. Perry RC, Shanker RR , Fineberg N, McGill J, Baron AD.Early Diabetes Intervention Program (EDIP). Diabetes Care2001;24:465.103
Angiotensin Converting Enzyme (ACE) inhibitors and Anogiotensin II Receptor Blockers (ARBs)S AhmedREVIEW ARTICLESAngiotensin Converting Enzyme (ACE) inhibitors andAnogiotensin II Receptor Blockers (ARBs) in renal diseaseS AHMEDSummary:Chronic Kidney disease is emerging as a new health problem.Therapy with angiotensin converting enzyme inhibitors (ACEI)and angiotensin II receptor blockers (ARBs) have shownimprovement in patients with hypertension, proteinuria andchronic renal failure. This improvement in GFR, fall in plasmarenin activity (PRA) is due to improved sympathetic activity,improved endothelial function, reduced inflammation orcombination of these factors. Several large scale, prospectiverandomized studies with clinical end point have stronglysuggested that both ACEI or ARBs can slow progression ofchronic glomerulonephritis alone. However, beneficial effect aremuch pronounced in combined group. Both ACEI & ARBs canprevent the progression from microalbuminuria to overtalbuminuria in both type I and type II diabetes. Whenprogression of renal disease is used as end point, protection hasbeen demonstrated with ACEI for type I, but not type II diabetes.In type II only ARB have shown to slow progression to ESRD.Combination of ACEI and ARB is superior than maximum ACEIdose in type I diabetes. Whereas calcium channel blocker (CCB)and ARB combination is better option for type II diabetes.Patients treated with ACEI or ARBs should be monitored forhypertension, decrease GFR and hyperkalaemia. These twodrugs should not be used in pregnancy for risk of foetalabnormality.(J Bangladesh Coll Phys Surg <strong>2004</strong>; 22 : 104-110)Introduction:Angiotensin converting enzyme inhibitors (ACEI)and angiotensin II receptor blockers (ARBs) arecurrently recommended for management andprevention of renal disease. In 1898, Tiegerstedt andBerg man found that crude saline extracts of kidneycontained a pressor substance which is termed renin 1 .Renin exists in both inactive (prorenin) and activerenin form. Active renin is a product primarily if notexclusively of the kidneys. Active renin is formed inthe secretary granules of the juxtaglomerular cellsand renin has a half life of 80 minutes or less in thecirculation. Renin acts on the basic substrateangiotensinogen, circulating (a 2globulin synthesizedin liver to form the decapeptide angiotensin I.Angitensin I is then transformed to the octapeptideangiotensin II by angiotensin coverting enzyme(ACE). Angiotensin II cause deleterious effect suchas vasoconstriction, salt retenion, inflammation,fibrosis and increased oxidative stress. Most of theconverting enzyme that form angiotensin II inAddress for Correspondence : Professor Shamim Ahmed, FCPS,Professor & Head, Dept of Nephrology, Dhaka Medical College &Hospital, Dhaka.circulation is located in the endothelial cellsparticularly the pulmonary vascular endothelium.This angiotensin II was synthesined by Schwyer andBumpus in 1957. Later, ACEI and ARB weredeveloped in the year 1982 & 1988 respectively 2,3 .Factors leading to progressive renal insufficiencyPatients with almost any form of renal disease are atrisk of progressive decline renal functions overvariable period of time. Risk factors are -1) Persistent immune insult to glomerulus ordisease gene abnormality2) Coexisting modifiers of risks like infection,obstruction & drugs to the kidney3) Systemic hypertension and glomerular capillaryhypertension and hyperperfusion leading toenhanced internal traffic of protein & structuralinjury.4) Proteinuria.5) Low number of nephrons caused by congenital oracquired nephropathy,6) Hyperlipidemia,7) Metabolic factors like phosphate, calcium &urate depositon 4 .