18^th Annual Conference on
Nephrology

Biography:

Shamim Ahmed now working as Professor of Nephrology and Senior Consultant, Kidney Foundation Hospital and Research Institute, Mirpur, Dhaka, Bangladesh. He was former Director and Professor of Nephrology National Institute of Kidney Disease and Urology (NIKDU). He also worked as Professor and Head, Department of Nephrology in Dhaka Medical College and Hospital. He graduated MBBS degree from Dhaka Medical College in 1979. He obtained FCPS (Medicine) degree from BCPS in 1987. He received clinical training in Nephrology for one year in 1992 from PGIMER Chandigarh, India under WHO fellowship. He also completed 13th Especial Foundation Training in 1989 from BATC, Saver. He was awarded FRCP (Edin) in 2003, FRCP (USA) in 2004, FRCP (Glasg) in 2005. He had more than 90 scientific papers published in different journals of home & abroad.  He is life member BRA, BMA, teachers Association of DMC & RMC, BCPS, Kidney Foundation Bangladesh. He is also member of ISN, New York Academy of Science & other organizations. He worked as Asstt. Editor, Bangladesh Renal Journal, editor of TAJ (Joumal of teachers Association RMC). He was Vice President and General Secretary of Bangladesh Renal Association. At present he is member of executive committee of Bangladesh renal Association and treasurer of Kidney Foundation. He attended Scientific conferences in different countries like India, Pakistan, Sri Lanka, Thailand, Singapore, Malaysia, Japan, UK, USA, Brazil, Italy, Sweden & South Africa, France, Germany, Cze Republic, Canada, Philippine, Nepal, Australia, Austria and Turkey. He was honored with Mother Terasha Gold Medal award, Mirror Health award, Netaji Subash Chandro Basu award, Bangabandhu Gold Medal award, Deshpramiksarmana award and Kazi Nazrul Islam sarmanona award by different organizations of the country. 

Abstract:

Normal metabolism of the body produce approximately 15000 mmol of carbon dioxide and 50 to 100 mmol of nonvolatile or fixed acid each day. Acid base balance is maintained by normal elimination of carbon dioxide by lungs and normal excretion of non volatile acid by kidneys. Metabolic acidosis occurs when either an increase in production non volatile acid or increase loss of bicarbonate from the body overwhelms the mechanism of homeostasis or when renal acidification mechanism are compromised. Metabolic acidosis (Chronic) is commonly associated with chronic kidney disease (CKD). The number of functioning nephrons declined in CKD, acid excretion is initially maintained by an increase in ammonium excretion. However total ammonium excretion begin to fall when glomerular filtration rate (GFR) is below 40ml/min. CKD leads to retention of hydrogen ion which is buffered by bicarbonate in the extra cellular fluid, tissue buffer and bone. With worsening of renal function progressive metabolic acidosis and academia develop. Serum bicarbonate concentration is <22meq/L is about 25% patient of non dialysis dependent CKD stage 5. Serum bicarbonate trends to stabilize 12 to 18 meq/L in CKD when GFR is < 10ml/min. Anion gap remains normal until late stage CKD when it begins to widen due to retaining anion such as phosphate and sulfate. The consequences in CKD are bone resorption and osteopenia, increase muscle protein catabolism, aggravation of secondary hyperparathyroidism, reduced respiratory reserve, exhaustion body buffer system, increase severity of acute intercurrent illness, reduce Na-K-ATPase activity in RBC, myocardial cells resulting impair myocardial contractility, producing heart failure, systemic inflammation and hypotension. Endocrine disorder in metabolic acidosis in CKD are resistance to growth hormone and insulin and hypertriglyceridemia. African American Study of Kidney disease (AASK) trial and CRIC observational study in patients of non dialysis depended CKD have found that lower serum bicarbonate concentration, higher net endogenous acid production, higher dietary acid load and inability to excrete acid are all associated with a higher risk of progressive renal function loss. Potential mechanism for progression of CKD is metabolic acidosis promotes increase of ammonium excreted per nephron is associated with activation of complement system, renin angiotensin system with increase production of endothelin which may produce tubulointerstitial inflammation and chronic damage to kidneys. Treatment of metabolic acidosis in CKD are sodium bicarbonate or sodium citrate. In mild acedemia (arterial ph>7.2 ) in asymptomatic adult does not require bicarbonate therapy. KDIGO guideline advocate alkali therapy in patient with CKD in a dose 0.5 to 1mg per/kg/day to maintain target range 23 to 28 meq/L. Sodium citrate should be avoided in patient also taking aluminum containing antacid. Sodium bicarbonate therapy may cause volume expansion and hypertension in CKD patients and raising  ph can precipitate tetany in patient with hypocalcaemia. Bicarbonate supplement appears to slow the progression of CKD, prevent or delay the progression of both osteopenia and hyperparathyroid bone disease and improved nutritional status and lean body mass. In conclusion several but not all studies of patients with chronic metabolic acidosis in CKD have demonstrated bicarbonate therapy improves or decrease the progression of bone disease, normalizes growth, reduce muscle degradation, improves of albumin synthesis and retards progression of CKD. At present recommendation to maintain bicarbonate level 22-23mmol/L in CKD patients.